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  • Cloning, Molecular
  • Transfection
  • American Association for the Advancement of Science (AAAS)  (663)
  • American Association of Petroleum Geologists (AAPG)
  • Emerald
  • 2005-2009  (158)
  • 1995-1999  (505)
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  • 1
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    Orc1 controls centriole and centrosome copy number in human cells (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-02-07
    Description: Centrosomes, each containing a pair of centrioles, organize microtubules in animal cells, particularly during mitosis. DNA and centrosomes are normally duplicated once before cell division to maintain optimal genome integrity. We report a new role for the Orc1 protein, a subunit of the origin recognition complex (ORC) that is a key component of the DNA replication licensing machinery, in controlling centriole and centrosome copy number in human cells, independent of its role in DNA replication. Cyclin A promotes Orc1 localization to centrosomes where Orc1 prevents Cyclin E-dependent reduplication of both centrioles and centrosomes in a single cell division cycle. The data suggest that Orc1 is a regulator of centriole and centrosome reduplication as well as the initiation of DNA replication.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2653626/" 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/PMC2653626/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hemerly, Adriana S -- Prasanth, Supriya G -- Siddiqui, Khalid -- Stillman, Bruce -- CA13106/CA/NCI NIH HHS/ -- P01 CA013106/CA/NCI NIH HHS/ -- P01 CA013106-310025/CA/NCI NIH HHS/ -- P01 CA013106-36/CA/NCI NIH HHS/ -- P01 CA013106-370025/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2009 Feb 6;323(5915):789-93. doi: 10.1126/science.1166745.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cold Spring Harbor Laboratory, 1 Bungtown Road, Cold Spring Harbor 11724, NY, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19197067" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Cycle ; Cell Line, Tumor ; Centrioles/*physiology ; Centrosome/*physiology ; Cyclin A/metabolism ; Cyclin E/metabolism ; Cyclin-Dependent Kinase 2/metabolism ; DNA Replication ; HeLa Cells ; Humans ; Kinetics ; Mutant Proteins/metabolism ; Origin Recognition Complex/genetics/*metabolism ; RNA Interference ; RNA, Small Interfering ; 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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  • 2
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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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  • 3
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    Stress-inducible regulation of heat shock factor 1 by the deacetylase SIRT1 (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-02-21
    Description: Heat shock factor 1 (HSF1) is essential for protecting cells from protein-damaging stress associated with misfolded proteins and regulates the insulin-signaling pathway and aging. Here, we show that human HSF1 is inducibly acetylated at a critical residue that negatively regulates DNA binding activity. Activation of the deacetylase and longevity factor SIRT1 prolonged HSF1 binding to the heat shock promoter Hsp70 by maintaining HSF1 in a deacetylated, DNA-binding competent state. Conversely, down-regulation of SIRT1 accelerated the attenuation of the heat shock response (HSR) and release of HSF1 from its cognate promoter elements. These results provide a mechanistic basis for the requirement of HSF1 in the regulation of life span and establish a role for SIRT1 in protein homeostasis and the HSR.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3429349/" 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/PMC3429349/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Westerheide, Sandy D -- Anckar, Julius -- Stevens, Stanley M Jr -- Sistonen, Lea -- Morimoto, Richard I -- R01 AG026647/AG/NIA NIH HHS/ -- R01 AG026647-01/AG/NIA NIH HHS/ -- R01 AG026647-02/AG/NIA NIH HHS/ -- R01 AG026647-03/AG/NIA NIH HHS/ -- R01 AG026647-04/AG/NIA NIH HHS/ -- R01 GM038109/GM/NIGMS NIH HHS/ -- R37 GM038109/GM/NIGMS NIH HHS/ -- R37 GM038109-19/GM/NIGMS NIH HHS/ -- R37 GM038109-20/GM/NIGMS NIH HHS/ -- R37 GM038109-21/GM/NIGMS NIH HHS/ -- R37 GM038109-22/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2009 Feb 20;323(5917):1063-6. doi: 10.1126/science.1165946.