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  • Cell Line  (341)
  • Chemical Engineering
  • American Association for the Advancement of Science (AAAS)  (342)
  • 2005-2009  (342)
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  • 1
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    Hemagglutinin receptor binding avidity drives influenza A virus antigenic drift (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-11-11
    Description: Rapid antigenic evolution in the influenza A virus hemagglutinin precludes effective vaccination with existing vaccines. To understand this phenomenon, we passaged virus in mice immunized with influenza vaccine. Neutralizing antibodies selected mutants with single-amino acid hemagglutinin substitutions that increased virus binding to cell surface glycan receptors. Passaging these high-avidity binding mutants in naive mice, but not immune mice, selected for additional hemagglutinin substitutions that decreased cellular receptor binding avidity. Analyzing a panel of monoclonal antibody hemagglutinin escape mutants revealed a positive correlation between receptor binding avidity and escape from polyclonal antibodies. We propose that in response to variation in neutralizing antibody pressure between individuals, influenza A virus evolves by adjusting receptor binding avidity via amino acid substitutions throughout the hemagglutinin globular domain, many of which simultaneously alter antigenicity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2784927/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2784927/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hensley, Scott E -- Das, Suman R -- Bailey, Adam L -- Schmidt, Loren M -- Hickman, Heather D -- Jayaraman, Akila -- Viswanathan, Karthik -- Raman, Rahul -- Sasisekharan, Ram -- Bennink, Jack R -- Yewdell, Jonathan W -- GM 57073/GM/NIGMS NIH HHS/ -- U54 GM62116/GM/NIGMS NIH HHS/ -- Z01 AI001014-01/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2009 Oct 30;326(5953):734-6. doi: 10.1126/science.1178258.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19900932" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Neutralizing/immunology ; Antibodies, Viral/immunology ; Antigenic Variation/genetics/*immunology ; Cell Line ; Hemagglutinin Glycoproteins, Influenza Virus/genetics/immunology/*metabolism ; Influenza A Virus, H1N1 Subtype/genetics/*immunology ; Influenza Vaccines/immunology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Models, Immunological ; Mutation ; Receptors, Virus/*metabolism ; Serial Passage
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    Biomedical research. Researchers generally happy with final stem cell rules (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-07-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holden, Constance -- New York, N.Y. -- Science. 2009 Jul 10;325(5937):131. doi: 10.1126/science.325_131.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19589969" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; *Embryo Research/economics ; *Embryonic Stem Cells ; Financing, Government ; *Guidelines as Topic ; Humans ; National Institutes of Health (U.S.) ; Registries ; *Research Support as Topic ; United States
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Pulsatile stimulation determines timing and specificity of NF-kappaB-dependent transcription (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-04-11
    Description: The nuclear factor kappaB (NF-kappaB) transcription factor regulates cellular stress responses and the immune response to infection. NF-kappaB activation results in oscillations in nuclear NF-kappaB abundance. To define the function of these oscillations, we treated cells with repeated short pulses of tumor necrosis factor-alpha at various intervals to mimic pulsatile inflammatory signals. At all pulse intervals that were analyzed, we observed synchronous cycles of NF-kappaB nuclear translocation. Lower frequency stimulations gave repeated full-amplitude translocations, whereas higher frequency pulses gave reduced translocation, indicating a failure to reset. Deterministic and stochastic mathematical models predicted how negative feedback loops regulate both the resetting of the system and cellular heterogeneity. Altering the stimulation intervals gave different patterns of NF-kappaB-dependent gene expression, which supports the idea that oscillation frequency has a functional role.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2785900/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2785900/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ashall, Louise -- Horton, Caroline A -- Nelson, David E -- Paszek, Pawel -- Harper, Claire V -- Sillitoe, Kate -- Ryan, Sheila -- Spiller, David G -- Unitt, John F -- Broomhead, David S -- Kell, Douglas B -- Rand, David A -- See, Violaine -- White, Michael R H -- BB/C007158/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/C008219/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/C520471/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/D010748/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/E004210/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/E012965/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/F005938/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BBC0071581/Biotechnology and Biological Sciences Research Council/United Kingdom -- BBC0082191/Biotechnology and Biological Sciences Research Council/United Kingdom -- BBC5204711/Biotechnology and Biological Sciences Research Council/United Kingdom -- BBD0107481/Biotechnology and Biological Sciences Research Council/United Kingdom -- BBF0059381/Biotechnology and Biological Sciences Research Council/United Kingdom -- G0500346/Medical Research Council/United Kingdom -- G0500346(73596)/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2009 Apr 10;324(5924):242-6. doi: 10.1126/science.1164860.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Cell Imaging, School of Biological Sciences, Bioscience Research Building, Crown Street, Liverpool, L69 7ZB, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19359585" target="_blank"〉PubMed〈/a〉
    Keywords: Active Transport, Cell Nucleus ; Animals ; Cell Line ; Cell Line, Tumor ; Cell Nucleus/metabolism ; Cytoplasm/metabolism ; Feedback, Physiological ; *Gene Expression ; Humans ; I-kappa B Proteins/metabolism ; Mice ; Models, Biological ; Models, Statistical ; NF-kappa B/*metabolism ; Phosphorylation ; Recombinant Fusion Proteins/metabolism ; Stochastic Processes ; Transcription Factor RelA/*metabolism ; *Transcription, Genetic ; Transfection ; Tumor Necrosis Factor-alpha/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Biomedical research. A first step in relaxing restrictions on stem cell research (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-03-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holden, Constance -- New York, N.Y. -- Science. 2009 Mar 13;323(5920):1412-3. doi: 10.1126/science.323.5920.1412.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19286523" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Embryo Research/economics/*legislation & jurisprudence ; *Embryonic Stem Cells ; Financing, Government/legislation & jurisprudence ; Guidelines as Topic ; Humans ; National Institutes of Health (U.S.) ; Pluripotent Stem Cells ; Research Support as Topic/*legislation & jurisprudence ; United States
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Reversal of RNA dominance by displacement of protein sequestered on triplet repeat RNA (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-07-18
    Description: Genomic expansions of simple tandem repeats can give rise to toxic RNAs that contain expanded repeats. In myotonic dystrophy, the expression of expanded CUG repeats (CUGexp) causes abnormal regulation of alternative splicing and neuromuscular dysfunction. We used a transgenic mouse model to show that derangements of myotonic dystrophy are reversed by a morpholino antisense oligonucleotide, CAG25, that binds to CUGexp RNA and blocks its interaction with muscleblind-like 1 (MBNL1), a CUGexp-binding protein. CAG25 disperses nuclear foci of CUGexp RNA and reduces the overall burden of this toxic RNA. As MBNL1 is released from sequestration, the defect of alternative splicing regulation is corrected, thereby restoring ion channel function. These findings suggest an alternative use of antisense methods, to inhibit deleterious interactions of proteins with pathogenic RNAs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4109973/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4109973/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wheeler, Thurman M -- Sobczak, Krzysztof -- Lueck, John D -- Osborne, Robert J -- Lin, Xiaoyan -- Dirksen, Robert T -- Thornton, Charles A -- AR/NS48143/AR/NIAMS NIH HHS/ -- AR046806/AR/NIAMS NIH HHS/ -- K08 NS064293/NS/NINDS NIH HHS/ -- K24 AR048143/AR/NIAMS NIH HHS/ -- NIDCR-T32DE07202/DE/NIDCR NIH HHS/ -- R01 AR046806/AR/NIAMS NIH HHS/ -- R01 AR049077/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 2009 Jul 17;325(5938):336-9. doi: 10.1126/science.1173110.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Neurology, Pharmacology and Physiology, University of Rochester, Rochester, NY 14642, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19608921" target="_blank"〉PubMed〈/a〉
    Keywords: 3' Untranslated Regions/genetics/*metabolism ; Actins/genetics ; Alternative Splicing ; Animals ; Cell Line ; Cell Nucleus/metabolism ; Chloride Channels/metabolism ; DNA-Binding Proteins/*metabolism ; Humans ; Mice ; Mice, Knockout ; Mice, Transgenic ; Myotonic Dystrophy/*drug therapy/*genetics/metabolism ; Myotonin-Protein Kinase ; Oligodeoxyribonucleotides, Antisense/*pharmacology/therapeutic use ; Protein-Serine-Threonine Kinases/genetics ; RNA, Messenger/genetics ; RNA-Binding Proteins/*metabolism ; Transcription, Genetic ; *Trinucleotide Repeat Expansion
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Biomedical policy. Draft stem cell guidelines please many, disappoint some (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-04-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holden, Constance -- Kaiser, Jocelyn -- New York, N.Y. -- Science. 2009 Apr 24;324(5926):446. doi: 10.1126/science.324_446.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19390007" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Embryo Research/economics/*legislation & jurisprudence ; Embryonic Stem Cells ; Financing, Government/*legislation & jurisprudence ; Guidelines as Topic ; Humans ; National Institutes of Health (U.S.) ; Public Policy ; Research Support as Topic/*legislation & jurisprudence ; *Stem Cells ; United States
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    S-nitrosylation of Drp1 mediates beta-amyloid-related mitochondrial fission and neuronal injury (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-04-04
    Description: Mitochondria continuously undergo two opposing processes, fission and fusion. The disruption of this dynamic equilibrium may herald cell injury or death and may contribute to developmental and neurodegenerative disorders. Nitric oxide functions as a signaling molecule, but in excess it mediates neuronal injury, in part via mitochondrial fission or fragmentation. However, the underlying mechanism for nitric oxide-induced pathological fission remains unclear. We found that nitric oxide produced in response to beta-amyloid protein, thought to be a key mediator of Alzheimer's disease, triggered mitochondrial fission, synaptic loss, and neuronal damage, in part via S-nitrosylation of dynamin-related protein 1 (forming SNO-Drp1). Preventing nitrosylation of Drp1 by cysteine mutation abrogated these neurotoxic events. SNO-Drp1 is increased in brains of human Alzheimer's disease patients and may thus contribute to the pathogenesis of neurodegeneration.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2823371/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2823371/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cho, Dong-Hyung -- Nakamura, Tomohiro -- Fang, Jianguo -- Cieplak, Piotr -- Godzik, Adam -- Gu, Zezong -- Lipton, Stuart A -- P01 ES016738/ES/NIEHS NIH HHS/ -- P01 ES016738-01/ES/NIEHS NIH HHS/ -- P01 ES016738-010003/ES/NIEHS NIH HHS/ -- P01 ES016738-02/ES/NIEHS NIH HHS/ -- P01 ES016738-020003/ES/NIEHS NIH HHS/ -- P01 HD029587/HD/NICHD NIH HHS/ -- P01 HD029587-16/HD/NICHD NIH HHS/ -- P01 HD29587/HD/NICHD NIH HHS/ -- P30 NS057096/NS/NINDS NIH HHS/ -- P30 NS057096-04/NS/NINDS NIH HHS/ -- R01 EY005477/EY/NEI NIH HHS/ -- R01 EY005477-25/EY/NEI NIH HHS/ -- R01 EY05477/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 2009 Apr 3;324(5923):102-5. doi: 10.1126/science.1171091.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Neuroscience, Aging, and Stem Cell Research, Burnham Institute for Medical Research, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19342591" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/metabolism/pathology ; Amino Acid Motifs ; Amyloid beta-Peptides/*metabolism/pharmacology ; Animals ; Cell Line ; Cell Line, Tumor ; Cerebral Cortex/cytology ; Cysteine/analogs & derivatives/genetics/metabolism/pharmacology ; Female ; GTP Phosphohydrolases/chemistry/*metabolism ; Humans ; Male ; Mice ; Mice, Transgenic ; Microtubule-Associated Proteins/chemistry/*metabolism ; Mitochondria/drug effects/physiology/*ultrastructure ; Mitochondrial Proteins/chemistry/*metabolism ; Models, Molecular ; Mutation ; Neurons/drug effects/*ultrastructure ; Nitric Oxide/*metabolism ; Peptide Fragments/metabolism/pharmacology ; Protein Multimerization ; Protein Structure, Tertiary ; S-Nitrosothiols/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    Regulation of neuronal survival factor MEF2D by chaperone-mediated autophagy (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-01-03
    Description: Chaperone-mediated autophagy controls the degradation of selective cytosolic proteins and may protect neurons against degeneration. In a neuronal cell line, we found that chaperone-mediated autophagy regulated the activity of myocyte enhancer factor 2D (MEF2D), a transcription factor required for neuronal survival. MEF2D was observed to continuously shuttle to the cytoplasm, interact with the chaperone Hsc70, and undergo degradation. Inhibition of chaperone-mediated autophagy caused accumulation of inactive MEF2D in the cytoplasm. MEF2D levels were increased in the brains of alpha-synuclein transgenic mice and patients with Parkinson's disease. Wild-type alpha-synuclein and a Parkinson's disease-associated mutant disrupted the MEF2D-Hsc70 binding and led to neuronal death. Thus, chaperone-mediated autophagy modulates the neuronal survival machinery, and dysregulation of this pathway is associated with Parkinson's disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2666000/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2666000/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yang, Qian -- She, Hua -- Gearing, Marla -- Colla, Emanuela -- Lee, Michael -- Shacka, John J -- Mao, Zixu -- AG023695/AG/NIA NIH HHS/ -- NS038065/NS/NINDS NIH HHS/ -- NS048254/NS/NINDS NIH HHS/ -- NS055077/NS/NINDS NIH HHS/ -- NS47466/NS/NINDS NIH HHS/ -- NS57098/NS/NINDS NIH HHS/ -- P30 NS055077/NS/NINDS NIH HHS/ -- P30 NS055077-01A2/NS/NINDS NIH HHS/ -- P50 AG025688/AG/NIA NIH HHS/ -- P50 AG025688-03/AG/NIA NIH HHS/ -- R01 AG023695/AG/NIA NIH HHS/ -- R01 AG023695-02/AG/NIA NIH HHS/ -- R01 AG023695-03/AG/NIA NIH HHS/ -- R01 AG023695-04/AG/NIA NIH HHS/ -- R01 AG023695-05/AG/NIA NIH HHS/ -- R01 NS048254/NS/NINDS NIH HHS/ -- R01 NS048254-02/NS/NINDS NIH HHS/ -- R01 NS048254-03/NS/NINDS NIH HHS/ -- R01 NS048254-04/NS/NINDS NIH HHS/ -- R01 NS048254-05/NS/NINDS NIH HHS/ -- R01 NS048254-06/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2009 Jan 2;323(5910):124-7. doi: 10.1126/science.1166088.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Emory University School of Medicine, Atlanta, GA 30322, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19119233" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Ammonium Chloride/pharmacology ; Animals ; *Autophagy ; Brain/metabolism ; Cell Line ; Cell Nucleus/metabolism ; Cell Survival ; Cytoplasm/metabolism ; DNA/metabolism ; HSC70 Heat-Shock Proteins/metabolism ; Lysosomal-Associated Membrane Protein 2/metabolism ; Lysosomes/metabolism ; MADS Domain Proteins/*metabolism ; MEF2 Transcription Factors ; Mice ; Mice, Transgenic ; Molecular Chaperones/*metabolism ; Myogenic Regulatory Factors/chemistry/*metabolism ; Neurons/cytology/*metabolism ; Parkinson Disease/metabolism ; Protein Binding ; Protein Transport ; Rats ; Rats, Long-Evans ; alpha-Synuclein/genetics/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    Genome-wide RNAi screen identifies Letm1 as a mitochondrial Ca2+/H+ antiporter (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-10-03
    Description: Mitochondria are integral components of cellular calcium (Ca2+) signaling. Calcium stimulates mitochondrial adenosine 5'-triphosphate production, but can also initiate apoptosis. In turn, cytoplasmic Ca2+ concentrations are regulated by mitochondria. Although several transporter and ion-channel mechanisms have been measured in mitochondria, the molecules that govern Ca2+ movement across the inner mitochondrial membrane are unknown. We searched for genes that regulate mitochondrial Ca2+ and H+ concentrations using a genome-wide Drosophila RNA interference (RNAi) screen. The mammalian homolog of one Drosophila gene identified in the screen, Letm1, was found to specifically mediate coupled Ca2+/H+ exchange. RNAi knockdown, overexpression, and liposome reconstitution of the purified Letm1 protein demonstrate that Letm1 is a mitochondrial Ca2+/H+ antiporter.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4067766/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4067766/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jiang, Dawei -- Zhao, Linlin -- Clapham, David E -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Oct 2;326(5949):144-7. doi: 10.1126/science.1175145.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cardiology, Howard Hughes Medical Institute, Children's Hospital Boston, Manton Center for Orphan Disease, and Department of Neurobiology, Harvard Medical School, Enders Building 1309, 320 Longwood Avenue, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19797662" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antiporters/*genetics/metabolism ; Calcium/*metabolism ; Calcium-Binding Proteins/*genetics/*metabolism ; Cation Transport Proteins/genetics/metabolism ; Cell Line ; Drosophila Proteins/*genetics/metabolism ; Drosophila melanogaster/*genetics/metabolism ; Genome, Human ; Genome, Insect ; HeLa Cells ; Humans ; Hydrogen/metabolism ; Hydrogen-Ion Concentration ; Ion Transport ; Membrane Potential, Mitochondrial ; Membrane Proteins/*genetics/*metabolism ; Mitochondria/*metabolism ; Mitochondrial Membranes/metabolism ; Mitochondrial Proteins/genetics/*metabolism ; Proteolipids/metabolism ; *RNA Interference
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    Cell biology. Overcoming opposition, Brazil banks on stem cells (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-04-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Leite, Marcelo -- New York, N.Y. -- Science. 2009 Apr 3;324(5923):26. doi: 10.1126/science.324.5923.26.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19342562" target="_blank"〉PubMed〈/a〉
    Keywords: Biomedical Research/economics ; Bioreactors ; Brazil ; Cell Culture Techniques ; Cell Line ; *Embryo Research/economics ; *Embryonic Stem Cells/cytology ; Financing, Government ; Humans ; *Pluripotent Stem Cells/cytology ; Research Support as Topic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 11
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    The hallucinogen N,N-dimethyltryptamine (DMT) is an endogenous sigma-1 receptor regulator (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-02-14
    Description: The sigma-1 receptor is widely distributed in the central nervous system and periphery. Originally mischaracterized as an opioid receptor, the sigma-1 receptor binds a vast number of synthetic compounds but does not bind opioid peptides; it is currently considered an orphan receptor. The sigma-1 receptor pharmacophore includes an alkylamine core, also found in the endogenous compound N,N-dimethyltryptamine (DMT). DMT acts as a hallucinogen, but its receptor target has been unclear. DMT bound to sigma-1 receptors and inhibited voltage-gated sodium ion (Na+) channels in both native cardiac myocytes and heterologous cells that express sigma-1 receptors. DMT induced hypermobility in wild-type mice but not in sigma-1 receptor knockout mice. These biochemical, physiological, and behavioral experiments indicate that DMT is an endogenous agonist for the sigma-1 receptor.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2947205/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2947205/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fontanilla, Dominique -- Johannessen, Molly -- Hajipour, Abdol R -- Cozzi, Nicholas V -- Jackson, Meyer B -- Ruoho, Arnold E -- F31 DA022932/DA/NIDA NIH HHS/ -- NS30016/NS/NINDS NIH HHS/ -- R01 MH065503/MH/NIMH NIH HHS/ -- R01 MH065503-01A1/MH/NIMH NIH HHS/ -- R01 NS030016/NS/NINDS NIH HHS/ -- R01 NS030016-08/NS/NINDS NIH HHS/ -- R01 NS030016-09/NS/NINDS NIH HHS/ -- T32 GM08688/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2009 Feb 13;323(5916):934-7. doi: 10.1126/science.1166127.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of Wisconsin School of Medicine and Public Health, Madison, WI 53706, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19213917" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; COS Cells ; Cell Line ; Cells, Cultured ; Cercopithecus aethiops ; Guinea Pigs ; Hallucinogens/*metabolism ; Ligands ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Myocardium/metabolism ; N,N-Dimethyltryptamine/*metabolism ; Rats ; Receptors, sigma/agonists/antagonists & inhibitors/*metabolism ; Tryptamines/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 12
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    The aryl hydrocarbon nuclear translocator alters CD30-mediated NF-kappaB-dependent transcription (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-01-10
    Description: Expression and signaling of CD30, a tumor necrosis factor receptor family member, is up-regulated in numerous lymphoid-derived neoplasias, most notably anaplastic large-cell lymphoma (ALCL) and Hodgkin's lymphoma. To gain insight into the mechanism of CD30 signaling, we used an affinity purification strategy that led to the identification of the aryl hydrocarbon receptor nuclear translocator (ARNT) as a CD30-interacting protein that modulated the activity of the RelB subunit of the transcription factor nuclear factor kappaB (NF-kappaB). ALCL cells that were deficient in ARNT exhibited defects in RelB recruitment to NF-kappaB-responsive promoters, whereas RelA recruitment to the same sites was potentiated, resulting in the augmented expression of these NF-kappaB-responsive genes. These findings indicate that ARNT functions in concert with RelB in a CD30-induced negative feedback mechanism.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2682336/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2682336/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wright, Casey W -- Duckett, Colin S -- R01 GM067827/GM/NIGMS NIH HHS/ -- R01 GM067827-04/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2009 Jan 9;323(5911):251-5. doi: 10.1126/science.1162818.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19131627" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Antigens, CD30/*metabolism ; Aryl Hydrocarbon Receptor Nuclear Translocator/chemistry/genetics/*metabolism ; Cell Line ; Cell Line, Tumor ; DNA/metabolism ; Feedback, Physiological ; Gene Expression Regulation ; Humans ; Lymphoma, Large-Cell, Anaplastic/genetics/metabolism ; Molecular Sequence Data ; NF-kappa B/genetics/metabolism ; Promoter Regions, Genetic ; Protein Structure, Tertiary ; Receptors, Tumor Necrosis Factor, Type II/metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Transcription Factor RelB/genetics/*metabolism ; *Transcription, Genetic ; Transcriptional Activation
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  • 13
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    The cAMP sensor Epac2 is a direct target of antidiabetic sulfonylurea drugs (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-08-01
    Description: Epac2, a guanine nucleotide exchange factor for the small guanosine triphosphatase Rap1, is activated by adenosine 3',5'-monophosphate. Fluorescence resonance energy transfer and binding experiments revealed that sulfonylureas, widely used antidiabetic drugs, interact directly with Epac2. Sulfonylureas activated Rap1 specifically through Epac2. Sulfonylurea-stimulated insulin secretion was reduced both in vitro and in vivo in mice lacking Epac2, and the glucose-lowering effect of the sulfonylurea tolbutamide was decreased in these mice. Epac2 thus contributes to the effect of sulfonylureas to promote insulin secretion. Because Epac2 is also required for the action of incretins, gut hormones crucial for potentiating insulin secretion, it may be a promising target for antidiabetic drug development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Chang-Liang -- Katoh, Megumi -- Shibasaki, Tadao -- Minami, Kohtaro -- Sunaga, Yasuhiro -- Takahashi, Harumi -- Yokoi, Norihide -- Iwasaki, Masahiro -- Miki, Takashi -- Seino, Susumu -- New York, N.Y. -- Science. 2009 Jul 31;325(5940):607-10. doi: 10.1126/science.1172256.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Cellular and Molecular Medicine, Department of Physiology and Cell Biology, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19644119" target="_blank"〉PubMed〈/a〉
    Keywords: 8-Bromo Cyclic Adenosine Monophosphate/pharmacology ; Animals ; Blood Glucose/analysis ; COS Cells ; Carrier Proteins/genetics/*metabolism ; Cell Line ; Cercopithecus aethiops ; Cyclic AMP/*metabolism ; Fluorescence Resonance Energy Transfer ; Glucose/administration & dosage ; Glyburide/metabolism/pharmacology ; Guanine Nucleotide Exchange Factors/genetics/*metabolism ; Hypoglycemic Agents/chemistry/*metabolism/pharmacology ; Insulin/blood/secretion ; Islets of Langerhans/secretion ; Mice ; Mice, Inbred C57BL ; Sulfonylurea Compounds/chemistry/*metabolism/pharmacology ; Tolbutamide/metabolism/pharmacology ; rap1 GTP-Binding Proteins/metabolism
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  • 14
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    RIP3, an energy metabolism regulator that switches TNF-induced cell death from apoptosis to necrosis (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-06-06