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Molecular Biology and Cell Biology, Rice Institute for Biomedical Research, Northwestern University, Evanston, IL, 60208, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19229036" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Amino Acid Sequence ; Animals ; Cell Aging/*physiology ; Chromatin Immunoprecipitation ; DNA/metabolism ; DNA-Binding Proteins/*metabolism ; Down-Regulation ; HSP70 Heat-Shock Proteins/*genetics ; HeLa Cells ; *Heat-Shock Response ; Homeostasis ; Humans ; Mice ; Molecular Sequence Data ; *Promoter Regions, Genetic ; RNA, Small Interfering ; Sirtuin 1 ; Sirtuins/genetics/*metabolism ; *Stress, Psychological ; Transcription Factors/*metabolism ; 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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  • 4
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    Coding-sequence determinants of gene expression in Escherichia coli (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-04-11
    Description: Synonymous mutations do not alter the encoded protein, but they can influence gene expression. To investigate how, we engineered a synthetic library of 154 genes that varied randomly at synonymous sites, but all encoded the same green fluorescent protein (GFP). When expressed in Escherichia coli, GFP protein levels varied 250-fold across the library. GFP messenger RNA (mRNA) levels, mRNA degradation patterns, and bacterial growth rates also varied, but codon bias did not correlate with gene expression. Rather, the stability of mRNA folding near the ribosomal binding site explained more than half the variation in protein levels. In our analysis, mRNA folding and associated rates of translation initiation play a predominant role in shaping expression levels of individual genes, whereas codon bias influences global translation efficiency and cellular fitness.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3902468/" 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/PMC3902468/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kudla, Grzegorz -- Murray, Andrew W -- Tollervey, David -- Plotkin, Joshua B -- BB/D019621/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/DO19621/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/DO19621/1/Wellcome Trust/United Kingdom -- P50 GM068763/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2009 Apr 10;324(5924):255-8. doi: 10.1126/science.1170160.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology and Program in Applied Mathematics and Computational Science, University of Pennsylvania, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19359587" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Substitution ; Base Composition ; Cloning, Molecular ; *Codon ; Escherichia coli/*genetics/growth & development/metabolism ; *Gene Expression ; Gene Library ; Genes, Synthetic ; Green Fluorescent Proteins/*genetics/metabolism ; Mutation ; Nucleic Acid Conformation ; Protein Biosynthesis ; RNA Stability ; RNA, Bacterial/chemistry/genetics/metabolism ; RNA, Messenger/chemistry/*genetics/metabolism ; Spectrometry, Fluorescence
    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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    HDAC4 regulates neuronal survival in normal and diseased retinas (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-01-10
    Description: Histone deacetylase 4 (HDAC4) shuttles between the nucleus and cytoplasm and serves as a nuclear co-repressor that regulates bone and muscle development. We report that HDAC4 regulates the survival of retinal neurons in the mouse in normal and pathological conditions. Reduction in HDAC4 expression during normal retinal development led to apoptosis of rod photoreceptors and bipolar (BP) interneurons, whereas overexpression reduced naturally occurring cell death of the BP cells. HDAC4 overexpression in a mouse model of retinal degeneration prolonged photoreceptor survival. The survival effect was due to the activity of HDAC4 in the cytoplasm and relied at least partly on the activity of hypoxia-inducible factor 1alpha (HIF1alpha). These data provide evidence that HDAC4 plays an important role in promoting the survival of retinal neurons.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3339762/" 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/PMC3339762/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Bo -- Cepko, Constance L -- EYO 14466/PHS HHS/ -- R01 EY014466/EY/NEI NIH HHS/ -- R01 EY014466-05/EY/NEI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Jan 9;323(5911):256-9. doi: 10.1126/science.1166226.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics and Howard Hughes Medical Institute, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02115, USA. bochen@genetics.med.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19131628" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Animals ; Apoptosis ; Cell Nucleus/enzymology ; Cell Survival ; Cytoplasm/enzymology ; Electroporation ; Histone Deacetylases/genetics/*metabolism ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; Mice ; Mutation ; Retina/cytology/*enzymology ; Retinal Degeneration/*enzymology/pathology ; Retinal Neurons/enzymology/*physiology ; Retinal Rod Photoreceptor Cells/enzymology/*physiology ; Rhodopsin/genetics/metabolism ; 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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  • 6
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    Structure of a type IV secretion system core complex (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-01-10
    Description: Type IV secretion systems (T4SSs) are important virulence factors used by Gram-negative bacterial pathogens to inject effectors into host cells or to spread plasmids harboring antibiotic resistance genes. We report the 15 angstrom resolution cryo-electron microscopy structure of the core complex of a T4SS. The core complex is composed of three proteins, each present in 14 copies and forming a approximately 1.1-megadalton two-chambered, double membrane-spanning channel. The structure is double-walled, with each component apparently spanning a large part of the channel. The complex is open on the cytoplasmic side and constricted on the extracellular side. Overall, the T4SS core complex structure is different in both architecture and composition from the other known double membrane-spanning secretion system that has been structurally characterized.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fronzes, Remi -- Schafer, Eva -- Wang, Luchun -- Saibil, Helen R -- Orlova, Elena V -- Waksman, Gabriel -- 070776/Wellcome Trust/United Kingdom -- BB/C516144/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/C516179/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/F010281/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2009 Jan 9;323(5911):266-8. doi: 10.1126/science.1166101.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Structural and Molecular Biology, School of Crystallography, Birkbeck College, Malet Street, London, WC1E 7HX, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19131631" target="_blank"〉PubMed〈/a〉
    Keywords: Bacterial Outer Membrane Proteins/*chemistry/genetics/ultrastructure ; Bacterial Proteins/*chemistry/genetics/*ultrastructure ; Cloning, Molecular ; Cryoelectron Microscopy ; Gram-Negative Bacteria/*chemistry/genetics/pathogenicity ; Imaging, Three-Dimensional ; Models, Molecular ; Multiprotein Complexes/chemistry/ultrastructure ; *Plasmids ; Protein Conformation ; Protein Structure, Quaternary ; Virulence Factors/*chemistry/genetics
    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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    A kinase-START gene confers temperature-dependent resistance to wheat stripe rust (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-02-21
    Description: Stripe rust is a devastating fungal disease that afflicts wheat in many regions of the world. New races of Puccinia striiformis, the pathogen responsible for this disease, have overcome most of the known race-specific resistance genes. We report the map-based cloning of the gene Yr36 (WKS1), which confers resistance to a broad spectrum of stripe rust races at relatively high temperatures (25 degrees to 35 degrees C). This gene includes a kinase and a putative START lipid-binding domain. Five independent mutations and transgenic complementation confirmed that both domains are necessary to confer resistance. Yr36 is present in wild wheat but is absent in modern pasta and bread wheat varieties, and therefore it can now be used to improve resistance to stripe rust in a broad set of varieties.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4737487/" 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/PMC4737487/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fu, Daolin -- Uauy, Cristobal -- Distelfeld, Assaf -- Blechl, Ann -- Epstein, Lynn -- Chen, Xianming -- Sela, Hanan -- Fahima, Tzion -- Dubcovsky, Jorge -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Mar 6;323(5919):1357-60. doi: 10.1126/science.1166289. Epub 2009 Feb 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Plant Sciences, University of California, Davis, CA 95616, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19228999" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Basidiomycota/*pathogenicity ; Cloning, Molecular ; Crosses, Genetic ; Down-Regulation ; *Genes, Plant ; Hot Temperature ; Immunity, Innate ; Molecular Sequence Data ; Phosphotransferases/chemistry/*genetics/metabolism ; Physical Chromosome Mapping ; *Plant Diseases/immunology/microbiology ; Plant Proteins/chemistry/genetics/metabolism ; Plants, Genetically Modified ; Triticum/*genetics/*microbiology