    Description: Necrosis can be induced by stimulating death receptors with tumor necrosis factor (TNF) or other agonists; however, the underlying mechanism differentiating necrosis from apoptosis is largely unknown. We identified the protein kinase receptor-interacting protein 3 (RIP3) as a molecular switch between TNF-induced apoptosis and necrosis in NIH 3T3 cells and found that RIP3 was required for necrosis in other cells. RIP3 did not affect RIP1-mediated apoptosis but was required for RIP1-mediated necrosis and the enhancement of necrosis by the caspase inhibitor zVAD. By activating key enzymes of metabolic pathways, RIP3 regulates TNF-induced reactive oxygen species production, which partially accounts for RIP3's ability to promote necrosis. Our data suggest that modulation of energy metabolism in response to death stimuli has an important role in the choice between apoptosis and necrosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Duan-Wu -- Shao, Jing -- Lin, Juan -- Zhang, Na -- Lu, Bao-Ju -- Lin, Sheng-Cai -- Dong, Meng-Qiu -- Han, Jiahuai -- New York, N.Y. -- Science. 2009 Jul 17;325(5938):332-6. doi: 10.1126/science.1172308. Epub 2009 Jun 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Key Laboratory of the Ministry of Education for Cell Biology and Tumor Cell Engineering, School of Life Sciences, Xiamen University, Xiamen, Fujian 361005, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19498109" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Chloromethyl Ketones/pharmacology ; Animals ; *Apoptosis ; Cell Line ; Energy Metabolism ; Glutamate Dehydrogenase/metabolism ; Glutamate-Ammonia Ligase/metabolism ; Glycogen Phosphorylase/metabolism ; Mice ; NIH 3T3 Cells ; *Necrosis ; RNA Interference ; Reactive Oxygen Species/metabolism ; Receptor-Interacting Protein Serine-Threonine Kinases/genetics/*metabolism ; Tumor Necrosis Factor-alpha/*pharmacology
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  • 15
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    Rab35 controls actin bundling by recruiting fascin as an effector protein (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-09-05
    Description: Actin filaments are key components of the eukaryotic cytoskeleton that provide mechanical structure and generate forces during cell shape changes, growth, and migration. Actin filaments are dynamically assembled into higher-order structures at specified locations to regulate diverse functions. The Rab family of small guanosine triphosphatases is evolutionarily conserved and mediates intracellular vesicle trafficking. We found that Rab35 regulates the assembly of actin filaments during bristle development in Drosophila and filopodia formation in cultured cells. These effects were mediated by the actin-bundling protein fascin, which directly associated with active Rab35. Targeting Rab35 to the outer mitochondrial membrane triggered actin recruitment, demonstrating a role for an intracellular trafficking protein in localized actin assembly.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Jun -- Fonovic, Marko -- Suyama, Kaye -- Bogyo, Matthew -- Scott, Matthew P -- U54 RR020843/RR/NCRR NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Sep 4;325(5945):1250-4. doi: 10.1126/science.1174921.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Biology, Stanford University School of Medicine, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19729655" target="_blank"〉PubMed〈/a〉
    Keywords: Actin Cytoskeleton/*metabolism/ultrastructure ; Actins/*metabolism ; Animals ; Carrier Proteins/*metabolism ; Cell Line ; Cell Membrane/metabolism ; Drosophila/anatomy & histology/growth & development/metabolism ; Drosophila Proteins/genetics/*metabolism ; HeLa Cells ; Humans ; Mice ; Microfilament Proteins/*metabolism ; Mitochondrial Membranes/metabolism ; NIH 3T3 Cells ; Pseudopodia/metabolism/ultrastructure ; RNA Interference ; Recombinant Fusion Proteins/metabolism ; rab GTP-Binding Proteins/genetics/*metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 16
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    The insect neuropeptide PTTH activates receptor tyrosine kinase torso to initiate metamorphosis (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-12-08
    Description: Holometabolous insects undergo complete metamorphosis to become sexually mature adults. Metamorphosis is initiated by brain-derived prothoracicotropic hormone (PTTH), which stimulates the production of the molting hormone ecdysone via an incompletely defined signaling pathway. Here we demonstrate that Torso, a receptor tyrosine kinase that regulates embryonic terminal cell fate in Drosophila, is the PTTH receptor. Trunk, the embryonic Torso ligand, is related to PTTH, and ectopic expression of PTTH in the embryo partially rescues trunk mutants. In larvae, torso is expressed specifically in the prothoracic gland (PG), and its loss phenocopies the removal of PTTH. The activation of Torso by PTTH stimulates extracellular signal-regulated kinase (ERK) phosphorylation, and the loss of ERK in the PG phenocopies the loss of PTTH and Torso. We conclude that PTTH initiates metamorphosis by activation of the Torso/ERK pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rewitz, Kim F -- Yamanaka, Naoki -- Gilbert, Lawrence I -- O'Connor, Michael B -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Dec 4;326(5958):1403-5. doi: 10.1126/science.1176450.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Cell Biology, and Development, University of Minnesota, Minneapolis, MN 55455, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965758" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Bombyx/*genetics/metabolism ; Cell Line ; Drosophila Proteins/chemistry/genetics/*metabolism ; Drosophila melanogaster/embryology/genetics/*growth & development/metabolism ; Embryo, Nonmammalian/metabolism ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Insect Hormones/chemistry/*metabolism ; Larva/growth & development ; Ligands ; *Metamorphosis, Biological ; Molecular Sequence Data ; Neurons/metabolism ; Phosphorylation ; Pupa/growth & development ; RNA Interference ; Receptor Protein-Tyrosine Kinases/genetics/*metabolism ; Signal Transduction
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  • 17
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    Glioma-derived mutations in IDH1 dominantly inhibit IDH1 catalytic activity and induce HIF-1alpha (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-04-11
    Description: Heterozygous mutations in the gene encoding isocitrate dehydrogenase-1 (IDH1) occur in certain human brain tumors, but their mechanistic role in tumor development is unknown. We have shown that tumor-derived IDH1 mutations impair the enzyme's affinity for its substrate and dominantly inhibit wild-type IDH1 activity through the formation of catalytically inactive heterodimers. Forced expression of mutant IDH1 in cultured cells reduces formation of the enzyme product, alpha-ketoglutarate (alpha-KG), and increases the levels of hypoxia-inducible factor subunit HIF-1alpha, a transcription factor that facilitates tumor growth when oxygen is low and whose stability is regulated by alpha-KG. The rise in HIF-1alpha levels was reversible by an alpha-KG derivative. HIF-1alpha levels were higher in human gliomas harboring an IDH1 mutation than in tumors without a mutation. Thus, IDH1 appears to function as a tumor suppressor that, when mutationally inactivated, contributes to tumorigenesis in part through induction of the HIF-1 pathway.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3251015/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3251015/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhao, Shimin -- Lin, Yan -- Xu, Wei -- Jiang, Wenqing -- Zha, Zhengyu -- Wang, Pu -- Yu, Wei -- Li, Zhiqiang -- Gong, Lingling -- Peng, Yingjie -- Ding, Jianping -- Lei, Qunying -- Guan, Kun-Liang -- Xiong, Yue -- R01 CA068377/CA/NCI NIH HHS/ -- R01 CA068377-14/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2009 Apr 10;324(5924):261-5. doi: 10.1126/science.1170944.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular and Cell Biology Laboratory, Institute of Biomedical Sciences, Fudan University, 130 Dong-An Road, Shanghai 200032, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19359588" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Aged ; Astrocytoma/genetics/metabolism ; Biocatalysis ; Brain Neoplasms/*genetics/metabolism ; Cell Line ; Child ; Female ; Gene Expression Regulation, Neoplastic ; Genes, Tumor Suppressor ; Glioblastoma/genetics/metabolism ; Glioma/*genetics/metabolism ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit/antagonists & ; inhibitors/genetics/*metabolism ; Isocitrate Dehydrogenase/chemistry/*genetics/*metabolism ; Ketoglutaric Acids/metabolism ; Male ; Middle Aged ; Mutant Proteins/chemistry/metabolism ; Oligodendroglioma/genetics/metabolism ; Oxalates/pharmacology ; Protein Multimerization
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  • 18
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    Stem cells. CIRM awards seek to move cell therapies to the clinic (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-11-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaiser, Jocelyn -- New York, N.Y. -- Science. 2009 Nov 6;326(5954):780-1. doi: 10.1126/science.326_780a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19892950" target="_blank"〉PubMed〈/a〉
    Keywords: *Academies and Institutes ; Adult Stem Cells ; *Biological Therapy ; California ; Cell Line ; Embryonic Stem Cells ; Genetic Therapy ; Humans ; Induced Pluripotent Stem Cells ; National Institutes of Health (U.S.) ; *Research Support as Topic ; *Stem Cell Transplantation ; *Stem Cells ; United States
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  • 19
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    Conversion of 5-methylcytosine to 5-hydroxymethylcytosine in mammalian DNA by MLL partner TET1 (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-04-18
    Description: DNA cytosine methylation is crucial for retrotransposon silencing and mammalian development. In a computational search for enzymes that could modify 5-methylcytosine (5mC), we identified TET proteins as mammalian homologs of the trypanosome proteins JBP1 and JBP2, which have been proposed to oxidize the 5-methyl group of thymine. We show here that TET1, a fusion partner of the MLL gene in acute myeloid leukemia, is a 2-oxoglutarate (2OG)- and Fe(II)-dependent enzyme that catalyzes conversion of 5mC to 5-hydroxymethylcytosine (hmC) in cultured cells and in vitro. hmC is present in the genome of mouse embryonic stem cells, and hmC levels decrease upon RNA interference-mediated depletion of TET1. Thus, TET proteins have potential roles in epigenetic regulation through modification of 5mC to hmC.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2715015/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2715015/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tahiliani, Mamta -- Koh, Kian Peng -- Shen, Yinghua -- Pastor, William A -- Bandukwala, Hozefa -- Brudno, Yevgeny -- Agarwal, Suneet -- Iyer, Lakshminarayan M -- Liu, David R -- Aravind, L -- Rao, Anjana -- AI44432/AI/NIAID NIH HHS/ -- K08 HL089150/HL/NHLBI NIH HHS/ -- R01 GM065865/GM/NIGMS NIH HHS/ -- R01 GM065865-05A1/GM/NIGMS NIH HHS/ -- R01GM065865/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2009 May 15;324(5929):930-5. doi: 10.1126/science.1170116. Epub 2009 Apr 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Harvard Medical School and Immune Disease Institute, 200 Longwood Avenue, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19372391" target="_blank"〉PubMed〈/a〉
    Keywords: 5-Methylcytosine/*metabolism ; Amino Acid Sequence ; Animals ; Cell Line ; Cytosine/*analogs & derivatives/analysis/metabolism ; DNA/chemistry/*metabolism ; DNA Methylation ; DNA-Binding Proteins/chemistry/genetics/*metabolism ; Dinucleoside Phosphates/metabolism ; Embryonic Stem Cells/chemistry/metabolism ; Humans ; Hydroxylation ; Mass Spectrometry ; Mice ; Molecular Sequence Data ; Proto-Oncogene Proteins/chemistry/genetics/*metabolism ; RNA Interference ; Sequence Alignment ; Transfection
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  • 20
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    Analysis of Drosophila segmentation network identifies a JNK pathway factor overexpressed in kidney cancer (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-01-24
    Description: We constructed a large-scale functional network model in Drosophila melanogaster built around two key transcription factors involved in the process of embryonic segmentation. Analysis of the model allowed the identification of a new role for the ubiquitin E3 ligase complex factor SPOP. In Drosophila, the gene encoding SPOP is a target of segmentation transcription factors. Drosophila SPOP mediates degradation of the Jun kinase phosphatase Puckered, thereby inducing tumor necrosis factor (TNF)/Eiger-dependent apoptosis. In humans, we found that SPOP plays a conserved role in TNF-mediated JNK signaling and was highly expressed in 99% of clear cell renal cell carcinomas (RCCs), the most prevalent form of kidney cancer. SPOP expression distinguished histological subtypes of RCC and facilitated identification of clear cell RCC as the primary tumor for metastatic lesions.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2756524/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2756524/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, Jiang -- Ghanim, Murad -- Xue, Lei -- Brown, Christopher D -- Iossifov, Ivan -- Angeletti, Cesar -- Hua, Sujun -- Negre, Nicolas -- Ludwig, Michael -- Stricker, Thomas -- Al-Ahmadie, Hikmat A -- Tretiakova, Maria -- Camp, Robert L -- Perera-Alberto, Montse -- Rimm, David L -- Xu, Tian -- Rzhetsky, Andrey -- White, Kevin P -- P50 GM081892/GM/NIGMS NIH HHS/ -- P50 GM081892-01A1/GM/NIGMS NIH HHS/ -- R01 HG003012/HG/NHGRI NIH HHS/ -- R01 HG003012-04/HG/NHGRI NIH HHS/ -- UL1 RR024999/RR/NCRR NIH HHS/ -- UL1 RR024999-02/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2009 Feb 27;323(5918):1218-22. doi: 10.1126/science.1157669. Epub 2009 Jan 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Genomics and Systems Biology, University of Chicago and Argonne National Laboratory, Chicago, IL 60637, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19164706" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Apoptosis ; Carcinoma, Renal Cell/*genetics/metabolism ; Cell Line ; Compound Eye, Arthropod/embryology/metabolism ; Drosophila Proteins/genetics/metabolism ; Drosophila melanogaster/embryology/*genetics/metabolism ; Embryo, Nonmammalian/metabolism ; Fushi Tarazu Transcription Factors/genetics/metabolism ; Gene Expression Profiling ; Gene Regulatory Networks ; Homeodomain Proteins/genetics/metabolism ; Humans ; Janus Kinases/*metabolism ; Kidney/metabolism ; Kidney Neoplasms/*genetics/metabolism ; Molecular Sequence Data ; Nervous System/embryology ; Nuclear Proteins/*genetics/metabolism ; Phosphoprotein Phosphatases/metabolism ; Phosphorylation ; Repressor Proteins/*genetics/metabolism ; *Signal Transduction ; Transcription Factors/genetics/metabolism ; Transcription, Genetic
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    Calcineurin/NFAT signaling is required for neuregulin-regulated Schwann cell differentiation (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-01-31
    Description: Schwann cells develop from multipotent neural crest cells and form myelin sheaths around axons that allow rapid transmission of action potentials. Neuregulin signaling through the ErbB receptor regulates Schwann cell development; however, the downstream pathways are not fully defined. We find that mice lacking calcineurin B1 in the neural crest have defects in Schwann cell differentiation and myelination. Neuregulin addition to Schwann cell precursors initiates an increase in cytoplasmic Ca2+, which activates calcineurin and the downstream transcription factors NFATc3 and c4. Purification of NFAT protein complexes shows that Sox10 is an NFAT nuclear partner and synergizes with NFATc4 to activate Krox20, which regulates genes necessary for myelination. Our studies demonstrate that calcineurin and NFAT are essential for neuregulin and ErbB signaling, neural crest diversification, and differentiation of Schwann cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2790385/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2790385/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kao, Shih-Chu -- Wu, Hai -- Xie, Jianming -- Chang, Ching-Pin -- Ranish, Jeffrey A -- Graef, Isabella A -- Crabtree, Gerald R -- AI60037/AI/NIAID NIH HHS/ -- HD55391/HD/NICHD NIH HHS/ -- NS046789/NS/NINDS NIH HHS/ -- R01 AI060037/AI/NIAID NIH HHS/ -- R01 AI060037-01/AI/NIAID NIH HHS/ -- R01 AI060037-02/AI/NIAID NIH HHS/ -- R01 AI060037-03/AI/NIAID NIH HHS/ -- R01 AI060037-04/AI/NIAID NIH HHS/ -- R01 AI060037-05/AI/NIAID NIH HHS/ -- R01 HD055391/HD/NICHD NIH HHS/ -- R01 NS046789/NS/NINDS NIH HHS/ -- R01 NS046789-01/NS/NINDS NIH HHS/ -- R01 NS046789-02/NS/NINDS NIH HHS/ -- R01 NS046789-03/NS/NINDS NIH HHS/ -- R01 NS046789-04/NS/NINDS NIH HHS/ -- R01 NS046789-05/NS/NINDS NIH HHS/ -- R21 NS061702/NS/NINDS NIH HHS/ -- R21 NS061702-01/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Jan 30;323(5914):651-4. doi: 10.1126/science.1166562.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Stanford University, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19179536" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcineurin/*metabolism ; Calcium/metabolism ; Cell Differentiation ; Cell Line ; Coculture Techniques ; Early Growth Response Protein 2/metabolism ; Ganglia, Spinal/cytology ; Mice ; Myelin Sheath/physiology ; NFATC Transcription Factors/*metabolism ; Neural Crest/cytology/metabolism ; Neuregulins/*metabolism ; Phosphorylation ; Receptor, ErbB-2/metabolism ; Receptor, ErbB-3 ; SOXE Transcription Factors/metabolism ; Schwann Cells/*cytology/*metabolism ; *Signal Transduction
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    Circadian control of the NAD+ salvage pathway by CLOCK-SIRT1 (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-03-17
    Description: Many metabolic and physiological processes display circadian oscillations. We have shown that the core circadian regulator, CLOCK, is a histone acetyltransferase whose activity is counterbalanced by the nicotinamide adenine dinucleotide (NAD+)-dependent histone deacetylase SIRT1. Here we show that intracellular NAD+ levels cycle with a 24-hour rhythm, an oscillation driven by the circadian clock. CLOCK:BMAL1 regulates the circadian expression of NAMPT (nicotinamide phosphoribosyltransferase), an enzyme that provides a rate-limiting step in the NAD+ salvage pathway. SIRT1 is recruited to the Nampt promoter and contributes to the circadian synthesis of its own coenzyme. Using the specific inhibitor FK866, we demonstrated that NAMPT is required to modulate circadian gene expression. Our findings in mouse embryo fibroblasts reveal an interlocked transcriptional-enzymatic feedback loop that governs the molecular interplay between cellular metabolism and circadian rhythms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nakahata, Yasukazu -- Sahar, Saurabh -- Astarita, Giuseppe -- Kaluzova, Milota -- Sassone-Corsi, Paolo -- R01-GM081634/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2009 May 1;324(5927):654-7. doi: 10.1126/science.1170803. Epub 2009 Mar 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, School of Medicine, University of California, Irvine, Irvine, CA 92697, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19286518" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors ; Acrylamides/pharmacology ; Animals ; Basic Helix-Loop-Helix Transcription Factors/metabolism ; Biological Clocks ; CLOCK Proteins ; Cell Line ; Chromatin Assembly and Disassembly ; *Circadian Rhythm ; Cytokines/antagonists & inhibitors/genetics/*metabolism ; Enzyme Inhibitors/pharmacology ; *Feedback, Physiological ; *Gene Expression Regulation ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Knockout ; NAD/*metabolism ; Niacinamide/metabolism ; Nicotinamide Phosphoribosyltransferase/antagonists & ; inhibitors/genetics/*metabolism ; Piperidines/pharmacology ; Promoter Regions, Genetic ; Sirtuin 1 ; Sirtuins/*metabolism ; Trans-Activators/genetics/*metabolism ; Transcription, Genetic
    Print ISSN: 0036-8075
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    A role for the CHC22 clathrin heavy-chain isoform in human glucose metabolism (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-05-30
    Description: Intracellular trafficking of the glucose transporter GLUT4 from storage compartments to the plasma membrane is triggered in muscle and fat during the body's response to insulin. Clathrin is involved in intracellular trafficking, and in humans, the clathrin heavy-chain isoform CHC22 is highly expressed in skeletal muscle. We found a role for CHC22 in the formation of insulin-responsive GLUT4 compartments in human muscle and adipocytes. CHC22 also associated with expanded GLUT4 compartments in muscle from type 2 diabetic patients. Tissue-specific introduction of CHC22 in mice, which have only a pseudogene for this protein, caused aberrant localization of GLUT4 transport pathway components in their muscle, as well as features of diabetes. Thus, CHC22-dependent membrane trafficking constitutes a species-restricted pathway in human muscle and fat with potential implications for type 2 diabetes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2975026/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2975026/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vassilopoulos, Stephane -- Esk, Christopher -- Hoshino, Sachiko -- Funke, Birgit H -- Chen, Chih-Ying -- Plocik, Alex M -- Wright, Woodring E -- Kucherlapati, Raju -- Brodsky, Frances M -- GM038093/GM/NIGMS NIH HHS/ -- HD47863/HD/NICHD NIH HHS/ -- R01 GM038093/GM/NIGMS NIH HHS/ -- R01 GM038093-19/GM/NIGMS NIH HHS/ -- R01 GM038093-19S1/GM/NIGMS NIH HHS/ -- R01 GM038093-20A1/GM/NIGMS NIH HHS/ -- R01 HD047863/HD/NICHD NIH HHS/ -- R01 HD047863-01/HD/NICHD NIH HHS/ -- R01 HD047863-02/HD/NICHD NIH HHS/ -- R01 HD047863-03/HD/NICHD NIH HHS/ -- R01 HD047863-04/HD/NICHD NIH HHS/ -- R01 HD047863-05/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2009 May 29;324(5931):1192-6. doi: 10.1126/science.1171529.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bioengineering and Therapeutic Sciences, University of California, School of Pharmacy, San Francisco (UCSF), San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19478182" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes/cytology/*metabolism/ultrastructure ; Animals ; Blood Glucose/metabolism ; Cell Differentiation ; Cell Line ; Cell Membrane/metabolism ; Clathrin/chemistry/*metabolism ; Clathrin Heavy Chains ; Clathrin-Coated Vesicles/*metabolism ; Diabetes Mellitus, Type 2/*metabolism ; Glucose/*metabolism ; Glucose Transporter Type 4/*metabolism ; Humans ; Insulin/blood/pharmacology ; Mice ; Mice, Transgenic ; Muscle Fibers, Skeletal/metabolism ; Muscle, Skeletal/*metabolism/ultrastructure ; Myoblasts/cytology/metabolism/ultrastructure ; Protein Isoforms/chemistry/metabolism ; Protein Transport ; Signal Transduction
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    Two chemoreceptors mediate developmental effects of dauer pheromone in C. elegans (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-10-03
    Description: Intraspecific chemical communication is mediated by signals called pheromones. Caenorhabditis elegans secretes a mixture of small molecules (collectively termed dauer pheromone) that regulates entry into the alternate dauer larval stage and also modulates adult behavior via as yet unknown receptors. Here, we identify two heterotrimeric GTP-binding protein (G protein)-coupled receptors (GPCRs) that mediate dauer formation in response to a subset of dauer pheromone components. The SRBC-64 and SRBC-66 GPCRs are members of the large Caenorhabditis-specific SRBC subfamily and are expressed in the ASK chemosensory neurons, which are required for pheromone-induced dauer formation. Expression of both, but not each receptor alone, confers pheromone-mediated effects on heterologous cells. Identification of dauer pheromone receptors will allow a better understanding of the signaling cascades that transduce the context-dependent effects of ecologically important chemical signals.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4448937/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4448937/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Kyuhyung -- Sato, Koji -- Shibuya, Mayumi -- Zeiger, Danna M -- Butcher, Rebecca A -- Ragains, Justin R -- Clardy, Jon -- Touhara, Kazushige -- Sengupta, Piali -- F32 GM077943/GM/NIGMS NIH HHS/ -- P30 NS045713/NS/NINDS NIH HHS/ -- P30 NS45713/NS/NINDS NIH HHS/ -- R01 CA024487/CA/NCI NIH HHS/ -- R01 CA24487/CA/NCI NIH HHS/ -- R01 GM056223/GM/NIGMS NIH HHS/ -- R01 GM56223/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2009 Nov 13;326(5955):994-8. doi: 10.1126/science.1176331. Epub 2009 Oct 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology and National Center for Behavioral Genomics, Brandeis University, Waltham, MA 02454, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19797623" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis elegans/genetics/*growth & development/*physiology ; Caenorhabditis elegans Proteins/genetics/physiology ; Calcium/metabolism ; Cell Line ; Chemoreceptor Cells/metabolism ; Cyclic AMP/metabolism ; Cyclic GMP/metabolism ; GTP-Binding Protein alpha Subunits, Gi-Go/physiology ; Gene Expression Regulation, Developmental ; Genes, Helminth ; Guanylate Cyclase/antagonists & inhibitors/metabolism ; Hexoses/chemistry/physiology ; Humans ; Mutation ; Pheromones/*physiology ; Receptors, G-Protein-Coupled ; Reproduction ; Signal Transduction ; Transfection
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    Global analysis of short RNAs reveals widespread promoter-proximal stalling and arrest of Pol II in Drosophila (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-12-17
    Description: Emerging evidence indicates that gene expression in higher organisms is regulated by RNA polymerase II stalling during early transcription elongation. To probe the mechanisms responsible for this regulation, we developed methods to isolate and characterize short RNAs derived from stalled RNA polymerase II in Drosophila cells. Significant levels of these short RNAs were generated from more than one-third of all genes, indicating that promoter-proximal stalling is a general feature of early polymerase elongation. Nucleotide composition of the initially transcribed sequence played an important role in promoting transcriptional stalling by rendering polymerase elongation complexes highly susceptible to backtracking and arrest. These results indicate that the intrinsic efficiency of early elongation can greatly affect gene expression.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3435875/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3435875/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nechaev, Sergei -- Fargo, David C -- dos Santos, Gilberto -- Liu, Liwen -- Gao, Yuan -- Adelman, Karen -- ZIA ES101987-05/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2010 Jan 15;327(5963):335-8. doi: 10.1126/science.1181421. Epub 2009 Dec 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20007866" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Composition ; Cell Line ; Drosophila melanogaster ; *Gene Expression Regulation ; *Genes, Insect ; Genome, Insect ; Oligonucleotide Array Sequence Analysis ; *Promoter Regions, Genetic ; RNA/genetics/*metabolism ; RNA Caps/genetics/metabolism ; RNA Polymerase II/*metabolism ; RNA, Messenger/genetics/metabolism ; Transcription Initiation Site ; *Transcription, Genetic
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    Common regulatory variation impacts gene expression in a cell type-dependent manner (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-08-01