    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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    KLF family members regulate intrinsic axon regeneration ability (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-10-10
    Description: Neurons in the central nervous system (CNS) lose their ability to regenerate early in development, but the underlying mechanisms are unknown. By screening genes developmentally regulated in retinal ganglion cells (RGCs), we identified Kruppel-like factor-4 (KLF4) as a transcriptional repressor of axon growth in RGCs and other CNS neurons. RGCs lacking KLF4 showed increased axon growth both in vitro and after optic nerve injury in vivo. Related KLF family members suppressed or enhanced axon growth to differing extents, and several growth-suppressive KLFs were up-regulated postnatally, whereas growth-enhancing KLFs were down-regulated. Thus, coordinated activities of different KLFs regulate the regenerative capacity of CNS neurons.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2882032/" 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/PMC2882032/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moore, Darcie L -- Blackmore, Murray G -- Hu, Ying -- Kaestner, Klaus H -- Bixby, John L -- Lemmon, Vance P -- Goldberg, Jeffrey L -- P30 EY014801/EY/NEI NIH HHS/ -- R01 NS059866/NS/NINDS NIH HHS/ -- R01 NS059866-01A2/NS/NINDS NIH HHS/ -- R01 NS061348/NS/NINDS NIH HHS/ -- R01 NS061348-01A2/NS/NINDS NIH HHS/ -- R01 NS061348-02/NS/NINDS NIH HHS/ -- R01 NS061348-03/NS/NINDS NIH HHS/ -- R01 NS061348-04/NS/NINDS NIH HHS/ -- R03 EY016790/EY/NEI NIH HHS/ -- R03 EY016790-01/EY/NEI NIH HHS/ -- R03 EY016790-02/EY/NEI NIH HHS/ -- R03 EY016790-03/EY/NEI NIH HHS/ -- T32 NS007459/NS/NINDS NIH HHS/ -- T32 NS07492/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2009 Oct 9;326(5950):298-301. doi: 10.1126/science.1175737.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Bascom Palmer Eye Institute, University of Miami Miller School of Medicine, Miami, FL 33136, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19815778" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*physiology/ultrastructure ; Cell Count ; Cell Survival ; Cells, Cultured ; Down-Regulation ; Gene Knockout Techniques ; Growth Cones/physiology ; Hippocampus/cytology/physiology ; Kruppel-Like Transcription Factors/genetics/*physiology ; Mice ; Nerve Crush ; Nerve Regeneration ; Neurites/physiology ; Neurons/*physiology ; Optic Nerve Injuries/physiopathology ; Rats ; Retinal Ganglion Cells/cytology/*physiology ; Transcription, Genetic ; Transfection ; Up-Regulation
    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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    Conversion of 5-methylcytosine to 5-hydroxymethylcytosine in mammalian DNA by MLL partner TET1 (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    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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    Crystal structure of the eukaryotic strong inward-rectifier K+ channel Kir2.2 at 3.1 A resolution (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-12-19
    Description: Inward-rectifier potassium (K+) channels conduct K+ ions most efficiently in one direction, into the cell. Kir2 channels control the resting membrane voltage in many electrically excitable cells, and heritable mutations cause periodic paralysis and cardiac arrhythmia. We present the crystal structure of Kir2.2 from chicken, which, excluding the unstructured amino and carboxyl termini, is 90% identical to human Kir2.2. Crystals containing rubidium (Rb+), strontium (Sr2+), and europium (Eu3+) reveal binding sites along the ion conduction pathway that are both conductive and inhibitory. The sites correlate with extensive electrophysiological data and provide a structural basis for understanding rectification. The channel's extracellular surface, with large structured turrets and an unusual selectivity filter entryway, might explain the relative insensitivity of eukaryotic inward rectifiers to toxins. These same surface features also suggest a possible approach to the development of inhibitory agents specific to each member of the inward-rectifier K+ channel family.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2819303/" 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/PMC2819303/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tao, Xiao -- Avalos, Jose L -- Chen, Jiayun -- MacKinnon, Roderick -- P30 EB009998/EB/NIBIB NIH HHS/ -- R01 GM043949/GM/NIGMS NIH HHS/ -- R01 GM043949-10/GM/NIGMS NIH HHS/ -- R01 GM043949-11/GM/NIGMS NIH HHS/ -- R01 GM043949-12/GM/NIGMS NIH HHS/ -- R01 GM043949-13/GM/NIGMS NIH HHS/ -- R01 GM043949-14/GM/NIGMS NIH HHS/ -- R01 GM043949-15/GM/NIGMS NIH HHS/ -- R01 GM043949-16/GM/NIGMS NIH HHS/ -- R01 GM043949-17/GM/NIGMS NIH HHS/ -- R01 GM043949-18/GM/NIGMS NIH HHS/ -- R01 GM043949-19/GM/NIGMS NIH HHS/ -- R01 GM043949-20/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Dec 18;326(5960):1668-74. doi: 10.1126/science.1180310.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Neurobiology and Biophysics, Rockefeller University, Howard Hughes Medical Institute, 1230 York Avenue, New York, NY 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20019282" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Amino Acid Sequence ; Animals ; Binding Sites ; Chickens ; Cloning, Molecular ; Crystallography, X-Ray ; Europium/metabolism ; Hydrogen Bonding ; Hydrophobic and Hydrophilic Interactions ; Models, Molecular ; Molecular Sequence Data ; Oocytes ; Patch-Clamp Techniques ; Potassium/metabolism ; Potassium Channel Blockers/pharmacology ; Potassium Channels, Inwardly Rectifying/antagonists & ; inhibitors/*chemistry/metabolism ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Protein Subunits/chemistry ; Rubidium/metabolism ; Sequence Alignment ; Strontium/metabolism ; Xenopus laevis
    Print ISSN: 0036-8075
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  • 11
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    Input-specific spine entry of soma-derived Vesl-1S protein conforms to synaptic tagging (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-05-16
    Description: Late-phase synaptic plasticity depends on the synthesis of new proteins that must function only in the activated synapses. The synaptic tag hypothesis requires input-specific functioning of these proteins after undirected transport. Confirmation of this hypothesis requires specification of a biochemical tagging activity and an example protein that behaves as the hypothesis predicts. We found that in rat neurons, soma-derived Vesl-1S (Homer-1a) protein, a late-phase plasticity-related synaptic protein, prevailed in every dendrite and did not enter spines. N-methyl-d-aspartate receptor activation triggered input-specific spine entry of Vesl-1S proteins, which met many criteria for synaptic tagging. These results suggest that Vesl-1S supports the hypothesis and that the activity-dependent regulation of spine entry functions as a synaptic tag.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Okada, Daisuke -- Ozawa, Fumiko -- Inokuchi, Kaoru -- New York, N.Y. -- Science. 2009 May 15;324(5929):904-9. doi: 10.1126/science.1171498.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Mitsubishi Kagaku Institute of Life Sciences (MITILS), 11 Minamiooya, Machida, Tokyo 194-8511, Japan. dada@mitils.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19443779" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; Carrier Proteins/genetics/*metabolism ; Cells, Cultured ; Dendrites/*metabolism ; Dendritic Spines/*metabolism/ultrastructure ; Hippocampus/cytology/metabolism ; Mice ; *Neuronal Plasticity ; Plasmids ; Protein Transport ; Rats ; Rats, Wistar ; Receptors, N-Methyl-D-Aspartate/metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Synapses/*metabolism ; Synaptic Transmission ; Transfection
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  • 12
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    Complete reconstitution of a highly reducing iterative polyketide synthase (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-11-11