    Description: Studies correlating genetic variation to gene expression facilitate the interpretation of common human phenotypes and disease. As functional variants may be operating in a tissue-dependent manner, we performed gene expression profiling and association with genetic variants (single-nucleotide polymorphisms) on three cell types of 75 individuals. We detected cell type-specific genetic effects, with 69 to 80% of regulatory variants operating in a cell type-specific manner, and identified multiple expressive quantitative trait loci (eQTLs) per gene, unique or shared among cell types and positively correlated with the number of transcripts per gene. Cell type-specific eQTLs were found at larger distances from genes and at lower effect size, similar to known enhancers. These data suggest that the complete regulatory variant repertoire can only be uncovered in the context of cell-type specificity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2867218/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2867218/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dimas, Antigone S -- Deutsch, Samuel -- Stranger, Barbara E -- Montgomery, Stephen B -- Borel, Christelle -- Attar-Cohen, Homa -- Ingle, Catherine -- Beazley, Claude -- Gutierrez Arcelus, Maria -- Sekowska, Magdalena -- Gagnebin, Marilyne -- Nisbett, James -- Deloukas, Panos -- Dermitzakis, Emmanouil T -- Antonarakis, Stylianos E -- 077011/Wellcome Trust/United Kingdom -- 077046/Wellcome Trust/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2009 Sep 4;325(5945):1246-50. doi: 10.1126/science.1174148. Epub 2009 Jul 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, CB10 1HH, Cambridge, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19644074" target="_blank"〉PubMed〈/a〉
    Keywords: Allelic Imbalance ; B-Lymphocytes ; Cell Line ; Enhancer Elements, Genetic ; Fibroblasts ; Gene Expression Profiling ; *Gene Expression Regulation ; Gene Frequency ; Genotype ; Humans ; *Polymorphism, Single Nucleotide ; *Quantitative Trait Loci ; RNA, Messenger/genetics/metabolism ; *Regulatory Elements, Transcriptional ; Statistics, Nonparametric ; T-Lymphocytes
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  • 27
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    Regulation of hypoxia-inducible factor 2alpha signaling by the stress-responsive deacetylase sirtuin 1 (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-06-06
    Description: To survive in hostile environments, organisms activate stress-responsive transcriptional regulators that coordinately increase production of protective factors. Hypoxia changes cellular metabolism and thus activates redox-sensitive as well as oxygen-dependent signal transducers. We demonstrate that Sirtuin 1 (Sirt1), a redox-sensing deacetylase, selectively stimulates activity of the transcription factor hypoxia-inducible factor 2 alpha (HIF-2alpha) during hypoxia. The effect of Sirt1 on HIF-2alpha required direct interaction of the proteins and intact deacetylase activity of Sirt1. Select lysine residues in HIF-2alpha that are acetylated during hypoxia confer repression of Sirt1 augmentation by small-molecule inhibitors. In cultured cells and mice, decreasing or increasing Sirt1 activity or levels affected expression of the HIF-2alpha target gene erythropoietin accordingly. Thus, Sirt1 promotes HIF-2 signaling during hypoxia and likely other environmental stresses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dioum, Elhadji M -- Chen, Rui -- Alexander, Matthew S -- Zhang, Quiyang -- Hogg, Richard T -- Gerard, Robert D -- Garcia, Joseph A -- I01 BX000446/BX/BLRD VA/ -- New York, N.Y. -- Science. 2009 Jun 5;324(5932):1289-93. doi: 10.1126/science.1169956.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Veterans Affairs North Texas Health Care System, Department of Medicine, 4500 South Lancaster Road, Dallas, TX 75216, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19498162" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Amino Acid Substitution ; Animals ; Basic Helix-Loop-Helix Transcription Factors/chemistry/genetics/*metabolism ; *Cell Hypoxia ; Cell Line ; Cell Line, Tumor ; Erythropoietin/genetics ; Gene Expression Regulation ; Humans ; Kidney/metabolism ; Liver/embryology/metabolism ; Mice ; Mice, Knockout ; Mutant Proteins/chemistry/metabolism ; Oxidation-Reduction ; *Signal Transduction ; Sirtuin 1 ; Sirtuins/genetics/*metabolism
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    Poly(ADP-ribose)-dependent regulation of DNA repair by the chromatin remodeling enzyme ALC1 (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-08-08
    Description: Posttranslational modifications play key roles in regulating chromatin plasticity. Although various chromatin-remodeling enzymes have been described that respond to specific histone modifications, little is known about the role of poly[adenosine 5'-diphosphate (ADP)-ribose] in chromatin remodeling. Here, we identify a chromatin-remodeling enzyme, ALC1 (Amplified in Liver Cancer 1, also known as CHD1L), that interacts with poly(ADP-ribose) and catalyzes PARP1-stimulated nucleosome sliding. Our results define ALC1 as a DNA damage-response protein whose role in this process is sustained by its association with known DNA repair factors and its rapid poly(ADP-ribose)-dependent recruitment to DNA damage sites. Furthermore, we show that depletion or overexpression of ALC1 results in sensitivity to DNA-damaging agents. Collectively, these results provide new insights into the mechanisms by which poly(ADP-ribose) regulates DNA repair.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3443743/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3443743/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ahel, Dragana -- Horejsi, Zuzana -- Wiechens, Nicola -- Polo, Sophie E -- Garcia-Wilson, Elisa -- Ahel, Ivan -- Flynn, Helen -- Skehel, Mark -- West, Stephen C -- Jackson, Stephen P -- Owen-Hughes, Tom -- Boulton, Simon J -- 064414/Wellcome Trust/United Kingdom -- 11224/Cancer Research UK/United Kingdom -- A3549/Cancer Research UK/United Kingdom -- A5290/Cancer Research UK/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Cancer Research UK/United Kingdom -- Department of Health/United Kingdom -- New York, N.Y. -- Science. 2009 Sep 4;325(5945):1240-3. doi: 10.1126/science.1177321. Epub 2009 Aug 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉DNA Damage Response Laboratory, Clare Hall, London Research Institute, South Mimms EN6 3LD, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19661379" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphatases/metabolism ; Adenosine Triphosphate/metabolism ; Cell Line ; Chromatin/*metabolism ; *Chromatin Assembly and Disassembly ; DNA Damage ; DNA Helicases/chemistry/genetics/*metabolism ; *DNA Repair ; DNA-Binding Proteins/chemistry/genetics/*metabolism ; Humans ; Hydrogen Peroxide/pharmacology ; Immunoprecipitation ; Kinetics ; Mutant Proteins/chemistry/metabolism ; Nucleosomes/metabolism ; Phleomycins/pharmacology ; Poly Adenosine Diphosphate Ribose/*metabolism ; Poly(ADP-ribose) Polymerase Inhibitors ; Poly(ADP-ribose) Polymerases/metabolism ; Protein Structure, Tertiary ; Radiation, Ionizing ; Recombinant Proteins/chemistry/metabolism
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    Ankyrin-G promotes cyclic nucleotide-gated channel transport to rod photoreceptor sensory cilia (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-03-21
    Description: Cyclic nucleotide-gated (CNG) channels localize exclusively to the plasma membrane of photosensitive outer segments of rod photoreceptors where they generate the electrical response to light. Here, we report the finding that targeting of CNG channels to the rod outer segment required their interaction with ankyrin-G. Ankyrin-G localized exclusively to rod outer segments, coimmunoprecipitated with the CNG channel, and bound to the C-terminal domain of the channel beta1 subunit. Ankyrin-G depletion in neonatal mouse retinas markedly reduced CNG channel expression. Transgenic expression of CNG channel beta-subunit mutants in Xenopus rods showed that ankyrin-G binding was necessary and sufficient for targeting of the beta1 subunit to outer segments. Thus, ankyrin-G is required for transport of CNG channels to the plasma membrane of rod outer segments.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2792576/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2792576/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kizhatil, Krishnakumar -- Baker, Sheila A -- Arshavsky, Vadim Y -- Bennett, Vann -- EY12859/EY/NEI NIH HHS/ -- P30 EY005722/EY/NEI NIH HHS/ -- P30 EY005722-23/EY/NEI NIH HHS/ -- R01 EY012859/EY/NEI NIH HHS/ -- R01 EY012859-10/EY/NEI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Mar 20;323(5921):1614-7. doi: 10.1126/science.1169789.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Duke University Medical Center, Durham, NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19299621" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Animals, Genetically Modified ; Ankyrins/*metabolism ; Cattle ; Cell Line ; Cell Membrane/metabolism ; Cilia/*metabolism ; Cyclic Nucleotide-Gated Cation Channels/*metabolism ; Humans ; Mice ; Molecular Sequence Data ; Nerve Tissue Proteins/metabolism ; Recombinant Fusion Proteins/metabolism ; Rod Cell Outer Segment/*metabolism ; Xenopus laevis
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    Generation of functional ventricular heart muscle from mouse ventricular progenitor cells (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-10-17
    Description: The mammalian heart is formed from distinct sets of first and second heart field (FHF and SHF, respectively) progenitors. Although multipotent progenitors have previously been shown to give rise to cardiomyocytes, smooth muscle, and endothelial cells, the mechanism governing the generation of large numbers of differentiated progeny remains poorly understood. We have employed a two-colored fluorescent reporter system to isolate FHF and SHF progenitors from developing mouse embryos and embryonic stem cells. Genome-wide profiling of coding and noncoding transcripts revealed distinct molecular signatures of these progenitor populations. We further identify a committed ventricular progenitor cell in the Islet 1 lineage that is capable of limited in vitro expansion, differentiation, and assembly into functional ventricular muscle tissue, representing a combination of tissue engineering and stem cell biology.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2895998/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2895998/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Domian, Ibrahim J -- Chiravuri, Murali -- van der Meer, Peter -- Feinberg, Adam W -- Shi, Xi -- Shao, Ying -- Wu, Sean M -- Parker, Kevin Kit -- Chien, Kenneth R -- K08 HL081086/HL/NHLBI NIH HHS/ -- K08 HL081086-01/HL/NHLBI NIH HHS/ -- K08 HL091209/HL/NHLBI NIH HHS/ -- R01 HL079126/HL/NHLBI NIH HHS/ -- R01 HL079126-01A1/HL/NHLBI NIH HHS/ -- T32 HL002807/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2009 Oct 16;326(5951):426-9. doi: 10.1126/science.1177350.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cardiovascular Research Center, Massachusetts General Hospital, Charles River Plaza, CPZN 3200, 185 Cambridge Street, Boston, MA 02114-2790, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19833966" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Cell Cycle ; Cell Differentiation ; Cell Line ; Cell Lineage ; Cells, Cultured ; Embryonic Stem Cells/*cytology/physiology ; Gene Expression ; Heart/embryology ; Heart Ventricles/*cytology/embryology ; Mice ; Mice, Transgenic ; Muscle Development ; Myocardial Contraction ; Myocytes, Cardiac/*cytology/physiology ; Oligonucleotide Array Sequence Analysis ; *Tissue Engineering ; *Ventricular Function
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    RSY-1 is a local inhibitor of presynaptic assembly in C. elegans (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-03-17
    Description: As fundamental units of neuronal communication, chemical synapses are composed of presynaptic and postsynaptic specializations that form at specific locations with defined shape and size. Synaptic assembly must be tightly regulated to prevent overgrowth of the synapse size and number, but the molecular mechanisms that inhibit synapse assembly are poorly understood. We identified regulator of synaptogenesis-1 (RSY-1) as an evolutionarily conserved molecule that locally antagonized presynaptic assembly. The loss of RSY-1 in Caenorhabditis elegans led to formation of extra synapses and recruitment of excessive synaptic material to presynaptic sites. RSY-1 directly interacted with and negatively regulated SYD-2/liprin-alpha, a master assembly molecule that recruits numerous synaptic components to presynaptic sites. RSY-1 also bound and regulated SYD-1, a synaptic protein required for proper functioning of SYD-2. Thus, local inhibitory mechanisms govern synapse formation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3087376/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3087376/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Patel, Maulik R -- Shen, Kang -- 1R01NS048392/NS/NINDS NIH HHS/ -- R01 NS048392/NS/NINDS NIH HHS/ -- R01 NS048392-05/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Mar 13;323(5920):1500-3. doi: 10.1126/science.1169025.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neurosciences Program, Stanford University, 385 Serra Mall, Herrin Labs, Room 144, Stanford University, Stanford,CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19286562" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Genetically Modified ; Caenorhabditis elegans/genetics/*physiology ; Caenorhabditis elegans Proteins/chemistry/genetics/*metabolism ; Carrier Proteins/metabolism ; Cell Line ; Cell Nucleus/metabolism ; Humans ; Mutation ; Nerve Tissue Proteins/metabolism ; Nuclear Proteins/chemistry/genetics/*metabolism ; Phosphoproteins/genetics/metabolism ; Protein Binding ; Protein Interaction Mapping ; Protein Isoforms/chemistry/genetics/metabolism ; Protein Structure, Tertiary ; Recombinant Fusion Proteins/metabolism ; Synapses/metabolism/*physiology
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    Mammalian expression of infrared fluorescent proteins engineered from a bacterial phytochrome (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-05-09
    Description: Visibly fluorescent proteins (FPs) from jellyfish and corals have revolutionized many areas of molecular and cell biology, but the use of FPs in intact animals, such as mice, has been handicapped by poor penetration of excitation light. We now show that a bacteriophytochrome from Deinococcus radiodurans, incorporating biliverdin as the chromophore, can be engineered into monomeric, infrared-fluorescent proteins (IFPs), with excitation and emission maxima of 684 and 708 nm, respectively; extinction coefficient 〉90,000 M(-1) cm(-1); and quantum yield of 0.07. IFPs express well in mammalian cells and mice and spontaneously incorporate biliverdin, which is ubiquitous as the initial intermediate in heme catabolism but has negligible fluorescence by itself. Because their wavelengths penetrate tissue well, IFPs are suitable for whole-body imaging. The IFPs developed here provide a scaffold for further engineering.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2763207/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2763207/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shu, Xiaokun -- Royant, Antoine -- Lin, Michael Z -- Aguilera, Todd A -- Lev-Ram, Varda -- Steinbach, Paul A -- Tsien, Roger Y -- R01 CA158448/CA/NCI NIH HHS/ -- R01 GM086197/GM/NIGMS NIH HHS/ -- R01 GM086197-01/GM/NIGMS NIH HHS/ -- R01 NS027177/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 May 8;324(5928):804-7. doi: 10.1126/science.1168683.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of California at San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0647, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19423828" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviridae/genetics ; Amino Acid Sequence ; Animals ; *Biliverdine/chemistry/metabolism ; Cell Line ; Deinococcus/*chemistry ; Diagnostic Imaging ; Fluorescence ; Humans ; Liver/anatomy & histology ; *Luminescent Proteins/chemistry/metabolism ; Mice ; Molecular Sequence Data ; *Phytochrome/chemistry/genetics/metabolism ; *Protein Engineering ; Recombinant Fusion Proteins/chemistry/metabolism ; Spectrophotometry, Infrared ; Whole Body Imaging
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    Apicomplexan parasites co-opt host calpains to facilitate their escape from infected cells (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-04-04
    Description: Apicomplexan parasites, including Plasmodium falciparum and Toxoplasma gondii (the causative agents of malaria and toxoplasmosis, respectively), are responsible for considerable morbidity and mortality worldwide. These pathogenic protozoa replicate within an intracellular vacuole inside of infected host cells, from which they must escape to initiate a new lytic cycle. By integrating cell biological, pharmacological, and genetic approaches, we provide evidence that both Plasmodium and Toxoplasma hijack host cell calpain proteases to facilitate parasite egress. Immunodepletion or inhibition of calpain-1 in hypotonically lysed and resealed erythrocytes prevented the escape of P. falciparum parasites, which was restored by adding purified calpain-1. Similarly, efficient egress of T. gondii from mammalian fibroblasts was blocked by either small interfering RNA-mediated suppression or genetic deletion of calpain activity and could be restored by genetic complementation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3391539/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3391539/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chandramohanadas, Rajesh -- Davis, Paul H -- Beiting, Daniel P -- Harbut, Michael B -- Darling, Claire -- Velmourougane, Geetha -- Lee, Ming Yeh -- Greer, Peter A -- Roos, David S -- Greenbaum, Doron C -- F32 AI075846/AI/NIAID NIH HHS/ -- F32 AI075846-02/AI/NIAID NIH HHS/ -- F32 AI077268/AI/NIAID NIH HHS/ -- F32 AI077268-02/AI/NIAID NIH HHS/ -- R37 AI028724/AI/NIAID NIH HHS/ -- R37 AI028724-17/AI/NIAID NIH HHS/ -- T32 GM008076/GM/NIGMS NIH HHS/ -- T32 GM008076-24/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2009 May 8;324(5928):794-7. doi: 10.1126/science.1171085. Epub 2009 Apr 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of Pennsylvania, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19342550" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calpain/blood/genetics/*metabolism ; Cell Line ; Cell Line, Tumor ; Erythrocytes/*parasitology ; Fibroblasts/parasitology ; Humans ; Leucine/analogs & derivatives/pharmacology ; Life Cycle Stages ; Merozoites/physiology ; Mice ; Mice, Knockout ; Plasmodium falciparum/growth & development/metabolism/*pathogenicity/physiology ; RNA, Small Interfering ; Schizonts/physiology ; Toxoplasma/growth & development/metabolism/*pathogenicity/physiology
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    Jmjd6 catalyses lysyl-hydroxylation of U2AF65, a protein associated with RNA splicing (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-07-04
    Description: The finding that the metazoan hypoxic response is regulated by oxygen-dependent posttranslational hydroxylations, which regulate the activity and lifetime of hypoxia-inducible factor (HIF), has raised the question of whether other hydroxylases are involved in the regulation of gene expression. We reveal that the splicing factor U2 small nuclear ribonucleoprotein auxiliary factor 65-kilodalton subunit (U2AF65) undergoes posttranslational lysyl-5-hydroxylation catalyzed by the Fe(II) and 2-oxoglutarate-dependent dioxygenase Jumonji domain-6 protein (Jmjd6). Jmjd6 is a nuclear protein that has an important role in vertebrate development and is a human homolog of the HIF asparaginyl-hydroxylase. Jmjd6 is shown to change alternative RNA splicing of some, but not all, of the endogenous and reporter genes, supporting a specific role for Jmjd6 in the regulation of RNA splicing.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Webby, Celia J -- Wolf, Alexander -- Gromak, Natalia -- Dreger, Mathias -- Kramer, Holger -- Kessler, Benedikt -- Nielsen, Michael L -- Schmitz, Corinna -- Butler, Danica S -- Yates, John R 3rd -- Delahunty, Claire M -- Hahn, Phillip -- Lengeling, Andreas -- Mann, Matthias -- Proudfoot, Nicholas J -- Schofield, Christopher J -- Bottger, Angelika -- 084655/Wellcome Trust/United Kingdom -- G9826944/Medical Research Council/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2009 Jul 3;325(5936):90-3. doi: 10.1126/science.1175865.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Chemistry Research Laboratory and Oxford Centre for Integrative Systems Biology, University of Oxford, 12 Mansfield Road, Oxford, Oxon OX1 3TA, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19574390" target="_blank"〉PubMed〈/a〉
    Keywords: *Alternative Splicing ; Amino Acid Sequence ; Biocatalysis ; Cell Line ; Chromatography, Liquid ; HeLa Cells ; Humans ; Hydroxylation ; Jumonji Domain-Containing Histone Demethylases ; Lysine/metabolism ; Molecular Sequence Data ; Nuclear Proteins/chemistry/*metabolism ; Protein Processing, Post-Translational ; RNA, Small Interfering ; Receptors, Cell Surface/genetics/*metabolism ; Recombinant Proteins/metabolism ; Ribonucleoproteins/chemistry/*metabolism ; Tandem Mass Spectrometry ; Tropomyosin/genetics
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    The nuclear DNA base 5-hydroxymethylcytosine is present in Purkinje neurons and the brain (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-04-18
    Description: Despite the importance of epigenetic regulation in neurological disorders, little is known about neuronal chromatin. Cerebellar Purkinje neurons have large and euchromatic nuclei, whereas granule cell nuclei are small and have a more typical heterochromatin distribution. While comparing the abundance of 5-methylcytosine in Purkinje and granule cell nuclei, we detected the presence of an unusual DNA nucleotide. Using thin-layer chromatography, high-pressure liquid chromatography, and mass spectrometry, we identified the nucleotide as 5-hydroxymethyl-2'-deoxycytidine (hmdC). hmdC constitutes 0.6% of total nucleotides in Purkinje cells, 0.2% in granule cells, and is not present in cancer cell lines. hmdC is a constituent of nuclear DNA that is highly abundant in the brain, suggesting a role in epigenetic control of neuronal function.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3263819/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3263819/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kriaucionis, Skirmantas -- Heintz, Nathaniel -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 May 15;324(5929):929-30. doi: 10.1126/science.1169786. Epub 2009 Apr 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Biology, Howard Hughes Medical Institute, Rockefeller University, New York, NY 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19372393" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Brain Chemistry ; Cell Line ; Cerebellum/*chemistry/cytology ; Chromatography, High Pressure Liquid ; Chromatography, Thin Layer ; Cytosine/*analogs & derivatives/analysis ; DNA/*chemistry ; DNA Damage ; Deoxycytidine/*analogs & derivatives/analysis ; Humans ; Mass Spectrometry ; Mice ; Purkinje Cells/*chemistry
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    Norbin is an endogenous regulator of metabotropic glutamate receptor 5 signaling (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-12-17
    Description: Metabotropic glutamate receptor 5 (mGluR5) is highly expressed in the mammalian central nervous system (CNS). It is involved in multiple physiological functions and is a target for treatment of various CNS disorders, including schizophrenia. We report that Norbin, a neuron-specific protein, physically interacts with mGluR5 in vivo, increases the cell surface localization of the receptor, and positively regulates mGluR5 signaling. Genetic deletion of Norbin attenuates mGluR5-dependent stable changes in synaptic function measured as long-term depression or long-term potentiation of synaptic transmission in the hippocampus. As with mGluR5 knockout mice or mice treated with mGluR5-selective antagonists, Norbin knockout mice showed a behavioral phenotype associated with a rodent model of schizophrenia, as indexed by alterations both in sensorimotor gating and psychotomimetic-induced locomotor activity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2796550/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2796550/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Hong -- Westin, Linda -- Nong, Yi -- Birnbaum, Shari -- Bendor, Jacob -- Brismar, Hjalmar -- Nestler, Eric -- Aperia, Anita -- Flajolet, Marc -- Greengard, Paul -- DA 10044/DA/NIDA NIH HHS/ -- MH074866/MH/NIMH NIH HHS/ -- MH66172/MH/NIMH NIH HHS/ -- P01 DA010044/DA/NIDA NIH HHS/ -- P01 DA010044-020002/DA/NIDA NIH HHS/ -- P01 DA010044-030002/DA/NIDA NIH HHS/ -- P01 DA010044-04/DA/NIDA NIH HHS/ -- P01 DA010044-040002/DA/NIDA NIH HHS/ -- P01 DA010044-05/DA/NIDA NIH HHS/ -- P01 DA010044-050002/DA/NIDA NIH HHS/ -- P01 DA010044-06/DA/NIDA NIH HHS/ -- P01 DA010044-060002/DA/NIDA NIH HHS/ -- P01 DA010044-07/DA/NIDA NIH HHS/ -- P01 DA010044-070002/DA/NIDA NIH HHS/ -- P01 DA010044-08/DA/NIDA NIH HHS/ -- P01 DA010044-080002/DA/NIDA NIH HHS/ -- P01 DA010044-09/DA/NIDA NIH HHS/ -- P01 DA010044-090002/DA/NIDA NIH HHS/ -- P01 DA010044-10/DA/NIDA NIH HHS/ -- P01 DA010044-100002/DA/NIDA NIH HHS/ -- P01 DA010044-11/DA/NIDA NIH HHS/ -- P01 DA010044-110005/DA/NIDA NIH HHS/ -- P01 DA010044-12/DA/NIDA NIH HHS/ -- P01 DA010044-120005/DA/NIDA NIH HHS/ -- P01 DA010044-129002/DA/NIDA NIH HHS/ -- P01 DA010044-13/DA/NIDA NIH HHS/ -- P01 DA010044-130005/DA/NIDA NIH HHS/ -- P01 DA010044-139002/DA/NIDA NIH HHS/ -- P01 DA010044-14/DA/NIDA NIH HHS/ -- P01 DA010044-140005/DA/NIDA NIH HHS/ -- P01 DA010044-149002/DA/NIDA NIH HHS/ -- P01 DA010044-14S1/DA/NIDA NIH HHS/ -- P01 DA010044-14S10005/DA/NIDA NIH HHS/ -- P01 DA010044-14S19002/DA/NIDA NIH HHS/ -- P50 MH074866/MH/NIMH NIH HHS/ -- P50 MH074866-010001/MH/NIMH NIH HHS/ -- P50 MH074866-020001/MH/NIMH NIH HHS/ -- P50 MH074866-030001/MH/NIMH NIH HHS/ -- P50 MH074866-039001/MH/NIMH NIH HHS/ -- P50 MH074866-040001/MH/NIMH NIH HHS/ -- P50 MH074866-050001/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2009 Dec 11;326(5959):1554-7. doi: 10.1126/science.1178496.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular and Cellular Neuroscience, Rockefeller University, New York, NY 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20007903" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*metabolism ; Calcium/metabolism ; Calcium Signaling ; Cell Line ; Cell Membrane/metabolism ; Humans ; Mice ; Mice, Knockout ; Motor Activity ; Nerve Tissue Proteins/genetics/*metabolism ; Neuronal Plasticity ; Protein Binding ; Rats ; Receptor, Metabotropic Glutamate 5 ; Receptors, Metabotropic Glutamate/genetics/*metabolism ; Reflex, Startle ; Schizophrenia/physiopathology ; *Signal Transduction ; Synaptic Transmission ; Transfection
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    State stem cell initiatives. CIRM close-hauled, seeks bonds to sustain headway (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-03-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holden, Constance -- New York, N.Y. -- Science. 2009 Mar 27;323(5922):1660-1. doi: 10.1126/science.323.5922.1660a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19325091" target="_blank"〉PubMed〈/a〉
    Keywords: *Academies and Institutes/economics/organization & administration ; *Biomedical Research/economics ; California ; Cell Line ; Clinical Trials as Topic ; Embryo Research/economics/legislation & jurisprudence ; *Embryonic Stem Cells ; Financing, Government ; Humans ; National Institutes of Health (U.S.) ; Research Support as Topic ; State Government ; *Stem Cells ; United States
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    ATP-citrate lyase links cellular metabolism to histone acetylation (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-05-23