    Description: Highly reducing iterative polyketide synthases are large, multifunctional enzymes that make important metabolites in fungi, such as lovastatin, a cholesterol-lowering drug from Aspergillus terreus. We report efficient expression of the lovastatin nonaketide synthase (LovB) from an engineered strain of Saccharomyces cerevisiae, as well as complete reconstitution of its catalytic function in the presence and absence of cofactors (the reduced form of nicotinamide adenine dinucleotide phosphate and S-adenosylmethionine) and its partner enzyme, the enoyl reductase LovC. Our results demonstrate that LovB retains correct intermediates until completion of synthesis of dihydromonacolin L, but off-loads incorrectly processed compounds as pyrones or hydrolytic products. Experiments replacing LovC with analogous MlcG from compactin biosynthesis demonstrate a gate-keeping function for this partner enzyme. This study represents a key step in the understanding of the functions and structures of this family of enzymes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2875069/" 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/PMC2875069/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ma, Suzanne M -- Li, Jesse W-H -- Choi, Jin W -- Zhou, Hui -- Lee, K K Michael -- Moorthie, Vijayalakshmi A -- Xie, Xinkai -- Kealey, James T -- Da Silva, Nancy A -- Vederas, John C -- Tang, Yi -- 1R01GM085128/GM/NIGMS NIH HHS/ -- 1R21GM077264/GM/NIGMS NIH HHS/ -- R01 GM085128/GM/NIGMS NIH HHS/ -- R01 GM085128-02/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2009 Oct 23;326(5952):589-92. doi: 10.1126/science.1175602.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemical and Biomolecular Engineering, 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/19900898" target="_blank"〉PubMed〈/a〉
    Keywords: Aspergillus/enzymology/genetics/metabolism ; Biocatalysis ; Catalytic Domain ; Cloning, Molecular ; Fungal Proteins/metabolism ; Ketones/metabolism ; Lactones/metabolism ; Lovastatin/biosynthesis ; Malonyl Coenzyme A/metabolism ; Molecular Structure ; Multienzyme Complexes/metabolism ; NAD/metabolism ; Naphthalenes/*metabolism ; Polyketide Synthases/chemistry/genetics/isolation & purification/*metabolism ; Pyrones/metabolism ; Recombinant Proteins/chemistry/isolation & purification/metabolism ; S-Adenosylmethionine/metabolism ; Saccharomyces cerevisiae/enzymology/*genetics ; Substrate Specificity
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  • 13
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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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  • 14
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    Plant science. Anti-rust antitrust (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-03-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kliebenstein, Daniel J -- Rowe, Heather C -- New York, N.Y. -- Science. 2009 Mar 6;323(5919):1301-2. doi: 10.1126/science.1171410.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Plant Sciences and Genetics Graduate Group, University of California, Davis, One Shields Avenue, Davis, CA 95616, USA. kliebenstein@ucdavis.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19265010" target="_blank"〉PubMed〈/a〉
    Keywords: ATP-Binding Cassette Transporters/chemistry/genetics/metabolism ; Ascomycota/genetics/*pathogenicity ; Basidiomycota/genetics/*pathogenicity ; Cloning, Molecular ; Evolution, Molecular ; *Genes, Plant ; Immunity, Innate ; Phosphotransferases/chemistry/genetics/metabolism ; *Plant Diseases/immunology/microbiology ; Plant Proteins/chemistry/genetics/metabolism ; Protein Structure, Tertiary ; *Quantitative Trait Loci ; Selection, Genetic ; Triticum/genetics/*microbiology
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  • 15
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    tasselseed1 is a lipoxygenase affecting jasmonic acid signaling in sex determination of maize (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-01-10
    Description: Sex determination in maize is controlled by a developmental cascade leading to the formation of unisexual florets derived from an initially bisexual floral meristem. Abortion of pistil primordia in staminate florets is controlled by a tasselseed-mediated cell death process. We positionally cloned and characterized the function of the sex determination gene tasselseed1 (ts1). The TS1 protein encodes a plastid-targeted lipoxygenase with predicted 13-lipoxygenase specificity, which suggests that TS1 may be involved in the biosynthesis of the plant hormone jasmonic acid. In the absence of a functional ts1 gene, lipoxygenase activity was missing and endogenous jasmonic acid concentrations were reduced in developing inflorescences. Application of jasmonic acid to developing inflorescences rescued stamen development in mutant ts1 and ts2 inflorescences, revealing a role for jasmonic acid in male flower development in maize.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Acosta, Ivan F -- Laparra, Helene -- Romero, Sandra P -- Schmelz, Eric -- Hamberg, Mats -- Mottinger, John P -- Moreno, Maria A -- Dellaporta, Stephen L -- R01 GM038148/GM/NIGMS NIH HHS/ -- R01 GM038148-19/GM/NIGMS NIH HHS/ -- R01 GM38148/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2009 Jan 9;323(5911):262-5. doi: 10.1126/science.1164645.