    Description: Histone acetylation in single-cell eukaryotes relies on acetyl coenzyme A (acetyl-CoA) synthetase enzymes that use acetate to produce acetyl-CoA. Metazoans, however, use glucose as their main carbon source and have exposure only to low concentrations of extracellular acetate. We have shown that histone acetylation in mammalian cells is dependent on adenosine triphosphate (ATP)-citrate lyase (ACL), the enzyme that converts glucose-derived citrate into acetyl-CoA. We found that ACL is required for increases in histone acetylation in response to growth factor stimulation and during differentiation, and that glucose availability can affect histone acetylation in an ACL-dependent manner. Together, these findings suggest that ACL activity is required to link growth factor-induced increases in nutrient metabolism to the regulation of histone acetylation and gene expression.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2746744/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2746744/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wellen, Kathryn E -- Hatzivassiliou, Georgia -- Sachdeva, Uma M -- Bui, Thi V -- Cross, Justin R -- Thompson, Craig B -- R01 CA092660/CA/NCI NIH HHS/ -- R01 CA092660-09/CA/NCI NIH HHS/ -- R01 CA105463/CA/NCI NIH HHS/ -- T32-HL07439-27/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2009 May 22;324(5930):1076-80. doi: 10.1126/science.1164097.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cancer Biology, Abramson Family Cancer Research Institute, University of Pennsylvania, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19461003" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; ATP Citrate (pro-S)-Lyase/genetics/*metabolism ; Acetate-CoA Ligase/genetics/metabolism ; Acetyl Coenzyme A/metabolism ; Acetylation ; Adipocytes/cytology/metabolism ; Animals ; Cell Differentiation ; Cell Line ; Cell Line, Tumor ; Cell Nucleus/enzymology ; Cell Proliferation ; Citric Acid/metabolism ; Cytoplasm/enzymology ; Gene Expression Regulation ; Glucose/*metabolism ; Glycolysis ; Histone Deacetylase Inhibitors ; Histone Deacetylases/metabolism ; Histones/*metabolism ; Humans ; Intercellular Signaling Peptides and Proteins/metabolism ; Interleukin-3/metabolism ; Mice ; RNA Interference ; Transcription, Genetic
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    Obama executive order. For Congress and NIH, headaches ahead on stem cells (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-03-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holden, Constance -- New York, N.Y. -- Science. 2009 Mar 20;323(5921):1552-3. doi: 10.1126/science.323.5921.1552a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19299595" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Cloning, Organism/legislation & jurisprudence ; Embryo Research/ethics/*legislation & jurisprudence ; *Embryonic Stem Cells ; Financing, Government/legislation & jurisprudence ; Government Regulation ; Guidelines as Topic ; Humans ; National Institutes of Health (U.S.) ; Politics ; Research Support as Topic/*legislation & jurisprudence ; United States
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    The E3 ligase TRAF6 regulates Akt ubiquitination and activation (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-08-29
    Description: Akt signaling plays a central role in many biological functions, such as cell proliferation and apoptosis. Because Akt (also known as protein kinase B) resides primarily in the cytosol, it is not known how these signaling molecules are recruited to the plasma membrane and subsequently activated by growth factor stimuli. We found that the protein kinase Akt undergoes lysine-63 chain ubiquitination, which is important for Akt membrane localization and phosphorylation. TRAF6 was found to be a direct E3 ligase for Akt and was essential for Akt ubiquitination, membrane recruitment, and phosphorylation upon growth-factor stimulation. The human cancer-associated Akt mutant displayed an increase in Akt ubiquitination, in turn contributing to the enhancement of Akt membrane localization and phosphorylation. Thus, Akt ubiquitination is an important step for oncogenic Akt activation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3008763/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3008763/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yang, Wei-Lei -- Wang, Jing -- Chan, Chia-Hsin -- Lee, Szu-Wei -- Campos, Alejandro D -- Lamothe, Betty -- Hur, Lana -- Grabiner, Brian C -- Lin, Xin -- Darnay, Bryant G -- Lin, Hui-Kuan -- R01 CA149321/CA/NCI NIH HHS/ -- R01 CA149321-02/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2009 Aug 28;325(5944):1134-8. doi: 10.1126/science.1175065.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Oncology, The University of Texas M. D. Anderson Cancer Center, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19713527" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Animals ; Apoptosis ; Cell Line ; Cell Line, Tumor ; Cell Membrane/*metabolism ; Humans ; Insulin-Like Growth Factor I/pharmacology ; Interleukin-1beta/pharmacology ; Lipopolysaccharides/pharmacology ; Mice ; Neoplasm Transplantation ; Neoplasms, Experimental/metabolism ; Phosphatidylinositol Phosphates/metabolism ; Phosphorylation ; Proto-Oncogene Proteins c-akt/chemistry/*metabolism ; *Signal Transduction ; TNF Receptor-Associated Factor 6/genetics/*metabolism ; Transplantation, Heterologous ; Ubiquitin-Protein Ligases/*metabolism ; Ubiquitination
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 41
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    Circadian clock feedback cycle through NAMPT-mediated NAD+ biosynthesis (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-03-21
    Description: The circadian clock is encoded by a transcription-translation feedback loop that synchronizes behavior and metabolism with the light-dark cycle. Here we report that both the rate-limiting enzyme in mammalian nicotinamide adenine dinucleotide (NAD+) biosynthesis, nicotinamide phosphoribosyltransferase (NAMPT), and levels of NAD+ display circadian oscillations that are regulated by the core clock machinery in mice. Inhibition of NAMPT promotes oscillation of the clock gene Per2 by releasing CLOCK:BMAL1 from suppression by SIRT1. In turn, the circadian transcription factor CLOCK binds to and up-regulates Nampt, thus completing a feedback loop involving NAMPT/NAD+ and SIRT1/CLOCK:BMAL1.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2738420/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2738420/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ramsey, Kathryn Moynihan -- Yoshino, Jun -- Brace, Cynthia S -- Abrassart, Dana -- Kobayashi, Yumiko -- Marcheva, Biliana -- Hong, Hee-Kyung -- Chong, Jason L -- Buhr, Ethan D -- Lee, Choogon -- Takahashi, Joseph S -- Imai, Shin-Ichiro -- Bass, Joseph -- AG02150/AG/NIA NIH HHS/ -- P01 AG011412/AG/NIA NIH HHS/ -- P50 MH074924/MH/NIMH NIH HHS/ -- R01 AG024150/AG/NIA NIH HHS/ -- R01 AG024150-05/AG/NIA NIH HHS/ -- T32 DK007169/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 May 1;324(5927):651-4. doi: 10.1126/science.1171641. Epub 2009 Mar 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Northwestern University Feinberg School of Medicine, 2200 Campus Drive, Evanston, IL 60208-3500, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19299583" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors ; Acrylamides/pharmacology ; Adipose Tissue, White/metabolism ; Animals ; Basic Helix-Loop-Helix Transcription Factors/genetics/metabolism ; *Biological Clocks ; CLOCK Proteins ; Cell Cycle Proteins/genetics ; Cell Line ; Cell Line, Tumor ; *Circadian Rhythm ; Cytokines/antagonists & inhibitors/genetics/*metabolism ; Enzyme Inhibitors/pharmacology ; *Feedback, Physiological ; Gene Expression Regulation ; Hepatocytes/metabolism ; Humans ; Liver/metabolism ; Mice ; NAD/*biosynthesis ; Nicotinamide Phosphoribosyltransferase/antagonists & ; inhibitors/genetics/*metabolism ; Nuclear Proteins/genetics ; Period Circadian Proteins ; Piperidines/pharmacology ; Protein Binding ; Sirtuin 1 ; Sirtuins/metabolism ; Trans-Activators/genetics/metabolism ; Transcription Factors/genetics ; Transcription, Genetic
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Activation of the PI3K pathway in cancer through inhibition of PTEN by exchange factor P-REX2a (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-09-05
    Description: PTEN (phosphatase and tensin homolog on chromosome 10) is a tumor suppressor whose cellular regulation remains incompletely understood. We identified phosphatidylinositol 3,4,5-trisphosphate RAC exchanger 2a (P-REX2a) as a PTEN-interacting protein. P-REX2a mRNA was more abundant in human cancer cells and significantly increased in tumors with wild-type PTEN that expressed an activated mutant of PIK3CA encoding the p110 subunit of phosphoinositide 3-kinase subunit alpha (PI3Kalpha). P-REX2a inhibited PTEN lipid phosphatase activity and stimulated the PI3K pathway only in the presence of PTEN. P-REX2a stimulated cell growth and cooperated with a PIK3CA mutant to promote growth factor-independent proliferation and transformation. Depletion of P-REX2a reduced amounts of phosphorylated AKT and growth in human cell lines with intact PTEN. Thus, P-REX2a is a component of the PI3K pathway that can antagonize PTEN in cancer cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2936784/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2936784/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fine, Barry -- Hodakoski, Cindy -- Koujak, Susan -- Su, Tao -- Saal, Lao H -- Maurer, Matthew -- Hopkins, Benjamin -- Keniry, Megan -- Sulis, Maria Luisa -- Mense, Sarah -- Hibshoosh, Hanina -- Parsons, Ramon -- CA097403/CA/NCI NIH HHS/ -- P01 CA097403/CA/NCI NIH HHS/ -- P01 CA097403-01A10003/CA/NCI NIH HHS/ -- P01 CA097403-06A1/CA/NCI NIH HHS/ -- R01 CA082783/CA/NCI NIH HHS/ -- R01 CA082783-06/CA/NCI NIH HHS/ -- R01 CA082783-07/CA/NCI NIH HHS/ -- R01 CA082783-08/CA/NCI NIH HHS/ -- R01 CA082783-09/CA/NCI NIH HHS/ -- R01 CA082783-10/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2009 Sep 4;325(5945):1261-5. doi: 10.1126/science.1173569.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Cancer Genetics and Herbert Irving Comprehensive Cancer Center, Columbia University, 1130 St. Nicholas Avenue, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19729658" target="_blank"〉PubMed〈/a〉
    Keywords: Breast Neoplasms/genetics/metabolism/pathology ; Cell Line ; Cell Line, Tumor ; Cell Proliferation ; Female ; GTPase-Activating Proteins/genetics/*metabolism ; Guanine Nucleotide Exchange Factors ; Humans ; Male ; Mutation ; Neoplasms/genetics/*metabolism/pathology ; PTEN Phosphohydrolase/*antagonists & inhibitors/chemistry/genetics/*metabolism ; Phosphatidylinositol 3-Kinases/*metabolism ; Phosphorylation ; Protein Binding ; Protein Structure, Tertiary ; Proto-Oncogene Proteins c-akt/metabolism ; Signal Transduction
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    Generation of medaka fish haploid embryonic stem cells (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-10-17
    Description: Haploid embryonic stem (ES) cells combine haploidy and pluripotency, enabling direct genetic analyses of recessive phenotypes in vertebrate cells. Haploid cells have been elusive for culture, due to their inferior growth and genomic instability. Here, we generated gynogenetic medaka embryos and obtained three haploid ES cell lines that retained pluripotency and competitive growth. Upon nuclear transfer into unfertilized oocytes, the haploid ES cells, even after genetic engineering, generated viable offspring capable of germline transmission. Hence, haploid medaka ES cells stably maintain normal growth, pluripotency, and genomic integrity. Mosaic oocytes created by combining a mitotic nucleus and a meiotic nucleus can generate fertile fish offspring. Haploid ES cells may offer a yeast-like system for analyzing recessive phenotypes in numerous cell lineages of vertebrates in vitro.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yi, Meisheng -- Hong, Ni -- Hong, Yunhan -- New York, N.Y. -- Science. 2009 Oct 16;326(5951):430-3. doi: 10.1126/science.1175151.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, National University of Singapore, 10 Kent Ridge Crescent, Singapore 119260.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19833967" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Line ; Cell Proliferation ; Cell Shape ; Chromosomal Instability ; Cloning, Organism ; Crosses, Genetic ; Diploidy ; Embryo, Nonmammalian/cytology ; Embryonic Stem Cells/cytology/*physiology ; Female ; *Haploidy ; Male ; Nuclear Transfer Techniques ; Oocytes ; *Oryzias/embryology/genetics/physiology ; Phenotype ; Pluripotent Stem Cells/cytology/*physiology ; Transplantation Chimera
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    Developmental biology. Pluripotent chromatin state (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-01-10
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4126799/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4126799/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chi, Andrew S -- Bernstein, Bradley E -- U54 HG004570/HG/NHGRI NIH HHS/ -- U54 HG004570-01/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2009 Jan 9;323(5911):220-1. doi: 10.1126/science.1166261.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Pathology Unit and Center for Cancer Research, Massachusetts General Hospital, Charlestown, MA 02129, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19131621" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Line ; Cell Lineage ; Chromatin/*physiology ; Chromatin Assembly and Disassembly ; Embryonic Stem Cells/*physiology ; Gene Expression Regulation, Developmental ; Nucleosomes/physiology ; Pluripotent Stem Cells/*physiology ; Polycomb-Group Proteins ; Repressor Proteins/metabolism ; Transcription Factors/metabolism ; *Transcription, Genetic
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    AMPK regulates the circadian clock by cryptochrome phosphorylation and degradation (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-10-17
    Description: Circadian clocks coordinate behavioral and physiological processes with daily light-dark cycles by driving rhythmic transcription of thousands of genes. Whereas the master clock in the brain is set by light, pacemakers in peripheral organs, such as the liver, are reset by food availability, although the setting, or "entrainment," mechanisms remain mysterious. Studying mouse fibroblasts, we demonstrated that the nutrient-responsive adenosine monophosphate-activated protein kinase (AMPK) phosphorylates and destabilizes the clock component cryptochrome 1 (CRY1). In mouse livers, AMPK activity and nuclear localization were rhythmic and inversely correlated with CRY1 nuclear protein abundance. Stimulation of AMPK destabilized cryptochromes and altered circadian rhythms, and mice in which the AMPK pathway was genetically disrupted showed alterations in peripheral clocks. Thus, phosphorylation by AMPK enables cryptochrome to transduce nutrient signals to circadian clocks in mammalian peripheral organs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2819106/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2819106/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lamia, Katja A -- Sachdeva, Uma M -- DiTacchio, Luciano -- Williams, Elliot C -- Alvarez, Jacqueline G -- Egan, Daniel F -- Vasquez, Debbie S -- Juguilon, Henry -- Panda, Satchidananda -- Shaw, Reuben J -- Thompson, Craig B -- Evans, Ronald M -- CA104838/CA/NCI NIH HHS/ -- DK057978/DK/NIDDK NIH HHS/ -- DK062434/DK/NIDDK NIH HHS/ -- DK080425/DK/NIDDK NIH HHS/ -- EY016807/EY/NEI NIH HHS/ -- P01 CA104838/CA/NCI NIH HHS/ -- P01 CA104838-05S1/CA/NCI NIH HHS/ -- P30 CA014195/CA/NCI NIH HHS/ -- R01 DK080425/DK/NIDDK NIH HHS/ -- R01 DK080425-03/DK/NIDDK NIH HHS/ -- R01 EY016807/EY/NEI NIH HHS/ -- R01 EY016807-03/EY/NEI NIH HHS/ -- R37 DK057978/DK/NIDDK NIH HHS/ -- R37 DK057978-31/DK/NIDDK NIH HHS/ -- T32 HL007439/HL/NHLBI NIH HHS/ -- T32 HL007439-27/HL/NHLBI NIH HHS/ -- T32-HL07439-27/HL/NHLBI NIH HHS/ -- U19 DK062434/DK/NIDDK NIH HHS/ -- U19 DK062434-08S19002/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Oct 16;326(5951):437-40. doi: 10.1126/science.1172156.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gene Expression Laboratory, the Salk Institute, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19833968" target="_blank"〉PubMed〈/a〉
    Keywords: AMP-Activated Protein Kinases/*metabolism ; ARNTL Transcription Factors ; Amino Acid Substitution ; Aminoimidazole Carboxamide/analogs & derivatives/pharmacology ; Animals ; Basic Helix-Loop-Helix Transcription Factors/genetics ; Cell Line ; Cell Nucleus/metabolism ; Cells, Cultured ; Circadian Rhythm/*physiology ; Cryptochromes ; Culture Media ; Flavoproteins/genetics/*metabolism ; Food ; Glucose/metabolism/pharmacology ; Humans ; Liver/*metabolism ; Mice ; Mutagenesis, Site-Directed ; Mutant Proteins/metabolism ; Phosphorylation ; Promoter Regions, Genetic ; Protein Stability ; Recombinant Fusion Proteins/metabolism ; Ribonucleotides/pharmacology ; Signal Transduction
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    Exchange of genetic material between cells in plant tissue grafts (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-05-02
    Description: Tissue grafting includes applications ranging from plant breeding to animal organ transplantation. Donor and recipient are generally believed to maintain their genetic integrity, in that the grafted tissues are joined but their genetic materials do not mix. We grafted tobacco plants from two transgenic lines carrying different marker and reporter genes in different cellular compartments, the nucleus and the plastid. Analysis of the graft sites revealed the frequent occurrence of cells harboring both antibiotic resistances and both fluorescent reporters. Our data demonstrate that plant grafting can result in the exchange of genetic information via either large DNA pieces or entire plastid genomes. This observation of novel combinations of genetic material has implications for grafting techniques and also provides a possible path for horizontal gene transfer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stegemann, Sandra -- Bock, Ralph -- New York, N.Y. -- Science. 2009 May 1;324(5927):649-51. doi: 10.1126/science.1170397.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max-Planck-Institut fur Molekulare Pflanzenphysiologie, Am Muhlenberg 1, D-14476 Potsdam-Golm, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19407205" target="_blank"〉PubMed〈/a〉
    Keywords: Breeding ; Cell Line ; Cell Nucleus/genetics ; Chloroplasts/genetics ; Drug Resistance/genetics ; *Gene Transfer, Horizontal ; *Genes, Plant ; Genes, Reporter ; Green Fluorescent Proteins/analysis ; Kanamycin/pharmacology ; Luminescent Proteins/analysis ; Plants, Genetically Modified ; Selection, Genetic ; Spectinomycin/pharmacology ; Tobacco/cytology/*genetics
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    Cell-specific information processing in segregating populations of Eph receptor ephrin-expressing cells (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-12-17
    Description: Cells have self-organizing properties that control their behavior in complex tissues. Contact between cells expressing either B-type Eph receptors or their transmembrane ephrin ligands initiates bidirectional signals that regulate cell positioning. However, simultaneously investigating how information is processed in two interacting cell types remains a challenge. We implemented a proteomic strategy to systematically determine cell-specific signaling networks underlying EphB2- and ephrin-B1-controlled cell sorting. Quantitative mass spectrometric analysis of mixed populations of EphB2- and ephrin-B1-expressing cells that were labeled with different isotopes revealed cell-specific tyrosine phosphorylation events. Functional associations between these phosphotyrosine signaling networks and cell sorting were established with small interfering RNA screening. Data-driven network modeling revealed that signaling between mixed EphB2- and ephrin-B1-expressing cells is asymmetric and that the distinct cell types use different tyrosine kinases and targets to process signals induced by cell-cell contact. We provide systems- and cell-specific network models of contact-initiated signaling between two distinct cell types.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jorgensen, Claus -- Sherman, Andrew -- Chen, Ginny I -- Pasculescu, Adrian -- Poliakov, Alexei -- Hsiung, Marilyn -- Larsen, Brett -- Wilkinson, David G -- Linding, Rune -- Pawson, Tony -- MC_U117532048/Medical Research Council/United Kingdom -- MOP-6849/Canadian Institutes of Health Research/Canada -- New York, N.Y. -- Science. 2009 Dec 11;326(5959):1502-9. doi: 10.1126/science.1176615.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Samuel Lunenfeld Research Institute (SLRI), Mount Sinai Hospital, Toronto M5G 1X5, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20007894" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/metabolism ; Algorithms ; Cell Line ; Ephrin-B1/genetics/*metabolism ; Humans ; Ligands ; Mass Spectrometry ; Models, Biological ; PDZ Domains ; Phosphorylation ; Protein Binding ; Protein Interaction Domains and Motifs ; Protein-Tyrosine Kinases/metabolism ; Proteomics ; RNA, Small Interfering ; Receptor, EphB2/genetics/*metabolism ; *Signal Transduction ; Tyrosine/metabolism ; src Homology Domains
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    Nuclear hormone receptor regulation of microRNAs controls developmental progression (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-04-04
    Description: In response to small-molecule signals such as retinoids or steroids, nuclear receptors activate gene expression to regulate development in different tissues. MicroRNAs turn off target gene expression within cells by binding complementary regions in messenger RNA transcripts, and they have been broadly implicated in development and disease. Here we show that the Caenorhabditis elegans nuclear receptor DAF-12 and its steroidal ligand directly activate promoters of let-7 microRNA family members to down-regulate the microRNA target hbl-1, which drives progression of epidermal stem cells from second to third larval stage patterns of cell division. Conversely, the receptor without the ligand represses microRNA expression during developmental arrest. These findings identify microRNAs as components of a hormone-coupled molecular switch that shuts off earlier developmental programs to allow for later ones.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2757405/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2757405/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bethke, Axel -- Fielenbach, Nicole -- Wang, Zhu -- Mangelsdorf, David J -- Antebi, Adam -- GM077201/GM/NIGMS NIH HHS/ -- R01 GM077201/GM/NIGMS NIH HHS/ -- R01 GM077201-03/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Apr 3;324(5923):95-8. doi: 10.1126/science.1164899.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Huffington Center on Aging, Department of Molecular and Cellular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19342589" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Genetically Modified ; Caenorhabditis elegans/cytology/genetics/*growth & development/*metabolism ; Caenorhabditis elegans Proteins/genetics/*metabolism ; Cell Line ; Cholestenes/*metabolism ; DNA-Binding Proteins/genetics/metabolism ; Down-Regulation ; Gene Expression Regulation, Developmental ; Genes, Helminth ; Humans ; Ligands ; MicroRNAs/*genetics ; Mutation ; RNA, Helminth/genetics/metabolism ; Receptors, Cytoplasmic and Nuclear/genetics/*metabolism ; Response Elements ; Signal Transduction ; Transcription Factors/genetics/metabolism ; Transfection ; Up-Regulation
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    Rhes, a striatal specific protein, mediates mutant-huntingtin cytotoxicity (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-06-06
    Description: Huntington's disease (HD) is caused by a polyglutamine repeat in the protein huntingtin (Htt) with mutant Htt (mHtt) expressed throughout the body and similarly in all brain regions. Yet, HD neuropathology is largely restricted to the corpus striatum. We report that the small guanine nucleotide-binding protein Rhes, which is localized very selectively to the striatum, binds physiologically to mHtt. Using cultured cells, we found Rhes induces sumoylation of mHtt, which leads to cytotoxicity. Thus, Rhes-mHtt interactions can account for the localized neuropathology of HD.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2745286/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2745286/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Subramaniam, Srinivasa -- Sixt, Katherine M -- Barrow, Roxanne -- Snyder, Solomon H -- DA00074/DA/NIDA NIH HHS/ -- MH18501/MH/NIMH NIH HHS/ -- R37 MH018501/MH/NIMH NIH HHS/ -- R37 MH018501-40/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2009 Jun 5;324(5932):1327-30. doi: 10.1126/science.1172871.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19498170" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Death ; Cell Line ; Cell Survival ; Corpus Striatum/metabolism ; GTP-Binding Proteins/*metabolism ; Humans ; Mice ; Mice, Transgenic ; Mutant Proteins/metabolism ; Nerve Tissue Proteins/chemistry/*metabolism ; Nuclear Proteins/chemistry/*metabolism ; PC12 Cells ; RNA Interference ; Rats ; Recombinant Fusion Proteins/metabolism ; SUMO-1 Protein/genetics/metabolism ; Small Ubiquitin-Related Modifier Proteins/metabolism ; Substrate Specificity
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    Recombination of retrotransposon and exogenous RNA virus results in nonretroviral cDNA integration (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-01-20
    Description: Retroviruses have the potential to acquire host cell-derived genetic material during reverse transcription and can integrate into the genomes of larger, more complex DNA viruses. In contrast, RNA viruses were believed not to integrate into the host's genome under any circumstances. We found that illegitimate recombination between an exogenous nonretroviral RNA virus, lymphocytic choriomeningitis virus, and the endogenous intracisternal A-type particle (IAP) retrotransposon occurred and led to reverse transcription of exogenous viral RNA. The resulting complementary DNA was integrated into the host's genome with an IAP element. Thus, RNA viruses should be closely scrutinized for any capacity to interact with endogenous retroviral elements before their approval for therapeutic use in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Geuking, Markus B -- Weber, Jacqueline -- Dewannieux, Marie -- Gorelik, Elieser -- Heidmann, Thierry -- Hengartner, Hans -- Zinkernagel, Rolf M -- Hangartner, Lars -- New York, N.Y. -- Science. 2009 Jan 16;323(5912):393-6. doi: 10.1126/science.1167375.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Experimental Immunology, University Hospital Zurich, Schmelzbergstrasse 12, 8091 Zurich, Switzerland. geuking@mcmaster.ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19150848" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arenaviridae Infections/virology ; Base Sequence ; Cell Line ; DNA, Complementary/*genetics ; Genes, Intracisternal A-Particle/*genetics ; Glycoproteins/genetics ; Humans ; Lymphocytic choriomeningitis virus/*genetics ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Polymerase Chain Reaction ; RNA, Viral/*genetics ; *Recombination, Genetic ; *Reverse Transcription ; Transfection ; Viral Proteins/genetics ; *Virus Integration
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    HIN-200 proteins regulate caspase activation in response to foreign cytoplasmic DNA (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-01-10
    Description: The mammalian innate immune system is activated by foreign nucleic acids. Detection of double-stranded DNA (dsDNA) in the cytoplasm triggers characteristic antiviral responses and macrophage cell death. Cytoplasmic dsDNA rapidly activated caspase 3 and caspase 1 in bone marrow-derived macrophages. We identified the HIN-200 family member and candidate lupus susceptibility factor, p202, as a dsDNA binding protein that bound stably and rapidly to transfected DNA. Knockdown studies showed p202 to be an inhibitor of DNA-induced caspase activation. Conversely, the related pyrin domain-containing HIN-200 factor, AIM2 (p210), was required for caspase activation by cytoplasmic dsDNA. This work indicates that HIN-200 proteins can act as pattern recognition receptors mediating responses to cytoplasmic dsDNA.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roberts, Tara L -- Idris, Adi -- Dunn, Jasmyn A -- Kelly, Greg M -- Burnton, Carol M -- Hodgson, Samantha -- Hardy, Lani L -- Garceau, Valerie -- Sweet, Matthew J -- Ross, Ian L -- Hume, David A -- Stacey, Katryn J -- New York, N.Y. -- Science. 2009 Feb 20;323(5917):1057-60. doi: 10.1126/science.1169841. Epub 2009 Jan 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The University of Queensland, Institute for Molecular Bioscience, QLD 4072, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19131592" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caspase 1/*metabolism ; Caspase 3/*metabolism ; Cell Line ; Cytoplasm/*metabolism ; DNA/immunology/*metabolism ; DNA-Binding Proteins/isolation & purification/metabolism ; Enzyme Activation ; Immunity, Innate ; Intracellular Signaling Peptides and Proteins/chemistry/genetics/isolation & ; purification/*metabolism ; Macrophages/immunology/*metabolism ; Membrane Proteins/chemistry/genetics/*metabolism ; Mice ; Mice, Inbred Strains ; RNA, Small Interfering ; Receptors, Pattern Recognition/*metabolism ; Symporters ; Transfection
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    Cytosolic viral sensor RIG-I is a 5'-triphosphate-dependent translocase on double-stranded RNA (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-01-03
    Description: Retinoic acid inducible-gene I (RIG-I) is a cytosolic multidomain protein that detects viral RNA and elicits an antiviral immune response. Two N-terminal caspase activation and recruitment domains (CARDs) transmit the signal, and the regulatory domain prevents signaling in the absence of viral RNA. 5'-triphosphate and double-stranded RNA (dsRNA) are two molecular patterns that enable RIG-I to discriminate pathogenic from self-RNA. However, the function of the DExH box helicase domain that is also required for activity is less clear. Using single-molecule protein-induced fluorescence enhancement, we discovered a robust adenosine 5'-triphosphate-powered dsRNA translocation activity of RIG-I. The CARDs dramatically suppress translocation in the absence of 5'-triphosphate, and the activation by 5'-triphosphate triggers RIG-I to translocate preferentially on dsRNA in cis. This functional integration of two RNA molecular patterns may provide a means to specifically sense and counteract replicating viruses.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3567915/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3567915/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Myong, Sua -- Cui, Sheng -- Cornish, Peter V -- Kirchhofer, Axel -- Gack, Michaela U -- Jung, Jae U -- Hopfner, Karl-Peter -- Ha, Taekjip -- CA82057/CA/NCI NIH HHS/ -- R01 GM065367/GM/NIGMS NIH HHS/ -- R01-GM065367/GM/NIGMS NIH HHS/ -- U19 AI083025/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Feb 20;323(5917):1070-4. doi: 10.1126/science.1168352. Epub 2009 Jan 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Genomic Biology, University of Illinois at Urbana-Champaign, 1206 West Gregory Drive, Champaign, IL 61801, USA. smyong@uiuc.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19119185" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/*metabolism ; Animals ; Cell Line ; Cytosol/metabolism ; DEAD-box RNA Helicases/chemistry/genetics/*metabolism ; Kinetics ; Nucleic Acid Heteroduplexes ; Protein Structure, Tertiary ; RNA/metabolism ; RNA, Double-Stranded/*metabolism ; RNA, Viral/metabolism ; Receptors, Pattern Recognition/chemistry/genetics/*metabolism ; Signal Transduction ; Temperature
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    Genetic code supports targeted insertion of two amino acids by one codon (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-01-10
    Description: Strict one-to-one correspondence between codons and amino acids is thought to be an essential feature of the genetic code. However, we report that one codon can code for two different amino acids with the choice of the inserted amino acid determined by a specific 3' untranslated region structure and location of the dual-function codon within the messenger RNA (mRNA). We found that the codon UGA specifies insertion of selenocysteine and cysteine in the ciliate Euplotes crassus, that the dual use of this codon can occur even within the same gene, and that the structural arrangements of Euplotes mRNA preserve location-dependent dual function of UGA when expressed in mammalian cells. Thus, the genetic code supports the use of one codon to code for multiple amino acids.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3088105/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3088105/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Turanov, Anton A -- Lobanov, Alexey V -- Fomenko, Dmitri E -- Morrison, Hilary G -- Sogin, Mitchell L -- Klobutcher, Lawrence A -- Hatfield, Dolph L -- Gladyshev, Vadim N -- AI058054/AI/NIAID NIH HHS/ -- GM061603/GM/NIGMS NIH HHS/ -- GM065204/GM/NIGMS NIH HHS/ -- R01 GM061603/GM/NIGMS NIH HHS/ -- R01 GM061603-04S2/GM/NIGMS NIH HHS/ -- ZIA BC010767-03/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2009 Jan 9;323(5911):259-61. doi: 10.1126/science.1164748.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Redox Biology Center, University of Nebraska, Lincoln, NE 68588, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19131629" target="_blank"〉PubMed〈/a〉
    Keywords: 3' Untranslated Regions ; Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; Codon/*genetics ; Codon, Terminator/*genetics ; Cysteine/*genetics/metabolism ; Euplotes/chemistry/*genetics ; *Genetic Code ; Humans ; Molecular Sequence Data ; Mutation ; Protozoan Proteins/biosynthesis/chemistry/genetics ; RNA, Protozoan/genetics/metabolism ; RNA, Transfer, Amino Acid-Specific/chemistry/genetics ; RNA, Transfer, Cys/chemistry/genetics ; Recombinant Fusion Proteins/metabolism ; Selenocysteine/*genetics/metabolism ; Selenoproteins/biosynthesis/chemistry/*genetics
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    The orphan G protein-coupled receptor 3 modulates amyloid-beta peptide generation in neurons (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-02-14
    Description: Deposition of the amyloid-beta peptide is a pathological hallmark of Alzheimer's disease. A high-throughput functional genomics screen identified G protein-coupled receptor 3 (GPR3), a constitutively active orphan G protein-coupled receptor, as a modulator of amyloid-beta production. Overexpression of GPR3 stimulated amyloid-beta production, whereas genetic ablation of GPR3 prevented accumulation of the amyloid-beta peptide in vitro and in an Alzheimer's disease mouse model. GPR3 expression led to increased formation and cell-surface localization of the mature gamma-secretase complex in the absence of an effect on Notch processing. GPR3 is highly expressed in areas of the normal human brain implicated in Alzheimer's disease and is elevated in the sporadic Alzheimer's disease brain. Thus, GPR3 represents a potential therapeutic target for the treatment of Alzheimer's disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thathiah, Amantha -- Spittaels, Kurt -- Hoffmann, Marcel -- Staes, Mik -- Cohen, Adrian -- Horre, Katrien -- Vanbrabant, Mieke -- Coun, Frea -- Baekelandt, Veerle -- Delacourte, Andre -- Fischer, David F -- Pollet, Dirk -- De Strooper, Bart -- Merchiers, Pascal -- New York, N.Y. -- Science. 2009 Feb 13;323(5916):946-51. doi: 10.1126/science.1160649.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Developmental Genetics, Vlaams Institute for Biotechnology, Center for Human Genetics, Catholic University of Leuven, Herestraat 49, 3000 Leuven, Belgium.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19213921" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Amyloid Precursor Protein Secretases/metabolism ; Amyloid beta-Peptides/*biosynthesis ; Animals ; Cell Line ; Cell Line, Tumor ; Cells, Cultured ; Female ; Humans ; Male ; Mice ; Middle Aged ; Neurons/*metabolism ; Protein Structure, Tertiary ; Receptors, G-Protein-Coupled/*metabolism ; Receptors, Notch/metabolism ; Signal Transduction
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    Detection of an infectious retrovirus, XMRV, in blood cells of patients with chronic fatigue syndrome (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-10-10
    Description: Chronic fatigue syndrome (CFS) is a debilitating disease of unknown etiology that is estimated to affect 17 million people worldwide. Studying peripheral blood mononuclear cells (PBMCs) from CFS patients, we identified DNA from a human gammaretrovirus, xenotropic murine leukemia virus-related virus (XMRV), in 68 of 101 patients (67%) as compared to 8 of 218 (3.7%) healthy controls. Cell culture experiments revealed that patient-derived XMRV is infectious and that both cell-associated and cell-free transmission of the virus are possible. Secondary viral infections were established in uninfected primary lymphocytes and indicator cell lines after their exposure to activated PBMCs, B cells, T cells, or plasma derived from CFS patients. These findings raise the possibility that XMRV may be a contributing factor in the pathogenesis of CFS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lombardi, Vincent C -- Ruscetti, Francis W -- Das Gupta, Jaydip -- Pfost, Max A -- Hagen, Kathryn S -- Peterson, Daniel L -- Ruscetti, Sandra K -- Bagni, Rachel K -- Petrow-Sadowski, Cari -- Gold, Bert -- Dean, Michael -- Silverman, Robert H -- Mikovits, Judy A -- CA104943/CA/NCI NIH HHS/ -- HHSN26120080001E/PHS HHS/ -- New York, N.Y. -- Science. 2009 Oct 23;326(5952):585-9. doi: 10.1126/science.1179052. Epub 2009 Oct 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whittemore Peterson Institute, Reno, NV 89557, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19815723" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Viral/blood ; B-Lymphocytes/immunology/virology ; Base Sequence ; Cell Line ; Cell Line, Tumor ; Coculture Techniques ; DNA/genetics ; Fatigue Syndrome, Chronic/*virology ; Gammaretrovirus/genetics/immunology/*isolation & purification/physiology ; Gene Products, env/analysis ; Gene Products, gag/analysis ; Genome, Viral ; Humans ; Leukocytes, Mononuclear/*virology ; Lymphocyte Activation ; Male ; Mice ; Molecular Sequence Data ; Prostatic Neoplasms/virology ; Retroviridae Infections/epidemiology/transmission/*virology ; T-Lymphocytes/immunology/virology ; Tumor Virus Infections/epidemiology/transmission/*virology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Meningococcal type IV pili recruit the polarity complex to cross the brain endothelium (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-06-13
    Description: Type IV pili mediate the initial interaction of many bacterial pathogens with their host cells. In Neisseria meningitidis, the causative agent of cerebrospinal meningitis, type IV pili-mediated adhesion to brain endothelial cells is required for bacteria to cross the blood-brain barrier. Here, type IV pili-mediated adhesion of N. meningitidis to human brain endothelial cells was found to recruit the Par3/Par6/PKCzeta polarity complex that plays a pivotal role in the establishment of eukaryotic cell polarity and the formation of intercellular junctions. This recruitment leads to the formation of ectopic intercellular junctional domains at the site of bacteria-host cell interaction and a subsequent depletion of junctional proteins at the cell-cell interface with opening of the intercellular junctions of the brain-endothelial interface.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3980637/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3980637/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Coureuil, Mathieu -- Mikaty, Guillain -- Miller, Florence -- Lecuyer, Herve -- Bernard, Christine -- Bourdoulous, Sandrine -- Dumenil, Guillaume -- Mege, Rene-Marc -- Weksler, Babette B -- Romero, Ignacio A -- Couraud, Pierre-Olivier -- Nassif, Xavier -- New York, N.Y. -- Science. 2009 Jul 3;325(5936):83-7. doi: 10.1126/science.1173196. Epub 2009 Jun 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Universite Paris Descartes, Faculte de Medecine, INSERM (U-570), 75015 Paris, France. mathieu.coureuil@inserm.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19520910" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/metabolism ; Antigens, CD/metabolism ; *Bacterial Adhesion ; Blood-Brain Barrier/metabolism/*microbiology ; Brain/*blood supply/cytology/microbiology ; Cadherins/metabolism ; Catenins ; Cell Adhesion Molecules/metabolism ; Cell Cycle Proteins/metabolism ; Cell Line ; Cell Polarity ; Endothelial Cells/metabolism/microbiology ; Endothelium, Vascular/metabolism/*microbiology/ultrastructure ; Fimbriae, Bacterial/*physiology ; Humans ; Intercellular Junctions/*metabolism/microbiology/ultrastructure ; Membrane Proteins/metabolism ; Neisseria meningitidis/pathogenicity/*physiology ; Phosphoproteins/metabolism ; Protein Kinase C/metabolism ; cdc42 GTP-Binding Protein/metabolism
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    Translocator protein (18 kD) as target for anxiolytics without benzodiazepine-like side effects (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-06-23
    Description: Most antianxiety drugs (anxiolytics) work by modulating neurotransmitters in the brain. Benzodiazepines are fast and effective anxiolytic drugs; however, their long-term use is limited by the development of tolerance and withdrawal symptoms. Ligands of the translocator protein [18 kilodaltons (kD)] may promote the synthesis of endogenous neurosteroids, which also exert anxiolytic effects in animal models. Here, we found that the translocator protein (18 kD) ligand XBD173 enhanced gamma-aminobutyric acid-mediated neurotransmission and counteracted induced panic attacks in rodents in the absence of sedation and tolerance development. XBD173 also exerted antipanic activity in humans and, in contrast to benzodiazepines, did not cause sedation or withdrawal symptoms. Thus, translocator protein (18 kD) ligands are promising candidates for fast-acting anxiolytic drugs with less severe side effects than benzodiazepines.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rupprecht, Rainer -- Rammes, Gerhard -- Eser, Daniela -- Baghai, Thomas C -- Schule, Cornelius -- Nothdurfter, Caroline -- Troxler, Thomas -- Gentsch, Conrad -- Kalkman, Hans O -- Chaperon, Frederique -- Uzunov, Veska -- McAllister, Kevin H -- Bertaina-Anglade, Valerie -- La Rochelle, Christophe Drieu -- Tuerck, Dietrich -- Floesser, Annette -- Kiese, Beate -- Schumacher, Michael -- Landgraf, Rainer -- Holsboer, Florian -- Kucher, Klaus -- New York, N.Y. -- Science. 2009 Jul 24;325(5939):490-3. doi: 10.1126/science.1175055. Epub 2009 Jun 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry and Psychotherapy, Ludwig Maximilian University, Nussbaumstrasse 7, Munich 80336, Germany. rainer.rupprecht@med.uni-muenchen.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19541954" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Alprazolam/pharmacology ; Animals ; Anti-Anxiety Agents/adverse effects/*metabolism ; Benzodiazepines/adverse effects ; Cell Line ; Drug Tolerance ; Humans ; Isoquinolines/pharmacology ; Male ; Mice ; Mice, Inbred C57BL ; Neurotransmitter Agents/metabolism ; Panic Disorder/drug therapy ; Purines/*therapeutic use ; Rats ; Rats, Sprague-Dawley ; Receptors, GABA/*metabolism ; Receptors, GABA-A/metabolism ; Substance Withdrawal Syndrome/prevention & control ; Tetragastrin ; gamma-Aminobutyric Acid/metabolism
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    Sequential regulation of DOCK2 dynamics by two phospholipids during neutrophil chemotaxis (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-03-28
    Description: During chemotaxis, activation of the small guanosine triphosphatase Rac is spatially regulated to organize the extension of membrane protrusions in the direction of migration. In neutrophils, Rac activation is primarily mediated by DOCK2, an atypical guanine nucleotide exchange factor. Upon stimulation, we found that DOCK2 rapidly translocated to the plasma membrane in a phosphatidylinositol 3,4,5-trisphosphate-dependent manner. However, subsequent accumulation of DOCK2 at the leading edge required phospholipase D-mediated synthesis of phosphatidic acid, which stabilized DOCK2 there by means of interaction with a polybasic amino acid cluster, resulting in increased local actin polymerization. When this interaction was blocked, neutrophils failed to form leading edges properly and exhibited defects in chemotaxis. Thus, intracellular DOCK2 dynamics are sequentially regulated by distinct phospholipids to localize Rac activation during neutrophil chemotaxis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3761877/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3761877/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nishikimi, Akihiko -- Fukuhara, Hideo -- Su, Wenjuan -- Hongu, Tsunaki -- Takasuga, Shunsuke -- Mihara, Hisashi -- Cao, Qinhong -- Sanematsu, Fumiyuki -- Kanai, Motomu -- Hasegawa, Hiroshi -- Tanaka, Yoshihiko -- Shibasaki, Masakatsu -- Kanaho, Yasunori -- Sasaki, Takehiko -- Frohman, Michael A -- Fukui, Yoshinori -- R01 GM084251/GM/NIGMS NIH HHS/ -- R01GM71520/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2009 Apr 17;324(5925):384-7. doi: 10.1126/science.1170179. Epub 2009 Mar 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Immunogenetics, Department of Immunobiology and Neuroscience, Medical Institute of Bioregulation, Kyushu University, Fukuoka 812-8582, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19325080" target="_blank"〉PubMed〈/a〉
    Keywords: 1-Butanol/pharmacology ; Actins/metabolism ; Animals ; Cell Line ; Cell Membrane/*metabolism ; Cell Polarity ; *Chemotaxis, Leukocyte ; Enzyme Inhibitors/pharmacology ; GTPase-Activating Proteins/chemistry/genetics/*metabolism ; Humans ; Mice ; Neutrophils/cytology/drug effects/*physiology ; Phosphatidic Acids/*metabolism/pharmacology ; Phosphatidylinositol Phosphates/*metabolism ; Phospholipase D/genetics/metabolism ; Protein Binding ; Pseudopodia/metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; rac GTP-Binding Proteins/metabolism
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    Mitochondrial STAT3 supports Ras-dependent oncogenic transformation (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-06-27
    Description: Signal transducer and activator of transcription 3 (STAT3) is a latent cytoplasmic transcription factor responsive to cytokine signaling and tyrosine kinase oncoproteins by nuclear translocation when it is tyrosine-phosphorylated. We report that malignant transformation by activated Ras is impaired without STAT3, in spite of the inability of Ras to drive STAT3 tyrosine phosphorylation or nuclear translocation. Moreover, STAT3 mutants that cannot be tyrosine-phosphorylated, that are retained in the cytoplasm, or that cannot bind DNA nonetheless supported Ras-mediated transformation. Unexpectedly, STAT3 was detected within mitochondria, and exclusive targeting of STAT3 to mitochondria without nuclear accumulation facilitated Ras transformation. Mitochondrial STAT3 sustained altered glycolytic and oxidative phosphorylation activities characteristic of cancer cells. Thus, in addition to its nuclear transcriptional role, STAT3 regulates a metabolic function in mitochondria, supporting Ras-dependent malignant transformation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2840701/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2840701/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gough, Daniel J -- Corlett, Alicia -- Schlessinger, Karni -- Wegrzyn, Joanna -- Larner, Andrew C -- Levy, David E -- R01 AI028900/AI/NIAID NIH HHS/ -- R01 AI028900-19/AI/NIAID NIH HHS/ -- R01AI28900/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2009 Jun 26;324(5935):1713-6. doi: 10.1126/science.1171721.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and New York University Cancer Institute, New York University School of Medicine, 550 First Avenue, New York, NY 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19556508" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Line, Tumor ; Cell Nucleus/metabolism ; Cell Proliferation ; Cell Survival ; *Cell Transformation, Neoplastic ; Genes, ras ; Glycolysis ; Membrane Potential, Mitochondrial ; Mice ; Mice, Inbred BALB C ; Mitochondria/*metabolism ; Mutant Proteins/metabolism ; Neoplasms, Experimental/metabolism/pathology ; Neoplastic Stem Cells ; Oxidative Phosphorylation ; Phosphorylation ; STAT3 Transcription Factor/genetics/*metabolism ; Signal Transduction ; ras Proteins/*metabolism
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    Cell biology. A revolving door for calcium (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-10-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Demaurex, Nicolas -- Poburko, Damon -- New York, N.Y. -- Science. 2009 Oct 2;326(5949):57-8. doi: 10.1126/science.1180482.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Physiology and Metabolism, University of Geneva, 1 Rue Michel-Servet, 1211 Geneva, Switzerland. nicolas.demaurex@unige.ch〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19797650" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Animals ; Antiporters/deficiency/genetics/*metabolism ; Calcium/*metabolism ; *Calcium Signaling ; Calcium-Binding Proteins/deficiency/genetics/*metabolism ; Cation Transport Proteins/deficiency/genetics/metabolism ; Cell Line ; Cell Respiration ; Drosophila Proteins/genetics/*metabolism ; Drosophila melanogaster ; Genome ; Humans ; Hydrogen/*metabolism ; Hydrogen-Ion Concentration ; Ion Transport ; Membrane Proteins/deficiency/genetics/*metabolism ; Mitochondria/*metabolism ; Mitochondrial Membranes/metabolism ; Mitochondrial Proteins/*metabolism ; Potassium/metabolism ; RNA Interference ; Wolf-Hirschhorn Syndrome/metabolism
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    An E3 ligase possessing an iron-responsive hemerythrin domain is a regulator of iron homeostasis (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-09-19
    Description: Cellular iron homeostasis is maintained by the coordinate posttranscriptional regulation of genes responsible for iron uptake, release, use, and storage through the actions of the iron regulatory proteins IRP1 and IRP2. However, the manner in which iron levels are sensed to affect IRP2 activity is poorly understood. We found that an E3 ubiquitin ligase complex containing the FBXL5 protein targets IRP2 for proteasomal degradation. The stability of FBXL5 itself was regulated, accumulating under iron- and oxygen-replete conditions and degraded upon iron depletion. FBXL5 contains an iron- and oxygen-binding hemerythrin domain that acted as a ligand-dependent regulatory switch mediating FBXL5's differential stability. These observations suggest a mechanistic link between iron sensing via the FBXL5 hemerythrin domain, IRP2 regulation, and cellular responses to maintain mammalian iron homeostasis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3582197/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3582197/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Salahudeen, Ameen A -- Thompson, Joel W -- Ruiz, Julio C -- Ma, He-Wen -- Kinch, Lisa N -- Li, Qiming -- Grishin, Nick V -- Bruick, Richard K -- C06 RR 15437-01/RR/NCRR NIH HHS/ -- CA115962/CA/NCI NIH HHS/ -- R01 CA115962/CA/NCI NIH HHS/ -- R01 CA115962-05/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2009 Oct 30;326(5953):722-6. doi: 10.1126/science.1176326. Epub 2009 Sep 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19762597" target="_blank"〉PubMed〈/a〉
    Keywords: Catalytic Domain ; Cell Line ; F-Box Proteins/chemistry/*metabolism ; HeLa Cells ; Hemerythrin/*metabolism ; Homeostasis ; Humans ; Iron/*metabolism ; Iron Regulatory Protein 2/metabolism ; Oxygen/metabolism ; Protein Structure, Tertiary ; RNA, Small Interfering ; Recombinant Fusion Proteins/metabolism ; Ubiquitin-Protein Ligases/chemistry/*metabolism
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    Mutations in FUS, an RNA processing protein, cause familial amyotrophic lateral sclerosis type 6 (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-03-03
    Description: Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease that is familial in 10% of cases. We have identified a missense mutation in the gene encoding fused in sarcoma (FUS) in a British kindred, linked to ALS6. In a survey of 197 familial ALS index cases, we identified two further missense mutations in eight families. Postmortem analysis of three cases with FUS mutations showed FUS-immunoreactive cytoplasmic inclusions and predominantly lower motor neuron degeneration. Cellular expression studies revealed aberrant localization of mutant FUS protein. FUS is involved in the regulation of transcription and RNA splicing and transport, and it has functional homology to another ALS gene, TARDBP, which suggests that a common mechanism may underlie motor neuron degeneration.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4516382/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4516382/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vance, Caroline -- Rogelj, Boris -- Hortobagyi, Tibor -- De Vos, Kurt J -- Nishimura, Agnes Lumi -- Sreedharan, Jemeen -- Hu, Xun -- Smith, Bradley -- Ruddy, Deborah -- Wright, Paul -- Ganesalingam, Jeban -- Williams, Kelly L -- Tripathi, Vineeta -- Al-Saraj, Safa -- Al-Chalabi, Ammar -- Leigh, P Nigel -- Blair, Ian P -- Nicholson, Garth -- de Belleroche, Jackie -- Gallo, Jean-Marc -- Miller, Christopher C -- Shaw, Christopher E -- 078662/Wellcome Trust/United Kingdom -- G0300329/Medical Research Council/United Kingdom -- G0500289/Medical Research Council/United Kingdom -- G0501573/Medical Research Council/United Kingdom -- G0600676/Medical Research Council/United Kingdom -- G0600974/Medical Research Council/United Kingdom -- G0900688/Medical Research Council/United Kingdom -- MC_G1000733/Medical Research Council/United Kingdom -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2009 Feb 27;323(5918):1208-11. doi: 10.1126/science.1165942.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Clinical Neuroscience, King's College London, Medical Research Council (MRC) Centre for Neurodegeneration Research, Institute of Psychiatry, London SE5 8AF, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19251628" target="_blank"〉PubMed〈/a〉
    Keywords: Age of Onset ; Amino Acid Sequence ; Amyotrophic Lateral Sclerosis/*genetics/metabolism/pathology ; Animals ; Brain/pathology ; Cell Line ; Cell Nucleus/metabolism ; Cytoplasm/metabolism ; DNA-Binding Proteins/analysis/genetics/metabolism ; Female ; Humans ; Inclusion Bodies/chemistry/ultrastructure ; Male ; Molecular Sequence Data ; Motor Neurons/metabolism ; *Mutation, Missense ; Pedigree ; RNA-Binding Protein FUS/analysis/*genetics/*metabolism ; Rats ; Spinal Cord/pathology ; Transfection
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    A recessive mutation in the APP gene with dominant-negative effect on amyloidogenesis (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-03-17
    Description: beta-Amyloid precursor protein (APP) mutations cause familial Alzheimer's disease with nearly complete penetrance. We found an APP mutation [alanine-673--〉valine-673 (A673V)] that causes disease only in the homozygous state, whereas heterozygous carriers were unaffected, consistent with a recessive Mendelian trait of inheritance. The A673V mutation affected APP processing, resulting in enhanced beta-amyloid (Abeta) production and formation of amyloid fibrils in vitro. Co-incubation of mutated and wild-type peptides conferred instability on Abeta aggregates and inhibited amyloidogenesis and neurotoxicity. The highly amyloidogenic effect of the A673V mutation in the homozygous state and its anti-amyloidogenic effect in the heterozygous state account for the autosomal recessive pattern of inheritance and have implications for genetic screening and the potential treatment of Alzheimer's disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2728497/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2728497/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Di Fede, Giuseppe -- Catania, Marcella -- Morbin, Michela -- Rossi, Giacomina -- Suardi, Silvia -- Mazzoleni, Giulia -- Merlin, Marco -- Giovagnoli, Anna Rita -- Prioni, Sara -- Erbetta, Alessandra -- Falcone, Chiara -- Gobbi, Marco -- Colombo, Laura -- Bastone, Antonio -- Beeg, Marten -- Manzoni, Claudia -- Francescucci, Bruna -- Spagnoli, Alberto -- Cantu, Laura -- Del Favero, Elena -- Levy, Efrat -- Salmona, Mario -- Tagliavini, Fabrizio -- NS42029/NS/NINDS NIH HHS/ -- R01 NS042029/NS/NINDS NIH HHS/ -- R01 NS042029-01A1/NS/NINDS NIH HHS/ -- R01 NS042029-02/NS/NINDS NIH HHS/ -- R01 NS042029-03/NS/NINDS NIH HHS/ -- R01 NS042029-04/NS/NINDS NIH HHS/ -- R01 NS042029-05/NS/NINDS NIH HHS/ -- R01 NS042029-06/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2009 Mar 13;323(5920):1473-7. doi: 10.1126/science.1168979.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neurology and Neuropathology, "Carlo Besta" National Neurological Institute, 20133 Milan, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19286555" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Alzheimer Disease/*genetics/metabolism ; Amino Acid Substitution ; Amyloid/*metabolism ; Amyloid beta-Peptides/chemistry/metabolism ; Amyloid beta-Protein Precursor/*genetics/metabolism ; Cell Line ; Dementia/*genetics/metabolism ; Female ; *Genes, Recessive ; Heterozygote ; Homozygote ; Humans ; Kinetics ; Male ; *Mutation ; Pedigree ; Peptide Fragments/chemistry/metabolism ; Protein Binding ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Control of iron homeostasis by an iron-regulated ubiquitin ligase (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-09-19
    Description: Eukaryotic cells require iron for survival and have developed regulatory mechanisms for maintaining appropriate intracellular iron concentrations. The degradation of iron regulatory protein 2 (IRP2) in iron-replete cells is a key event in this pathway, but the E3 ubiquitin ligase responsible for its proteolysis has remained elusive. We found that a SKP1-CUL1-FBXL5 ubiquitin ligase protein complex associates with and promotes the iron-dependent ubiquitination and degradation of IRP2. The F-box substrate adaptor protein FBXL5 was degraded upon iron and oxygen depletion in a process that required an iron-binding hemerythrin-like domain in its N terminus. Thus, iron homeostasis is regulated by a proteolytic pathway that couples IRP2 degradation to intracellular iron levels through the stability and activity of FBXL5.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2929180/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2929180/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vashisht, Ajay A -- Zumbrennen, Kimberly B -- Huang, Xinhua -- Powers, David N -- Durazo, Armando -- Sun, Dahui -- Bhaskaran, Nimesh -- Persson, Anja -- Uhlen, Mathias -- Sangfelt, Olle -- Spruck, Charles -- Leibold, Elizabeth A -- Wohlschlegel, James A -- GM45201/GM/NIGMS NIH HHS/ -- R01 GM045201/GM/NIGMS NIH HHS/ -- R01 GM045201-17/GM/NIGMS NIH HHS/ -- R01 GM089778/GM/NIGMS NIH HHS/ -- R01 GM089778-01A1/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2009 Oct 30;326(5953):718-21. doi: 10.1126/science.1176333. Epub 2009 Sep 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Chemistry, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19762596" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Cullin Proteins/metabolism ; F-Box Proteins/*metabolism ; Hemerythrin/metabolism ; Homeostasis ; Humans ; Iron/*metabolism ; Iron Regulatory Protein 1/metabolism ; Iron Regulatory Protein 2/*metabolism ; Oxygen/metabolism ; Protein Structure, Tertiary ; Recombinant Proteins/metabolism ; SKP Cullin F-Box Protein Ligases/metabolism ; Ubiquitin-Protein Ligases/*metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Research ethics. The NIH draft guidelines on human stem cell research (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-06-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Majumder, Mary A -- Cohen, Cynthia B -- New York, N.Y. -- Science. 2009 Jun 26;324(5935):1648-9. doi: 10.1126/science.1176253.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Medical Ethics and Health Policy, Baylor College of Medicine, Houston, TX 77030, USA. majumder@bcm.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19556488" target="_blank"〉PubMed〈/a〉
    Keywords: Advisory Committees ; Cell Line ; *Embryo Research/economics/ethics/legislation & jurisprudence ; *Embryonic Stem Cells ; Ethics Committees, Research ; Financing, Government/legislation & jurisprudence ; *Government Regulation ; *Guidelines as Topic ; Humans ; Informed Consent ; National Academy of Sciences (U.S.) ; *National Institutes of Health (U.S.) ; *Pluripotent Stem Cells ; Public Policy ; Research Embryo Creation ; Research Support as Topic/legislation & jurisprudence ; United States
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    SDH5, a gene required for flavination of succinate dehydrogenase, is mutated in paraganglioma (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-07-25
    Description: Mammalian mitochondria contain about 1100 proteins, nearly 300 of which are uncharacterized. Given the well-established role of mitochondrial defects in human disease, functional characterization of these proteins may shed new light on disease mechanisms. Starting with yeast as a model system, we investigated an uncharacterized but highly conserved mitochondrial protein (named here Sdh5). Both yeast and human Sdh5 interact with the catalytic subunit of the succinate dehydrogenase (SDH) complex, a component of both the electron transport chain and the tricarboxylic acid cycle. Sdh5 is required for SDH-dependent respiration and for Sdh1 flavination (incorporation of the flavin adenine dinucleotide cofactor). Germline loss-of-function mutations in the human SDH5 gene, located on chromosome 11q13.1, segregate with disease in a family with hereditary paraganglioma, a neuroendocrine tumor previously linked to mutations in genes encoding SDH subunits. Thus, a mitochondrial proteomics analysis in yeast has led to the discovery of a human tumor susceptibility gene.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3881419/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3881419/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hao, Huai-Xiang -- Khalimonchuk, Oleh -- Schraders, Margit -- Dephoure, Noah -- Bayley, Jean-Pierre -- Kunst, Henricus -- Devilee, Peter -- Cremers, Cor W R J -- Schiffman, Joshua D -- Bentz, Brandon G -- Gygi, Steven P -- Winge, Dennis R -- Kremer, Hannie -- Rutter, Jared -- DK071962/DK/NIDDK NIH HHS/ -- GM087346/GM/NIGMS NIH HHS/ -- R01 ES003817/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 2009 Aug 28;325(5944):1139-42. doi: 10.1126/science.1175689. Epub 2009 Jul 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Utah School of Medicine, Salt Lake City, UT 84112, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19628817" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Cell Line ; Cell Line, Tumor ; Female ; Flavin-Adenine Dinucleotide/metabolism ; Flavoproteins/metabolism ; *Germ-Line Mutation ; Haplotypes ; Humans ; Inheritance Patterns ; Male ; Mitochondria/*metabolism ; Mitochondrial Proteins/chemistry/*genetics/metabolism ; Molecular Sequence Data ; Oxygen Consumption ; Paraganglioma/*genetics ; Pedigree ; Protein Subunits/metabolism ; Proteomics ; Saccharomyces cerevisiae/*genetics/growth & development/metabolism ; Saccharomyces cerevisiae Proteins/chemistry/*genetics/*metabolism ; Succinate Dehydrogenase/*metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Medicine. The cart before the horse (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-09-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rowley, Janet D -- Blumenthal, Thomas -- New York, N.Y. -- Science. 2008 Sep 5;321(5894):1302-4. doi: 10.1126/science.1163791.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Chicago, 5841 South Maryland Avenue, MC 2115, Chicago, IL 60637, USA. jrowley@medicine.bsd.uchicago.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18772424" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Chromosomes, Human, Pair 17/genetics ; Chromosomes, Human, Pair 7/genetics ; Endometrial Neoplasms/genetics ; Endometrium/cytology/*metabolism ; Female ; Gene Fusion ; Gene Rearrangement ; Humans ; Macaca mulatta ; Menstrual Cycle ; Neoplasm Proteins/*genetics ; RNA, Guide/genetics ; RNA, Messenger/*genetics ; *Trans-Splicing ; Transcription Factors/*genetics ; *Translocation, Genetic
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Molecular coupling of Xist regulation and pluripotency (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-09-20
    Description: During mouse embryogenesis, reversion of imprinted X chromosome inactivation in the pluripotent inner cell mass of the female blastocyst is initiated by the repression of Xist from the paternal X chromosome. Here we report that key factors supporting pluripotency-Nanog, Oct3/4, and Sox2-bind within Xist intron 1 in undifferentiated embryonic stem (ES) cells. Whereas Nanog null ES cells display a reversible and moderate up-regulation of Xist in the absence of any apparent modification of Oct3/4 and Sox2 binding, the drastic release of all three factors from Xist intron 1 triggers rapid ectopic accumulation of Xist RNA. We conclude that the three main genetic factors underlying pluripotency cooperate to repress Xist and thus couple X inactivation reprogramming to the control of pluripotency during embryogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Navarro, Pablo -- Chambers, Ian -- Karwacki-Neisius, Violetta -- Chureau, Corinne -- Morey, Celine -- Rougeulle, Claire -- Avner, Philip -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2008 Sep 19;321(5896):1693-5. doi: 10.1126/science.1160952.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut Pasteur, Unite de Genetique Moleculaire Murine, CNRS, URA2578, F-75015, Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18802003" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastocyst Inner Cell Mass/metabolism ; Cell Differentiation ; Cell Line ; DNA-Binding Proteins/*metabolism ; Embryonic Stem Cells/cytology/*metabolism ; Female ; HMGB Proteins/*metabolism ; Homeodomain Proteins/genetics/*metabolism ; Introns ; Male ; Mice ; Octamer Transcription Factor-3/genetics/*metabolism ; Pluripotent Stem Cells/cytology/*metabolism ; RNA, Long Noncoding ; RNA, Untranslated/*genetics/metabolism ; SOXB1 Transcription Factors ; Transcription Factors/*metabolism ; Up-Regulation ; X Chromosome/physiology ; *X Chromosome Inactivation
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    Regulation of CD45 alternative splicing by heterogeneous ribonucleoprotein, hnRNPLL (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-08-02
    Description: The transition from naive to activated T cells is marked by alternative splicing of pre-mRNA encoding the transmembrane phosphatase CD45. Using a short hairpin RNA interference screen, we identified heterogeneous ribonucleoprotein L-like (hnRNPLL) as a critical inducible regulator of CD45 alternative splicing. HnRNPLL was up-regulated in stimulated T cells, bound CD45 transcripts, and was both necessary and sufficient for CD45 alternative splicing. Depletion or overexpression of hnRNPLL in B and T cell lines and primary T cells resulted in reciprocal alteration of CD45RA and RO expression. Exon array analysis suggested that hnRNPLL acts as a global regulator of alternative splicing in activated T cells. Induction of hnRNPLL during hematopoietic cell activation and differentiation may allow cells to rapidly shift their transcriptomes to favor proliferation and inhibit cell death.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2791692/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2791692/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Oberdoerffer, Shalini -- Moita, Luis Ferreira -- Neems, Daniel -- Freitas, Rui P -- Hacohen, Nir -- Rao, Anjana -- AI40127/AI/NIAID NIH HHS/ -- AI44432/AI/NIAID NIH HHS/ -- CA42471/CA/NCI NIH HHS/ -- R01 AI040127/AI/NIAID NIH HHS/ -- R01 AI040127-18/AI/NIAID NIH HHS/ -- R01 AI040127-19/AI/NIAID NIH HHS/ -- R01 AI044432/AI/NIAID NIH HHS/ -- R01 AI044432-09/AI/NIAID NIH HHS/ -- R01 AI044432-10/AI/NIAID NIH HHS/ -- R01 AI080875/AI/NIAID NIH HHS/ -- R01 AI080875-01/AI/NIAID NIH HHS/ -- R01 CA042471/CA/NCI NIH HHS/ -- R01 CA042471-23/CA/NCI NIH HHS/ -- R21 AI071060/AI/NIAID NIH HHS/ -- R21 AI071060-01/AI/NIAID NIH HHS/ -- R21 AI071060-02/AI/NIAID NIH HHS/ -- T32 HL066987/HL/NHLBI NIH HHS/ -- U19 AI070352/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2008 Aug 1;321(5889):686-91. doi: 10.1126/science.1157610. Epub 2008 Jul 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Immune Disease Institute, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18669861" target="_blank"〉PubMed〈/a〉
    Keywords: *Alternative Splicing ; Antigens, CD45/chemistry/*genetics ; B-Lymphocytes/immunology/metabolism ; CD4-Positive T-Lymphocytes/*immunology/*metabolism ; Cell Line ; Cell Line, Tumor ; Heterogeneous-Nuclear Ribonucleoproteins/genetics/*metabolism ; Humans ; Lentivirus/genetics/physiology ; *Lymphocyte Activation ; Protein Isoforms/chemistry/genetics ; RNA Interference ; STAT5 Transcription Factor/genetics ; T-Lymphocytes/*immunology/*metabolism ; Tetradecanoylphorbol Acetate/pharmacology ; Transcription, Genetic ; Transduction, Genetic ; Up-Regulation
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    ERdj5 is required as a disulfide reductase for degradation of misfolded proteins in the ER (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-07-26
    Description: Membrane and secretory proteins cotranslationally enter and are folded in the endoplasmic reticulum (ER). Misfolded or unassembled proteins are discarded by a process known as ER-associated degradation (ERAD), which involves their retrotranslocation into the cytosol. ERAD substrates frequently contain disulfide bonds that must be cleaved before their retrotranslocation. Here, we found that an ER-resident protein ERdj5 had a reductase activity, cleaved the disulfide bonds of misfolded proteins, and accelerated ERAD through its physical and functional associations with EDEM (ER degradation-enhancing alpha-mannosidase-like protein) and an ER-resident chaperone BiP. Thus, ERdj5 is a member of a supramolecular ERAD complex that recognizes and unfolds misfolded proteins for their efficient retrotranslocation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ushioda, Ryo -- Hoseki, Jun -- Araki, Kazutaka -- Jansen, Gregor -- Thomas, David Y -- Nagata, Kazuhiro -- New York, N.Y. -- Science. 2008 Jul 25;321(5888):569-72. doi: 10.1126/science.1159293.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Institute for Frontier Medical Sciences, Kyoto University, Kyoto 606-8397, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18653895" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Amino Acid Substitution ; Animals ; Cell Line ; Endoplasmic Reticulum/*metabolism ; Glutathione/metabolism ; HSP40 Heat-Shock Proteins/chemistry/genetics/*metabolism ; Heat-Shock Proteins/metabolism ; Humans ; Immunoglobulin J-Chains/chemistry/metabolism ; Membrane Proteins/metabolism ; Mice ; Molecular Chaperones/chemistry/genetics/*metabolism ; Mutation ; Oxidation-Reduction ; Protein Disulfide Reductase (Glutathione)/metabolism ; Protein Disulfide-Isomerases/metabolism ; Protein Folding ; Protein Structure, Tertiary ; Proteins/chemistry/*metabolism ; Recombinant Proteins/chemistry/metabolism ; Transfection ; Two-Hybrid System Techniques ; alpha 1-Antitrypsin/chemistry/metabolism
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    Ceramide triggers budding of exosome vesicles into multivesicular endosomes (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-03-01
    Description: Intraluminal vesicles of multivesicular endosomes are either sorted for cargo degradation into lysosomes or secreted as exosomes into the extracellular milieu. The mechanisms underlying the sorting of membrane into the different populations of intraluminal vesicles are unknown. Here, we find that cargo is segregated into distinct subdomains on the endosomal membrane and that the transfer of exosome-associated domains into the lumen of the endosome did not depend on the function of the ESCRT (endosomal sorting complex required for transport) machinery, but required the sphingolipid ceramide. Purified exosomes were enriched in ceramide, and the release of exosomes was reduced after the inhibition of neutral sphingomyelinases. These results establish a pathway in intraendosomal membrane transport and exosome formation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Trajkovic, Katarina -- Hsu, Chieh -- Chiantia, Salvatore -- Rajendran, Lawrence -- Wenzel, Dirk -- Wieland, Felix -- Schwille, Petra -- Brugger, Britta -- Simons, Mikael -- New York, N.Y. -- Science. 2008 Feb 29;319(5867):1244-7. doi: 10.1126/science.1153124.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Biochemistry and Molecular Cell Biology, University of Gottingen, 37073 Gottingen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18309083" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Line, Tumor ; Ceramides/analysis/*metabolism ; Cytoplasmic Vesicles/chemistry/*metabolism/ultrastructure ; Endosomes/*metabolism/ultrastructure ; Humans ; Intracellular Membranes/*metabolism/ultrastructure ; Membrane Microdomains/*metabolism/ultrastructure ; Mice ; Myelin Proteolipid Protein/*metabolism ; Oligodendroglia/metabolism/ultrastructure ; Protein Transport ; Receptor, Epidermal Growth Factor/metabolism ; Recombinant Fusion Proteins/metabolism ; Sphingomyelin Phosphodiesterase/antagonists & inhibitors/metabolism
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    Evidence for editing of human papillomavirus DNA by APOBEC3 in benign and precancerous lesions (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-04-12
    Description: Cytidine deaminases of the APOBEC3 family all have specificity for single-stranded DNA, which may become exposed during replication or transcription of double-stranded DNA. Three human APOBEC3A (hA3A), hA3B, and hA3H genes are expressed in keratinocytes and skin, leading us to determine whether genetic editing of human papillomavirus (HPV) DNA occurred. In a study of HPV1a plantar warts and HPV16 precancerous cervical biopsies, hyperedited HPV1a and HPV16 genomes were found. Strictly analogous results were obtained from transfection experiments with HPV plasmid DNA and the three nuclear localized enzymes: hA3A, hA3C, and hA3H. Thus, stochastic or transient overexpression of APOBEC3 genes may expose the genome to a broad spectrum of mutations that could influence the development of tumors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vartanian, Jean-Pierre -- Guetard, Denise -- Henry, Michel -- Wain-Hobson, Simon -- New York, N.Y. -- Science. 2008 Apr 11;320(5873):230-3. doi: 10.1126/science.1153201.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Retrovirology Unit, Institut Pasteur, 28 Rue de Docteur Roux, 75724 Paris cedex 15, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18403710" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Cervix Uteri/virology ; Cytidine/metabolism ; Cytosine Deaminase/*metabolism ; DNA Mismatch Repair ; DNA, Viral/genetics/*metabolism ; Female ; Genome, Viral ; Human papillomavirus 16/*genetics ; Humans ; Mupapillomavirus/*genetics ; Mutation ; Papillomavirus Infections/enzymology/virology ; Precancerous Conditions/enzymology/*virology ; Transfection ; Uterine Cervical Neoplasms/enzymology/*virology ; Warts/enzymology/*virology
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    Asymmetric tethering of flat and curved lipid membranes by a golgin (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-05-03
    Description: Golgins, long stringlike proteins, tether cisternae and transport vesicles at the Golgi apparatus. We examined the attachment of golgin GMAP-210 to lipid membranes. GMAP-210 connected highly curved liposomes to flatter ones. This asymmetric tethering relied on motifs that sensed membrane curvature both in the N terminus of GMAP-210 and in ArfGAP1, which controlled the interaction of the C terminus of GMAP-210 with the small guanine nucleotide-binding protein Arf1. Because membrane curvature constantly changes during vesicular trafficking, this mode of tethering suggests a way to maintain the Golgi architecture without compromising membrane flow.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Drin, Guillaume -- Morello, Vincent -- Casella, Jean-Francois -- Gounon, Pierre -- Antonny, Bruno -- New York, N.Y. -- Science. 2008 May 2;320(5876):670-3. doi: 10.1126/science.1155821.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut de Pharmacologie Moleculaire et Cellulaire, Universite de Nice Sophia Antipolis and CNRS, 660 route des lucioles, 06560 Valbonne, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18451304" target="_blank"〉PubMed〈/a〉
    Keywords: ADP-Ribosylation Factor 1/metabolism ; Binding Sites ; Cell Line ; GTPase-Activating Proteins/metabolism ; Golgi Apparatus/chemistry/metabolism ; HeLa Cells ; Humans ; Intracellular Membranes/*chemistry/metabolism ; Liposomes ; Membrane Lipids/*chemistry ; Nuclear Proteins/*chemistry/metabolism ; Recombinant Proteins/chemistry/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Wnt3a-mediated formation of phosphatidylinositol 4,5-bisphosphate regulates LRP6 phosphorylation (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-09-06
    Description: The canonical Wnt-beta-catenin signaling pathway is initiated by inducing phosphorylation of one of the Wnt receptors, low-density lipoprotein receptor-related protein 6 (LRP6), at threonine residue 1479 (Thr1479) and serine residue 1490 (Ser1490). By screening a human kinase small interfering RNA library, we identified phosphatidylinositol 4-kinase type II alpha and phosphatidylinositol-4-phosphate 5-kinase type I (PIP5KI) as required for Wnt3a-induced LRP6 phosphorylation at Ser1490 in mammalian cells and confirmed that these kinases are important for Wnt signaling in Xenopus embryos. Wnt3a stimulates the formation of phosphatidylinositol 4,5-bisphosphates [PtdIns (4,5)P2] through frizzled and dishevelled, the latter of which directly interacted with and activated PIP5KI. In turn, PtdIns (4,5)P2 regulated phosphorylation of LRP6 at Thr1479 and Ser1490. Therefore, our study reveals a signaling mechanism for Wnt to regulate LRP6 phosphorylation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2532521/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2532521/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pan, Weijun -- Choi, Sun-Cheol -- Wang, He -- Qin, Yuanbo -- Volpicelli-Daley, Laura -- Swan, Laura -- Lucast, Louise -- Khoo, Cynthia -- Zhang, Xiaowu -- Li, Lin -- Abrams, Charles S -- Sokol, Sergei Y -- Wu, Dianqing -- AR051476/AR/NIAMS NIH HHS/ -- CA132317/CA/NCI NIH HHS/ -- DA018343/DA/NIDA NIH HHS/ -- HL080706/HL/NHLBI NIH HHS/ -- NS36251/NS/NINDS NIH HHS/ -- P30 DA018343/DA/NIDA NIH HHS/ -- R01 AR051476/AR/NIAMS NIH HHS/ -- R01 AR051476-01A1/AR/NIAMS NIH HHS/ -- R01 AR051476-02/AR/NIAMS NIH HHS/ -- R01 AR051476-03/AR/NIAMS NIH HHS/ -- R01 CA132317/CA/NCI NIH HHS/ -- R01 CA132317-01A2/CA/NCI NIH HHS/ -- R01 CA139395/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2008 Sep 5;321(5894):1350-3. doi: 10.1126/science.1160741.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Yale University School of Medicine, New Haven, CT 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18772438" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Axin Protein ; Cell Line ; Frizzled Receptors/metabolism ; Humans ; LDL-Receptor Related Proteins/*metabolism ; Low Density Lipoprotein Receptor-Related Protein-6 ; Mice ; Models, Biological ; Phosphatidylinositol 4,5-Diphosphate/*metabolism ; Phosphoproteins/metabolism ; Phosphorylation ; Phosphotransferases (Alcohol Group Acceptor)/metabolism ; RNA, Small Interfering ; Recombinant Proteins/metabolism ; Repressor Proteins/metabolism ; Serine/metabolism ; Signal Transduction ; Threonine/metabolism ; Wnt Proteins/*metabolism ; Wnt3 Protein ; Wnt3A Protein ; Xenopus/embryology ; Xenopus Proteins
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    Reversible compartmentalization of de novo purine biosynthetic complexes in living cells (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-04-05
    Description: Purines are synthesized de novo in 10 chemical steps that are catalyzed by six enzymes in eukaryotes. Studies in vitro have provided little evidence of anticipated protein-protein interactions that would enable substrate channeling and regulation of the metabolic flux. We applied fluorescence microscopy to HeLa cells and discovered that all six enzymes colocalize to form clusters in the cellular cytoplasm. The association and dissociation of these enzyme clusters can be regulated dynamically, by either changing the purine levels of or adding exogenous agents to the culture media. Collectively, the data provide strong evidence for the formation of a multi-enzyme complex, the "purinosome," to carry out de novo purine biosynthesis in cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉An, Songon -- Kumar, Ravindra -- Sheets, Erin D -- Benkovic, Stephen J -- R21 AG030949/AG/NIA NIH HHS/ -- R21 AG030949-01/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2008 Apr 4;320(5872):103-6. doi: 10.1126/science.1152241.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, Pennsylvania State University, University Park, PA 16802, USA. sua13@psu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18388293" target="_blank"〉PubMed〈/a〉
    Keywords: Azaserine/pharmacology ; Binding Sites ; Carbon-Nitrogen Ligases/genetics/*metabolism ; Carbon-Nitrogen Ligases with Glutamine as Amide-N-Donor/genetics/*metabolism ; Cell Compartmentation ; Cell Line ; Cell Line, Tumor ; Culture Media ; Cytoplasm/*enzymology ; Fluorescent Antibody Technique ; HeLa Cells ; Humans ; Hypoxanthine/pharmacology ; Microscopy, Fluorescence ; Multienzyme Complexes/genetics/*metabolism ; Phosphoribosylglycinamide Formyltransferase/genetics/*metabolism ; Purines/*biosynthesis ; Recombinant Fusion Proteins/metabolism ; Transfection
    Print ISSN: 0036-8075
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    The antisense transcriptomes of human cells (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-12-06
    Description: Transcription in mammalian cells can be assessed at a genome-wide level, but it has been difficult to reliably determine whether individual transcripts are derived from the plus or minus strands of chromosomes. This distinction can be critical for understanding the relationship between known transcripts (sense) and the complementary antisense transcripts that may regulate them. Here, we describe a technique that can be used to (i) identify the DNA strand of origin for any particular RNA transcript, and (ii) quantify the number of sense and antisense transcripts from expressed genes at a global level. We examined five different human cell types and in each case found evidence for antisense transcripts in 2900 to 6400 human genes. The distribution of antisense transcripts was distinct from that of sense transcripts, was nonrandom across the genome, and differed among cell types. Antisense transcripts thus appear to be a pervasive feature of human cells, which suggests that they are a fundamental component of gene regulation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2824178/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2824178/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉He, Yiping -- Vogelstein, Bert -- Velculescu, Victor E -- Papadopoulos, Nickolas -- Kinzler, Kenneth W -- CA121113/CA/NCI NIH HHS/ -- CA43460/CA/NCI NIH HHS/ -- CA57345/CA/NCI NIH HHS/ -- CA62924/CA/NCI NIH HHS/ -- R37 CA057345/CA/NCI NIH HHS/ -- R37 CA057345-17/CA/NCI NIH HHS/ -- R37 CA057345-18/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2008 Dec 19;322(5909):1855-7. doi: 10.1126/science.1163853. Epub 2008 Dec 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ludwig Center for Cancer Genetics and Therapeutics and Howard Hughes Medical Institute, Johns Hopkins Kimmel Cancer Center, Baltimore, MD 21231, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19056939" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Cell Line, Tumor ; Exons ; Gene Expression ; *Gene Expression Profiling ; *Genome, Human ; Humans ; Introns ; Leukocytes, Mononuclear/metabolism ; Promoter Regions, Genetic ; RNA, Antisense/*genetics/metabolism ; RNA, Messenger/genetics/metabolism ; *Transcription, Genetic
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    Induced pluripotent stem cells generated without viral integration (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-09-27
    Description: Pluripotent stem cells have been generated from mouse and human somatic cells by viral expression of the transcription factors Oct4, Sox2, Klf4, and c-Myc. A major limitation of this technology is the use of potentially harmful genome-integrating viruses. We generated mouse induced pluripotent stem (iPS) cells from fibroblasts and liver cells by using nonintegrating adenoviruses transiently expressing Oct4, Sox2, Klf4, and c-Myc. These adenoviral iPS (adeno-iPS) cells show DNA demethylation characteristic of reprogrammed cells, express endogenous pluripotency genes, form teratomas, and contribute to multiple tissues, including the germ line, in chimeric mice. Our results provide strong evidence that insertional mutagenesis is not required for in vitro reprogramming. Adenoviral reprogramming may provide an improved method for generating and studying patient-specific stem cells and for comparing embryonic stem cells and iPS cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3987909/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3987909/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stadtfeld, Matthias -- Nagaya, Masaki -- Utikal, Jochen -- Weir, Gordon -- Hochedlinger, Konrad -- DP2 OD003266/OD/NIH HHS/ -- New York, N.Y. -- Science. 2008 Nov 7;322(5903):945-9. doi: 10.1126/science.1162494. Epub 2008 Sep 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Massachusetts General Hospital Cancer Center and Center for Regenerative Medicine, 185 Cambridge Street, Boston, MA 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18818365" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviridae/*genetics/physiology ; Animals ; Cell Differentiation ; Cell Line ; *Cellular Reprogramming ; Chimera ; Cloning, Molecular ; Female ; Fibroblasts/*cytology/metabolism/virology ; Genes, myc ; *Genetic Vectors ; Hepatocytes/*cytology/metabolism/virology ; Kruppel-Like Transcription Factors/genetics/metabolism ; Liver/cytology/embryology ; Male ; Mice ; Mice, SCID ; Octamer Transcription Factor-3/genetics/metabolism ; *Pluripotent Stem Cells/cytology/metabolism/transplantation ; Proto-Oncogene Proteins c-myc/genetics/metabolism ; SOXB1 Transcription Factors/genetics/metabolism ; Teratoma/etiology ; Transgenes ; Virus Integration
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    Medicine. Sidestepping mutational meltdown (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-02-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shoubridge, Eric A -- Wai, Timothy -- New York, N.Y. -- Science. 2008 Feb 15;319(5865):914-5. doi: 10.1126/science.1154515.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Montreal Neurological Institute and Department of Human Genetics, McGill University, Montreal, Quebec H3A 2B4, Canada. eric@ericpc.mni.mcgill.ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18276880" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autophagy ; Cell Line ; DNA, Mitochondrial/*genetics ; DNA-Directed DNA Polymerase/genetics ; Electron Transport Complex IV/*genetics ; Embryonic Stem Cells ; Female ; Frameshift Mutation ; *Germ-Line Mutation ; Male ; Mice ; Mitochondria/physiology ; NADH Dehydrogenase/*genetics ; Oocytes/*physiology ; Oogenesis ; *Selection, Genetic
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    A mouse model of mitochondrial disease reveals germline selection against severe mtDNA mutations (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-02-16
    Description: The majority of mitochondrial DNA (mtDNA) mutations that cause human disease are mild to moderately deleterious, yet many random mtDNA mutations would be expected to be severe. To determine the fate of the more severe mtDNA mutations, we introduced mtDNAs containing two mutations that affect oxidative phosphorylation into the female mouse germ line. The severe ND6 mutation was selectively eliminated during oogenesis within four generations, whereas the milder COI mutation was retained throughout multiple generations even though the offspring consistently developed mitochondrial myopathy and cardiomyopathy. Thus, severe mtDNA mutations appear to be selectively eliminated from the female germ line, thereby minimizing their impact on population fitness.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3049809/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3049809/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fan, Weiwei -- Waymire, Katrina G -- Narula, Navneet -- Li, Peng -- Rocher, Christophe -- Coskun, Pinar E -- Vannan, Mani A -- Narula, Jagat -- Macgregor, Grant R -- Wallace, Douglas C -- AG13154/AG/NIA NIH HHS/ -- AG16573/AG/NIA NIH HHS/ -- AG24373/AG/NIA NIH HHS/ -- DK73691/DK/NIDDK NIH HHS/ -- HD45913/HD/NICHD NIH HHS/ -- NS21328/NS/NINDS NIH HHS/ -- U01 HD045913-01/HD/NICHD NIH HHS/ -- U01 HD045913-02/HD/NICHD NIH HHS/ -- U01 HD045913-03/HD/NICHD NIH HHS/ -- U01 HD045913-04/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2008 Feb 15;319(5865):958-62. doi: 10.1126/science.1147786.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Molecular and Mitochondrial Medicine and Genetics, University of California, Irvine, CA 92697, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18276892" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cardiomyopathies/genetics/pathology ; Cell Line ; Crosses, Genetic ; DNA, Mitochondrial/*genetics ; Electron Transport Complex I/metabolism ; Electron Transport Complex IV/*genetics/metabolism ; Embryonic Stem Cells ; Female ; Frameshift Mutation ; *Germ-Line Mutation ; Litter Size ; Male ; Mice ; Mitochondria/physiology ; Mitochondrial Myopathies/*genetics/pathology ; Mutation, Missense ; Myocardium/pathology ; NADH Dehydrogenase/*genetics ; Oocytes/*physiology ; Oogenesis ; Oxidative Phosphorylation ; Oxygen Consumption ; Point Mutation ; *Selection, Genetic
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    Adenovirus small e1a alters global patterns of histone modification (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-08-23
    Description: Adenovirus small early region 1a (e1a) protein drives cells into S phase by binding RB family proteins and the closely related histone acetyl transferases p300 and CBP. The interaction with RB proteins displaces them from DNA-bound E2F transcription factors, reversing their repression of cell cycle genes. However, it has been unclear how the e1a interaction with p300 and CBP promotes passage through the cell cycle. We show that this interaction causes a threefold reduction in total cellular histone H3 lysine 18 acetylation (H3K18ac). CBP and p300 are required for acetylation at this site because their knockdown causes specific hypoacetylation at H3K18. SV40 T antigen also induces H3K18 hypoacetylation. Because global hypoacetylation at this site is observed in prostate carcinomas with poor prognosis, this suggests that processes resulting in global H3K18 hypoacetylation may be linked to oncogenic transformation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2756290/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2756290/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Horwitz, Gregory A -- Zhang, Kangling -- McBrian, Matthew A -- Grunstein, Michael -- Kurdistani, Siavash K -- Berk, Arnold J -- CA25235/CA/NCI NIH HHS/ -- R37 CA025235/CA/NCI NIH HHS/ -- R37 CA025235-30/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2008 Aug 22;321(5892):1084-5. doi: 10.1126/science.1155544.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Biology Institute, University of California, Los Angeles, CA 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18719283" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Adenovirus E1A Proteins/genetics/*metabolism ; Adenoviruses, Human/*metabolism ; Antigens, Polyomavirus Transforming/metabolism ; CREB-Binding Protein/metabolism ; *Cell Cycle ; Cell Line ; Cell Transformation, Viral ; Cells, Cultured ; HeLa Cells ; Histones/*metabolism ; Humans ; Lysine/metabolism ; Mutation ; p300-CBP Transcription Factors/metabolism
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    Phosphorylation of retinoblastoma protein by viral protein with cyclin-dependent kinase function (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-05-10
    Description: As obligate intracellular parasites, viruses expertly modify cellular processes to facilitate their replication and spread, often by encoding genes that mimic the functions of cellular proteins while lacking regulatory features that modify their activity. We show that the human cytomegalovirus UL97 protein has activities similar to cellular cyclin-cyclin-dependent kinase (CDK) complexes. UL97 phosphorylated and inactivated the retinoblastoma tumor suppressor, stimulated cell cycle progression in mammalian cells, and rescued proliferation of Saccharomyces cerevisiae lacking CDK activity. UL97 is not inhibited by the CDK inhibitor p21 and lacks amino acid residues conserved in the CDKs that permit the attenuation of kinase activity. Thus, UL97 represents a functional ortholog of cellular CDKs that is immune from normal CDK control mechanisms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hume, Adam J -- Finkel, Jonathan S -- Kamil, Jeremy P -- Coen, Donald M -- Culbertson, Michael R -- Kalejta, Robert F -- AI26077/AI/NIAID NIH HHS/ -- GM65172/GM/NIGMS NIH HHS/ -- R56-AI064703/AI/NIAID NIH HHS/ -- T32 AI07245/AI/NIAID NIH HHS/ -- T32 CA009135-31/CA/NCI NIH HHS/ -- T32 GM007215/GM/NIGMS NIH HHS/ -- T32 GM077078-01/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2008 May 9;320(5877):797-9. doi: 10.1126/science.1152095.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Molecular Virology and McArdle Laboratory for Cancer Research, University of Wisconsin-Madison, Madison, WI 53706, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18467589" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Cycle ; Cell Line ; Cyclin-Dependent Kinases/antagonists & inhibitors/*metabolism ; Cytomegalovirus/enzymology/*physiology ; Humans ; Molecular Mimicry ; Phosphorylation ; Phosphotransferases (Alcohol Group Acceptor)/antagonists & inhibitors/*metabolism ; Protein Kinase Inhibitors/pharmacology ; Retinoblastoma Protein/*metabolism
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    Phosphorylation networks regulating JNK activity in diverse genetic backgrounds (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-10-18
    Description: Cellular signaling networks have evolved to enable swift and accurate responses, even in the face of genetic or environmental perturbation. Thus, genetic screens may not identify all the genes that regulate different biological processes. Moreover, although classical screening approaches have succeeded in providing parts lists of the essential components of signaling networks, they typically do not provide much insight into the hierarchical and functional relations that exist among these components. We describe a high-throughput screen in which we used RNA interference to systematically inhibit two genes simultaneously in 17,724 combinations to identify regulators of Drosophila JUN NH(2)-terminal kinase (JNK). Using both genetic and phosphoproteomics data, we then implemented an integrative network algorithm to construct a JNK phosphorylation network, which provides structural and mechanistic insights into the systems architecture of JNK signaling.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2581798/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2581798/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bakal, Chris -- Linding, Rune -- Llense, Flora -- Heffern, Elleard -- Martin-Blanco, Enrique -- Pawson, Tony -- Perrimon, Norbert -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Oct 17;322(5900):453-6. doi: 10.1126/science.1158739.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02215, USA. cbakal@receptor.med.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18927396" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Animals ; Cell Line ; Computational Biology ; Drosophila/*enzymology/genetics ; Drosophila Proteins/genetics/*metabolism ; Fluorescence Resonance Energy Transfer ; *Genes, Insect ; JNK Mitogen-Activated Protein Kinases/genetics/*metabolism ; *MAP Kinase Signaling System ; Metabolic Networks and Pathways ; Phosphorylation ; Proteomics ; RNA Interference ; Signal Transduction
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  • 83
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    Four-jointed is a Golgi kinase that phosphorylates a subset of cadherin domains (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-07-19
    Description: The atypical cadherin Fat acts as a receptor for a signaling pathway that regulates growth, gene expression, and planar cell polarity. Genetic studies in Drosophila identified the four-jointed gene as a regulator of Fat signaling. We show that four-jointed encodes a protein kinase that phosphorylates serine or threonine residues within extracellular cadherin domains of Fat and its transmembrane ligand, Dachsous. Four-jointed functions in the Golgi and is the first molecularly defined kinase that phosphorylates protein domains destined to be extracellular. An acidic sequence motif (Asp-Asn-Glu) within Four-jointed was essential for its kinase activity in vitro and for its biological activity in vivo. Our results indicate that Four-jointed regulates Fat signaling by phosphorylating cadherin domains of Fat and Dachsous as they transit through the Golgi.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2562711/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2562711/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ishikawa, Hiroyuki O -- Takeuchi, Hideyuki -- Haltiwanger, Robert S -- Irvine, Kenneth D -- CA123071/CA/NCI NIH HHS/ -- GM061126/GM/NIGMS NIH HHS/ -- GM078620/GM/NIGMS NIH HHS/ -- R01 CA123071/CA/NCI NIH HHS/ -- R01 CA123071-02/CA/NCI NIH HHS/ -- R01 GM061126/GM/NIGMS NIH HHS/ -- R01 GM061126-08/GM/NIGMS NIH HHS/ -- R01 GM078620/GM/NIGMS NIH HHS/ -- R01 GM078620-02/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Jul 18;321(5887):401-4. doi: 10.1126/science.1158159.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Waksman Institute and Department of Molecular Biology and Biochemistry, Rutgers University, Piscataway, NJ 08854, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18635802" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Amino Acid Sequence ; Animals ; Cadherins/chemistry/*metabolism ; Cell Adhesion Molecules/chemistry/*metabolism ; Cell Line ; Drosophila Proteins/chemistry/genetics/*metabolism ; Drosophila melanogaster ; Electrophoretic Mobility Shift Assay ; Glycosylation ; Golgi Apparatus/enzymology/*metabolism ; Kinetics ; Membrane Glycoproteins/chemistry/genetics/*metabolism ; Molecular Sequence Data ; Mutant Proteins/chemistry/metabolism ; Phosphorylation ; Protein Kinases/chemistry/genetics/*metabolism ; Protein Structure, Tertiary ; Recombinant Fusion Proteins/metabolism ; Serine/metabolism ; Signal Transduction ; Threonine/metabolism
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  • 84
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    Global protein stability profiling in mammalian cells (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-11-08
    Description: The abundance of cellular proteins is determined largely by the rate of transcription and translation coupled with the stability of individual proteins. Although we know a great deal about global transcript abundance, little is known about global protein stability. We present a highly parallel multiplexing strategy to monitor protein turnover on a global scale by coupling flow cytometry with microarray technology to track the stability of individual proteins within a complex mixture. We demonstrated the feasibility of this approach by measuring the stability of approximately 8000 human proteins and identifying proteasome substrates. The technology provides a general platform for proteome-scale analysis of protein turnover under various physiological and disease conditions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yen, Hsueh-Chi Sherry -- Xu, Qikai -- Chou, Danny M -- Zhao, Zhenming -- Elledge, Stephen J -- AG11085/AG/NIA NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Nov 7;322(5903):918-23. doi: 10.1126/science.1160489.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Center for Genetics and Genomics, Brigham and Women's Hospital, Howard Hughes Medical Institute, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18988847" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acids/analysis ; Cell Cycle ; Cell Line ; DNA, Complementary ; Flow Cytometry ; Green Fluorescent Proteins/analysis/metabolism ; Half-Life ; Humans ; Luminescent Proteins/analysis/metabolism ; Oligonucleotide Array Sequence Analysis ; Open Reading Frames ; Proteasome Endopeptidase Complex/*metabolism ; Protein Biosynthesis ; *Protein Stability ; Proteins/genetics/*metabolism ; RNA, Messenger/genetics/metabolism ; Recombinant Fusion Proteins/metabolism ; Transcription, Genetic
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  • 85
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    Membrane phosphatidylserine regulates surface charge and protein localization (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-01-12
    Description: Electrostatic interactions with negatively charged membranes contribute to the subcellular targeting of proteins with polybasic clusters or cationic domains. Although the anionic phospholipid phosphatidylserine is comparatively abundant, its contribution to the surface charge of individual cellular membranes is unknown, partly because of the lack of reagents to analyze its distribution in intact cells. We developed a biosensor to study the subcellular distribution of phosphatidylserine and found that it binds the cytosolic leaflets of the plasma membrane, as well as endosomes and lysosomes. The negative charge associated with the presence of phosphatidylserine directed proteins with moderately positive charge to the endocytic pathway. More strongly cationic proteins, normally associated with the plasma membrane, relocalized to endocytic compartments when the plasma membrane surface charge decreased on calcium influx.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yeung, Tony -- Gilbert, Gary E -- Shi, Jialan -- Silvius, John -- Kapus, Andras -- Grinstein, Sergio -- New York, N.Y. -- Science. 2008 Jan 11;319(5860):210-3. doi: 10.1126/science.1152066.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Cell Biology, Hospital for Sick Children, Toronto M5G 1X8, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18187657" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biosensing Techniques ; Cell Line ; Cell Membrane/*metabolism ; Endocytosis ; Endosomes/*metabolism ; Fluorescence ; Fluorescence Resonance Energy Transfer ; Humans ; Hydrophobic and Hydrophilic Interactions ; Intracellular Membranes/*metabolism ; Lysosomes/*metabolism ; Microscopy, Confocal ; Milk Proteins/metabolism ; Organelles/metabolism ; Phosphatidylserines/*metabolism ; Recombinant Fusion Proteins/metabolism ; Saccharomyces cerevisiae/metabolism ; Signal Transduction ; Static Electricity ; Surface Properties
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  • 86
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    Regulated protein denitrosylation by cytosolic and mitochondrial thioredoxins (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-05-24
    Description: Nitric oxide acts substantially in cellular signal transduction through stimulus-coupled S-nitrosylation of cysteine residues. The mechanisms that might subserve protein denitrosylation in cellular signaling remain uncharacterized. Our search for denitrosylase activities focused on caspase-3, an exemplar of stimulus-dependent denitrosylation, and identified thioredoxin and thioredoxin reductase in a biochemical screen. In resting human lymphocytes, thioredoxin-1 actively denitrosylated cytosolic caspase-3 and thereby maintained a low steady-state amount of S-nitrosylation. Upon stimulation of Fas, thioredoxin-2 mediated denitrosylation of mitochondria-associated caspase-3, a process required for caspase-3 activation, and promoted apoptosis. Inhibition of thioredoxin-thioredoxin reductases enabled identification of additional substrates subject to endogenous S-nitrosylation. Thus, specific enzymatic mechanisms may regulate basal and stimulus-induced denitrosylation in mammalian cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2754768/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2754768/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Benhar, Moran -- Forrester, Michael T -- Hess, Douglas T -- Stamler, Jonathan S -- P01 HL075443/HL/NHLBI NIH HHS/ -- P01 HL075443-050003/HL/NHLBI NIH HHS/ -- R01 HL059130/HL/NHLBI NIH HHS/ -- R01 HL059130-11/HL/NHLBI NIH HHS/ -- U19 ES012496/ES/NIEHS NIH HHS/ -- U19 ES012496-05/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 2008 May 23;320(5879):1050-4. doi: 10.1126/science.1158265.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18497292" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD95/metabolism ; Apoptosis ; Auranofin/pharmacology ; Binding Sites ; Caspase 3/metabolism ; Caspase Inhibitors ; Cell Line ; Cytosol/*metabolism ; Dinitrochlorobenzene/pharmacology ; HeLa Cells ; Humans ; Jurkat Cells ; Macrophages/metabolism ; Mitochondria/enzymology/*metabolism ; Mitochondrial Proteins/*metabolism ; Nitric Oxide/*metabolism ; Rats ; Recombinant Proteins/metabolism ; S-Nitrosothiols/*metabolism ; T-Lymphocytes/metabolism ; Thioredoxin-Disulfide Reductase/*metabolism ; Thioredoxins/*metabolism
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    Human CHN1 mutations hyperactivate alpha2-chimaerin and cause Duane's retraction syndrome (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-07-26
    Description: Duane's retraction syndrome (DRS) is a complex congenital eye movement disorder caused by aberrant innervation of the extraocular muscles by axons of brainstem motor neurons. Studying families with a variant form of the disorder (DURS2-DRS), we have identified causative heterozygous missense mutations in CHN1, a gene on chromosome 2q31 that encodes alpha2-chimaerin, a Rac guanosine triphosphatase-activating protein (RacGAP) signaling protein previously implicated in the pathfinding of corticospinal axons in mice. We found that these are gain-of-function mutations that increase alpha2-chimaerin RacGAP activity in vitro. Several of the mutations appeared to enhance alpha2-chimaerin translocation to the cell membrane or enhance its ability to self-associate. Expression of mutant alpha2-chimaerin constructs in chick embryos resulted in failure of oculomotor axons to innervate their target extraocular muscles. We conclude that alpha2-chimaerin has a critical developmental function in ocular motor axon pathfinding.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2593867/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2593867/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miyake, Noriko -- Chilton, John -- Psatha, Maria -- Cheng, Long -- Andrews, Caroline -- Chan, Wai-Man -- Law, Krystal -- Crosier, Moira -- Lindsay, Susan -- Cheung, Michelle -- Allen, James -- Gutowski, Nick J -- Ellard, Sian -- Young, Elizabeth -- Iannaccone, Alessandro -- Appukuttan, Binoy -- Stout, J Timothy -- Christiansen, Stephen -- Ciccarelli, Maria Laura -- Baldi, Alfonso -- Campioni, Mara -- Zenteno, Juan C -- Davenport, Dominic -- Mariani, Laura E -- Sahin, Mustafa -- Guthrie, Sarah -- Engle, Elizabeth C -- G9900837/Medical Research Council/United Kingdom -- G9900989/Medical Research Council/United Kingdom -- R01 EY015298/EY/NEI NIH HHS/ -- R01 EY015298-01/EY/NEI NIH HHS/ -- R01 EY015298-02/EY/NEI NIH HHS/ -- R01 EY015298-03/EY/NEI NIH HHS/ -- R01 EY015298-04/EY/NEI NIH HHS/ -- R01 EY015298-05/EY/NEI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Aug 8;321(5890):839-43. doi: 10.1126/science.1156121. Epub 2008 Jul 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine (Genetics), Children's Hospital Boston, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18653847" target="_blank"〉PubMed〈/a〉
    Keywords: Abducens Nerve/abnormalities ; Amino Acid Sequence ; Animals ; Axons/physiology ; Cell Line ; Cell Membrane/metabolism ; Chick Embryo ; Chimerin 1/chemistry/*genetics/*metabolism ; Duane Retraction Syndrome/*genetics ; Female ; Gene Expression Profiling ; Heterozygote ; Humans ; Male ; Molecular Sequence Data ; *Mutation, Missense ; Oculomotor Muscles/embryology/innervation/metabolism ; Oculomotor Nerve/abnormalities/embryology ; Pedigree
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    Polycomb proteins targeted by a short repeat RNA to the mouse X chromosome (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-11-01
    Description: To equalize X-chromosome dosages between the sexes, the female mammal inactivates one of her two X chromosomes. X-chromosome inactivation (XCI) is initiated by expression of Xist, a 17-kb noncoding RNA (ncRNA) that accumulates on the X in cis. Because interacting factors have not been isolated, the mechanism by which Xist induces silencing remains unknown. We discovered a 1.6-kilobase ncRNA (RepA) within Xist and identified the Polycomb complex, PRC2, as its direct target. PRC2 is initially recruited to the X by RepA RNA, with Ezh2 serving as the RNA binding subunit. The antisense Tsix RNA inhibits this interaction. RepA depletion abolishes full-length Xist induction and trimethylation on lysine 27 of histone H3 of the X. Likewise, PRC2 deficiency compromises Xist up-regulation. Therefore, RepA, together with PRC2, is required for the initiation and spread of XCI. We conclude that a ncRNA cofactor recruits Polycomb complexes to their target locus.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2748911/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2748911/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhao, Jing -- Sun, Bryan K -- Erwin, Jennifer A -- Song, Ji-Joon -- Lee, Jeannie T -- R01 GM058839/GM/NIGMS NIH HHS/ -- R01 GM058839-10/GM/NIGMS NIH HHS/ -- R01 GM110090/GM/NIGMS NIH HHS/ -- R01GM58839/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Oct 31;322(5902):750-6. doi: 10.1126/science.1163045.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18974356" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Line ; Chromatin Immunoprecipitation ; Electrophoretic Mobility Shift Assay ; Embryonic Stem Cells ; Female ; Fibroblasts ; Male ; Mice ; Mice, Transgenic ; Molecular Sequence Data ; Polycomb-Group Proteins ; Polymerase Chain Reaction ; RNA, Long Noncoding ; RNA, Untranslated/genetics/*metabolism ; Repetitive Sequences, Nucleic Acid ; Repressor Proteins/*metabolism ; Up-Regulation ; X Chromosome/*metabolism ; X Chromosome Inactivation
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    Research ethics. When embryonic stem cell lines fail to meet consent standards (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-10-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sugarman, Jeremy -- Siegel, Andrew W -- New York, N.Y. -- Science. 2008 Oct 17;322(5900):379. doi: 10.1126/science.1164441.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Berman Institute of Bioethics, Johns Hopkins University, Baltimore, MD 21205, USA. jsugarm1@jhmi.edu .〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18927375" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Embryo Disposition ; Embryo Research/*ethics/legislation & jurisprudence ; *Embryo, Mammalian ; *Embryonic Stem Cells ; Female ; Germ Cells ; Guidelines as Topic ; Humans ; *Informed Consent ; *Tissue Donors
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    A global view of gene activity and alternative splicing by deep sequencing of the human transcriptome (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-07-05
    Description: The functional complexity of the human transcriptome is not yet fully elucidated. We report a high-throughput sequence of the human transcriptome from a human embryonic kidney and a B cell line. We used shotgun sequencing of transcripts to generate randomly distributed reads. Of these, 50% mapped to unique genomic locations, of which 80% corresponded to known exons. We found that 66% of the polyadenylated transcriptome mapped to known genes and 34% to nonannotated genomic regions. On the basis of known transcripts, RNA-Seq can detect 25% more genes than can microarrays. A global survey of messenger RNA splicing events identified 94,241 splice junctions (4096 of which were previously unidentified) and showed that exon skipping is the most prevalent form of alternative splicing.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sultan, Marc -- Schulz, Marcel H -- Richard, Hugues -- Magen, Alon -- Klingenhoff, Andreas -- Scherf, Matthias -- Seifert, Martin -- Borodina, Tatjana -- Soldatov, Aleksey -- Parkhomchuk, Dmitri -- Schmidt, Dominic -- O'Keeffe, Sean -- Haas, Stefan -- Vingron, Martin -- Lehrach, Hans -- Yaspo, Marie-Laure -- New York, N.Y. -- Science. 2008 Aug 15;321(5891):956-60. doi: 10.1126/science.1160342. Epub 2008 Jul 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Vertebrate Genomics, Max Planck Institute for Molecular Genetics, Ihnestrasse 73, 14195 Berlin, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18599741" target="_blank"〉PubMed〈/a〉
    Keywords: *Alternative Splicing ; Cell Line ; Cell Line, Tumor ; Computational Biology ; DNA, Complementary ; DNA, Intergenic ; Exons ; *Gene Expression Profiling ; *Genome, Human ; Humans ; Introns ; Oligonucleotide Array Sequence Analysis ; RNA Polymerase II/metabolism ; *RNA Splice Sites ; RNA, Messenger/*genetics ; *Sequence Analysis, RNA
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    Nascent RNA sequencing reveals widespread pausing and divergent initiation at human promoters (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-12-06
    Description: RNA polymerases are highly regulated molecular machines. We present a method (global run-on sequencing, GRO-seq) that maps the position, amount, and orientation of transcriptionally engaged RNA polymerases genome-wide. In this method, nuclear run-on RNA molecules are subjected to large-scale parallel sequencing and mapped to the genome. We show that peaks of promoter-proximal polymerase reside on approximately 30% of human genes, transcription extends beyond pre-messenger RNA 3' cleavage, and antisense transcription is prevalent. Additionally, most promoters have an engaged polymerase upstream and in an orientation opposite to the annotated gene. This divergent polymerase is associated with active genes but does not elongate effectively beyond the promoter. These results imply that the interplay between polymerases and regulators over broad promoter regions dictates the orientation and efficiency of productive transcription.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2833333/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2833333/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Core, Leighton J -- Waterfall, Joshua J -- Lis, John T -- GM25232/GM/NIGMS NIH HHS/ -- R01 GM025232/GM/NIGMS NIH HHS/ -- R01 GM025232-32/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2008 Dec 19;322(5909):1845-8. doi: 10.1126/science.1162228. Epub 2008 Dec 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Genetics, Cornell University, Ithaca, NY 14853, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19056941" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; CpG Islands ; DNA-Directed RNA Polymerases/*metabolism ; Genome, Human ; Humans ; Nucleosomes/metabolism ; *Promoter Regions, Genetic ; RNA Polymerase II/*metabolism ; RNA, Antisense/genetics/metabolism ; RNA, Messenger/genetics/metabolism ; *Sequence Analysis, RNA ; Transcription Initiation Site ; *Transcription, Genetic
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  • 92
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    A neoplastic gene fusion mimics trans-splicing of RNAs in normal human cells (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-09-06
    Description: Chromosomal rearrangements that create gene fusions are common features of human tumors. The prevailing view is that the resultant chimeric transcripts and proteins are abnormal, tumor-specific products that provide tumor cells with a growth and/or survival advantage. We show that normal endometrial stromal cells contain a specific chimeric RNA joining 5' exons of the JAZF1 gene on chromosome 7p15 to 3' exons of the Polycomb group gene JJAZ1/SUZ12 on chromosome 17q11 and that this RNA is translated into JAZF1-JJAZ1, a protein with anti-apoptotic activity. The JAZF1-JJAZ1 RNA appears to arise from physiologically regulated trans-splicing between precursor messenger RNAs for JAZF1 and JJAZ1. The chimeric RNA and protein are identical to those produced from a gene fusion found in human endometrial stromal tumors. These observations suggest that certain gene fusions may be pro-neoplastic owing to constitutive expression of chimeric gene products normally generated by trans-splicing of RNAs in developing tissues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Hui -- Wang, Jinglan -- Mor, Gil -- Sklar, Jeffrey -- R01 CA85995/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2008 Sep 5;321(5894):1357-61. doi: 10.1126/science.1156725.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Yale University School of Medicine, New Haven, CT 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18772439" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Hypoxia ; Cell Line ; Cell Line, Tumor ; Chromosome Aberrations ; Chromosomes, Human, Pair 17/genetics ; Chromosomes, Human, Pair 7/genetics ; Deferoxamine/pharmacology ; Endometrial Neoplasms/genetics ; Endometrium/cytology/*metabolism ; Exons ; Female ; *Gene Fusion ; Humans ; Menstrual Cycle ; Mutant Chimeric Proteins/genetics ; Neoplasm Proteins/biosynthesis/*genetics ; Progesterone/pharmacology ; Protein Biosynthesis ; RNA Precursors/*genetics ; RNA, Messenger/genetics ; Stromal Cells/*metabolism ; *Trans-Splicing ; Transcription Factors/biosynthesis/*genetics ; Translocation, Genetic
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    The Rag GTPases bind raptor and mediate amino acid signaling to mTORC1 (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-05-24
    Description: The multiprotein mTORC1 protein kinase complex is the central component of a pathway that promotes growth in response to insulin, energy levels, and amino acids and is deregulated in common cancers. We find that the Rag proteins--a family of four related small guanosine triphosphatases (GTPases)--interact with mTORC1 in an amino acid-sensitive manner and are necessary for the activation of the mTORC1 pathway by amino acids. A Rag mutant that is constitutively bound to guanosine triphosphate interacted strongly with mTORC1, and its expression within cells made the mTORC1 pathway resistant to amino acid deprivation. Conversely, expression of a guanosine diphosphate-bound Rag mutant prevented stimulation of mTORC1 by amino acids. The Rag proteins do not directly stimulate the kinase activity of mTORC1, but, like amino acids, promote the intracellular localization of mTOR to a compartment that also contains its activator Rheb.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2475333/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2475333/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sancak, Yasemin -- Peterson, Timothy R -- Shaul, Yoav D -- Lindquist, Robert A -- Thoreen, Carson C -- Bar-Peled, Liron -- Sabatini, David M -- AI47389/AI/NIAID NIH HHS/ -- R01 AI047389/AI/NIAID NIH HHS/ -- R01 AI047389-09/AI/NIAID NIH HHS/ -- R01 CA103866/CA/NCI NIH HHS/ -- R01 CA103866-05/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2008 Jun 13;320(5882):1496-501. doi: 10.1126/science.1157535. Epub 2008 May 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research and Department of Biology, Massachusetts Institute of Technology (MIT), Nine Cambridge Center, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18497260" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Amino Acids/*metabolism ; Cell Line ; Cell Nucleus/metabolism ; Cytoplasm/metabolism ; Dimerization ; Guanosine Triphosphate/metabolism ; Humans ; Insulin/metabolism ; Leucine/metabolism ; Monomeric GTP-Binding Proteins/genetics/*metabolism ; Multiprotein Complexes ; Mutant Proteins/metabolism ; Mutation ; Neuropeptides/metabolism ; Phosphorylation ; Protein Binding ; Protein Kinases/metabolism ; Proteins/*metabolism ; *Signal Transduction ; TOR Serine-Threonine Kinases ; Transcription Factors/*metabolism
    Print ISSN: 0036-8075
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    Proliferating cells express mRNAs with shortened 3' untranslated regions and fewer microRNA target sites (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-06-21
    Description: Messenger RNA (mRNA) stability, localization, and translation are largely determined by sequences in the 3' untranslated region (3'UTR). We found a conserved increase in expression of mRNAs terminating at upstream polyadenylation sites after activation of primary murine CD4+ T lymphocytes. This program, resulting in shorter 3'UTRs, is a characteristic of gene expression during immune cell activation and correlates with proliferation across diverse cell types and tissues. Forced expression of full-length 3'UTRs conferred reduced protein expression. In some cases the reduction in protein expression could be reversed by deletion of predicted microRNA target sites in the variably included region. Our data indicate that gene expression is coordinately regulated, such that states of increased proliferation are associated with widespread reductions in the 3'UTR-based regulatory capacity of mRNAs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2587246/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2587246/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sandberg, Rickard -- Neilson, Joel R -- Sarma, Arup -- Sharp, Phillip A -- Burge, Christopher B -- P01 CA042063/CA/NCI NIH HHS/ -- P01 CA042063-22/CA/NCI NIH HHS/ -- P01-CA42063/CA/NCI NIH HHS/ -- P30-CA14051/CA/NCI NIH HHS/ -- R01 GM034277/GM/NIGMS NIH HHS/ -- R01 GM034277-23/GM/NIGMS NIH HHS/ -- R01 HG002439/HG/NHGRI NIH HHS/ -- R01 HG002439-07/HG/NHGRI NIH HHS/ -- R01-GM34277/GM/NIGMS NIH HHS/ -- R01-HG002439/HG/NHGRI NIH HHS/ -- U19 AI056900/AI/NIAID NIH HHS/ -- U19 AI056900-010001/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2008 Jun 20;320(5883):1643-7. doi: 10.1126/science.1155390.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18566288" target="_blank"〉PubMed〈/a〉
    Keywords: *3' Untranslated Regions ; Animals ; CD4-Positive T-Lymphocytes/cytology/immunology/*metabolism ; Cell Line ; Cell Line, Tumor ; *Cell Proliferation ; Cells, Cultured ; *Gene Expression Regulation ; Humans ; *Lymphocyte Activation ; Mice ; Mice, Inbred C57BL ; MicroRNAs/*metabolism ; Oligonucleotide Array Sequence Analysis ; Polyadenylation ; RNA Splicing ; RNA, Messenger/chemistry/genetics/*metabolism
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    Control of the reversibility of cellular quiescence by the transcriptional repressor HES1 (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-08-23
    Description: The mechanisms by which quiescent cells, including adult stem cells, preserve their ability to resume proliferation after weeks or even years of cell cycle arrest are not known. We report that reversibility is not a passive property of nondividing cells, because enforced cell cycle arrest for a period as brief as 4 days initiates spontaneous, premature, and irreversible senescence. Increased expression of the gene encoding the basic helix-loop-helix protein HES1 was required for quiescence to be reversible, because HES1 prevented both premature senescence and inappropriate differentiation in quiescent fibroblasts. In some human tumors, the HES1 pathway was activated, which allowed these cells to evade differentiation and irreversible cell cycle arrest. We conclude that HES1 safeguards against irreversible cell cycle exit both during normal cellular quiescence and pathologically in the setting of tumorigenesis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2721335/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2721335/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sang, Liyun -- Coller, Hilary A -- Roberts, James M -- P50 GM071508/GM/NIGMS NIH HHS/ -- P50 GM071508-05/GM/NIGMS NIH HHS/ -- R01 CA118043/CA/NCI NIH HHS/ -- R01 CA118043-03/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Aug 22;321(5892):1095-100. doi: 10.1126/science.1155998.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18719287" target="_blank"〉PubMed〈/a〉
    Keywords: Basic Helix-Loop-Helix Transcription Factors/genetics/*metabolism ; Cell Aging ; *Cell Cycle ; Cell Differentiation ; Cell Line ; Cell Line, Tumor ; *Cell Proliferation ; Cyclin-Dependent Kinase Inhibitor p21/metabolism ; Fibroblasts/*cytology/metabolism ; Homeodomain Proteins/genetics/*metabolism ; Humans ; Muscle Development ; MyoD Protein/metabolism ; Receptors, Notch/metabolism ; Recombinant Fusion Proteins/metabolism ; Repressor Proteins/genetics/*metabolism ; Rhabdomyosarcoma/metabolism/pathology ; Signal Transduction ; Transduction, Genetic
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    Self-assembled water-soluble nucleic acid probe tiles for label-free RNA hybridization assays (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-01-12
    Description: The DNA origami method, in which long, single-stranded DNA segments are folded into shapes by short staple segments, was used to create nucleic acid probe tiles that are molecular analogs of macroscopic DNA chips. One hundred trillion probe tiles were fabricated in one step and bear pairs of 20-nucleotide-long single-stranded DNA segments that act as probe sequences. These tiles can hybridize to their targets in solution and, after adsorption onto mica surfaces, can be examined by atomic force microscopy in order to quantify binding events, because the probe segments greatly increase in stiffness upon hybridization. The nucleic acid probe tiles have been used to study position-dependent hybridization on the nanoscale and have also been used for label-free detection of RNA.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ke, Yonggang -- Lindsay, Stuart -- Chang, Yung -- Liu, Yan -- Yan, Hao -- New York, N.Y. -- Science. 2008 Jan 11;319(5860):180-3. doi: 10.1126/science.1150082.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Single Molecule Biophysics, Arizona State University, Tempe, AZ 85287, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18187649" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/genetics ; Adsorption ; Aluminum Silicates ; Animals ; Cell Line ; DNA, Single-Stranded ; Gene Expression Profiling/*methods ; Genes, RAG-1 ; Genes, myc ; Mice ; Microscopy, Atomic Force ; *Molecular Probe Techniques ; *Nanostructures ; Nucleic Acid Hybridization/*methods ; *Oligonucleotide Probes ; RNA/*analysis/genetics ; Sensitivity and Specificity ; Solubility
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    Recognition of a ubiquitous self antigen by prostate cancer-infiltrating CD8+ T lymphocytes (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-01-12
    Description: Substantial evidence exists that many tumors can be specifically recognized by CD8+ T lymphocytes. The definition of antigens targeted by these cells is paramount for the development of effective immunotherapeutic strategies for treating human cancers. In a screen for endogenous tumor-associated T cell responses in a primary mouse model of prostatic adenocarcinoma, we identified a naturally arising CD8+ T cell response that is reactive to a peptide derived from histone H4. Despite the ubiquitous nature of histones, T cell recognition of histone H4 peptide was specifically associated with the presence of prostate cancer in these mice. Thus, the repertoire of antigens recognized by tumor-infiltrating T cells is broader than previously thought and includes peptides derived from ubiquitous self antigens that are normally sequestered from immune detection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Savage, Peter A -- Vosseller, Keith -- Kang, Chulho -- Larimore, Kevin -- Riedel, Elyn -- Wojnoonski, Kathleen -- Jungbluth, Achim A -- Allison, James P -- New York, N.Y. -- Science. 2008 Jan 11;319(5860):215-20. doi: 10.1126/science.1148886.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Howard Hughes Medical Institute, and Ludwig Center for Cancer Immunotherapy, Memorial Sloan-Kettering Cancer Center (MSKCC), New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18187659" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma/*immunology ; Adoptive Transfer ; Animals ; Antigen Presentation ; Antigens, Neoplasm/*immunology ; Autoantigens/*immunology ; CD8-Positive T-Lymphocytes/*immunology ; Cell Line ; Epitopes, T-Lymphocyte/immunology ; Histones/*immunology ; Hybridomas ; Lymphocytes, Tumor-Infiltrating/*immunology ; Male ; Mice ; Mice, Transgenic ; Peptide Fragments/immunology ; Prostatic Neoplasms/*immunology ; Receptors, Antigen, T-Cell, alpha-beta/immunology
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  • 98
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    Arabidopsis CLV3 peptide directly binds CLV1 ectodomain (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-01-19
    Description: CLV1, which encodes a leucine-rich repeat receptor kinase, and CLV3, which encodes a secreted peptide, function in the same genetic pathway to maintain stem cell populations in Arabidopsis shoot apical meristem. Here, we show biochemical evidence, by ligand binding assay and photoaffinity labeling, that the CLV3 peptide directly binds the CLV1 ectodomain with a dissociation constant of 17.5 nM. The CLV1 ectodomain also interacts with the structurally related CLE peptides, with distinct affinities depending on the specific amino acid sequence. Our results provide direct evidence that CLV3 and CLV1 function as a ligand-receptor pair involved in stem cell maintenance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ogawa, Mari -- Shinohara, Hidefumi -- Sakagami, Youji -- Matsubayashi, Yoshikatsu -- New York, N.Y. -- Science. 2008 Jan 18;319(5861):294. doi: 10.1126/science.1150083.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Graduate School of Bio-Agricultural Sciences, Nagoya University, Chikusa, Nagoya 464-8601, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18202283" target="_blank"〉PubMed〈/a〉
    Keywords: Arabidopsis/cytology/genetics/*metabolism ; Arabidopsis Proteins/chemistry/*metabolism ; Cell Line ; Genes, Plant ; Ligands ; Meristem/cytology/metabolism ; Peptides/chemistry/metabolism ; Plants, Genetically Modified ; Protein Binding ; Protein Structure, Tertiary ; Receptor Protein-Tyrosine Kinases/chemistry/*metabolism ; Tobacco
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  • 99
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    A cholesterol biosynthesis inhibitor blocks Staphylococcus aureus virulence (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-02-16
    Description: Staphylococcus aureus produces hospital- and community-acquired infections, with methicillin-resistant S. aureus posing a serious public health threat. The golden carotenoid pigment of S. aureus, staphyloxanthin, promotes resistance to reactive oxygen species and host neutrophil-based killing, and early enzymatic steps in staphyloxanthin production resemble those for cholesterol biosynthesis. We determined the crystal structures of S. aureus dehydrosqualene synthase (CrtM) at 1.58 angstrom resolution, finding structural similarity to human squalene synthase (SQS). We screened nine SQS inhibitors and determined the structures of three, bound to CrtM. One, previously tested for cholesterol-lowering activity in humans, blocked staphyloxanthin biosynthesis in vitro (median inhibitory concentration approximately 100 nM), resulting in colorless bacteria with increased susceptibility to killing by human blood and to innate immune clearance in a mouse infection model. This finding represents proof of principle for a virulence factor-based therapy against S. aureus.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2747771/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2747771/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, Chia-I -- Liu, George Y -- Song, Yongcheng -- Yin, Fenglin -- Hensler, Mary E -- Jeng, Wen-Yih -- Nizet, Victor -- Wang, Andrew H-J -- Oldfield, Eric -- AI07482/AI/NIAID NIH HHS/ -- GM073216/GM/NIGMS NIH HHS/ -- GM65307/GM/NIGMS NIH HHS/ -- HD051796/HD/NICHD NIH HHS/ -- R01 GM065307/GM/NIGMS NIH HHS/ -- R01 GM065307-07/GM/NIGMS NIH HHS/ -- R01 GM073216/GM/NIGMS NIH HHS/ -- R01 GM073216-29/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2008 Mar 7;319(5868):1391-4. doi: 10.1126/science.1153018. Epub 2008 Feb 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Biological Chemistry, Academia Sinica, Nankang, Taipei 11529, Taiwan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18276850" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Anti-Bacterial Agents/chemical synthesis/chemistry/*pharmacology/therapeutic use ; Bacterial Proteins/*antagonists & inhibitors/chemistry/isolation & ; purification/metabolism ; Cell Line ; Cell Proliferation/drug effects ; Cholesterol/biosynthesis ; Crystallography, X-Ray ; Enzyme Inhibitors/chemical synthesis/metabolism/*pharmacology ; Farnesyl-Diphosphate Farnesyltransferase/*antagonists & ; inhibitors/chemistry/isolation & purification/metabolism ; Humans ; Mice ; Molecular Sequence Data ; Organothiophosphorus Compounds/chemical ; synthesis/metabolism/*pharmacology/therapeutic use ; Polyisoprenyl Phosphates/chemistry/metabolism ; Protein Structure, Secondary ; Sesquiterpenes/chemistry/metabolism ; Staphylococcal Infections/*drug therapy/microbiology ; Staphylococcus aureus/drug effects/growth & development/metabolism/*pathogenicity ; Virulence/drug effects ; Xanthophylls/biosynthesis
    Print ISSN: 0036-8075
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    Germline allele-specific expression of TGFBR1 confers an increased risk of colorectal cancer (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-08-16
    Description: Much of the genetic predisposition to colorectal cancer (CRC) in humans is unexplained. Studying a Caucasian-dominated population in the United States, we showed that germline allele-specific expression (ASE) of the gene encoding transforming growth factor-beta (TGF-beta) type I receptor, TGFBR1, is a quantitative trait that occurs in 10 to 20% of CRC patients and 1 to 3% of controls. ASE results in reduced expression of the gene, is dominantly inherited, segregates in families, and occurs in sporadic CRC cases. Although subtle, the reduction in constitutive TGFBR1 expression alters SMAD-mediated TGF-beta signaling. Two major TGFBR1 haplotypes are predominant among ASE cases, which suggests ancestral mutations, but causative germline changes have not been identified. Conservative estimates suggest that ASE confers a substantially increased risk of CRC (odds ratio, 8.7; 95% confidence interval, 2.6 to 29.1), but these estimates require confirmation and will probably show ethnic differences.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2672914/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2672914/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Valle, Laura -- Serena-Acedo, Tarsicio -- Liyanarachchi, Sandya -- Hampel, Heather -- Comeras, Ilene -- Li, Zhongyuan -- Zeng, Qinghua -- Zhang, Hong-Tao -- Pennison, Michael J -- Sadim, Maureen -- Pasche, Boris -- Tanner, Stephan M -- de la Chapelle, Albert -- CA108741/CA/NCI NIH HHS/ -- CA112520/CA/NCI NIH HHS/ -- CA16058/CA/NCI NIH HHS/ -- CA67941/CA/NCI NIH HHS/ -- R01 CA108741/CA/NCI NIH HHS/ -- R01 CA108741-01A2/CA/NCI NIH HHS/ -- R01 CA112520/CA/NCI NIH HHS/ -- R01 CA112520-01A1/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2008 Sep 5;321(5894):1361-5. doi: 10.1126/science.1159397. Epub 2008 Aug 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Human Cancer Genetics Program, Comprehensive Cancer Center, Ohio State University, Columbus, OH 43210, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18703712" target="_blank"〉PubMed〈/a〉
    Keywords: 3' Untranslated Regions ; Adult ; Aged ; Aged, 80 and over ; Alleles ; Cell Line ; Colorectal Neoplasms/*genetics ; Female ; *Gene Expression ; *Genetic Predisposition to Disease ; Haplotypes ; Heterozygote ; Humans ; Linkage Disequilibrium ; Male ; Middle Aged ; Polymorphism, Single Nucleotide ; Protein-Serine-Threonine Kinases/*genetics ; Quantitative Trait, Heritable ; Receptors, Transforming Growth Factor beta/*genetics ; Risk Factors ; Signal Transduction ; Smad3 Protein/metabolism ; Transforming Growth Factor beta/metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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