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular, Cellular and Developmental Biology, Yale University, New Haven, CT 06511, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19131630" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Cloning, Molecular ; Cyclopentanes/*metabolism/pharmacology ; Flowers/growth & development ; Genes, Plant ; Lipoxygenase/chemistry/genetics/*metabolism ; Molecular Sequence Data ; Mutation ; Oxylipins/*metabolism/pharmacology ; Plant Proteins/chemistry/*genetics/*metabolism ; Plastids/enzymology ; *Signal Transduction ; Zea mays/enzymology/*genetics/growth & development/*metabolism
    Print ISSN: 0036-8075
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  • 16
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    A putative ABC transporter confers durable resistance to multiple fungal pathogens in wheat (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-02-21
    Description: Agricultural crops benefit from resistance to pathogens that endures over years and generations of both pest and crop. Durable disease resistance, which may be partial or complete, can be controlled by several genes. Some of the most devastating fungal pathogens in wheat are leaf rust, stripe rust, and powdery mildew. The wheat gene Lr34 has supported resistance to these pathogens for more than 50 years. Lr34 is now shared by wheat cultivars around the world. Here, we show that the LR34 protein resembles adenosine triphosphate-binding cassette transporters of the pleiotropic drug resistance subfamily. Alleles of Lr34 conferring resistance or susceptibility differ by three genetic polymorphisms. The Lr34 gene, which functions in the adult plant, stimulates senescence-like processes in the flag leaf tips and edges.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Krattinger, Simon G -- Lagudah, Evans S -- Spielmeyer, Wolfgang -- Singh, Ravi P -- Huerta-Espino, Julio -- McFadden, Helen -- Bossolini, Eligio -- Selter, Liselotte L -- Keller, Beat -- New York, N.Y. -- Science. 2009 Mar 6;323(5919):1360-3. doi: 10.1126/science.1166453. Epub 2009 Feb 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Plant Biology, University of Zurich, Zollikerstrasse 107, 8008 Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19229000" target="_blank"〉PubMed〈/a〉
    Keywords: ATP-Binding Cassette Transporters/chemistry/*genetics/*metabolism ; Amino Acid Sequence ; Ascomycota/genetics/*pathogenicity ; Basidiomycota/genetics/*pathogenicity ; Chromosome Mapping ; Chromosomes, Plant/genetics ; Cloning, Molecular ; Exons ; Genes, Plant ; Immunity, Innate ; Molecular Sequence Data ; Mutation ; *Plant Diseases/immunology/microbiology ; Plant Leaves/microbiology ; Plant Proteins/chemistry/genetics/metabolism ; Polymorphism, Single Nucleotide ; Quantitative Trait Loci ; Triticum/*genetics/growth & development/immunology/*microbiology
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  • 17
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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
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 18
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    Loss of function of a proline-containing protein confers durable disease resistance in rice (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-08-22
    Description: Blast disease is a devastating fungal disease of rice, one of the world's staple foods. Race-specific resistance to blast disease has usually not been durable. Here, we report the cloning of a previously unknown type of gene that confers non-race-specific resistance and its successful use in breeding. Pi21 encodes a proline-rich protein that includes a putative heavy metal-binding domain and putative protein-protein interaction motifs. Wild-type Pi21 appears to slow the plant's defense responses, which may support optimization of defense mechanisms. Deletions in its proline-rich motif inhibit this slowing. Pi21 is separable from a closely linked gene conferring poor flavor. The resistant pi21 allele, which is found in some strains of japonica rice, could improve blast resistance of rice worldwide.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fukuoka, Shuichi -- Saka, Norikuni -- Koga, Hironori -- Ono, Kazuko -- Shimizu, Takehiko -- Ebana, Kaworu -- Hayashi, Nagao -- Takahashi, Akira -- Hirochika, Hirohiko -- Okuno, Kazutoshi -- Yano, Masahiro -- New York, N.Y. -- Science. 2009 Aug 21;325(5943):998-1001. doi: 10.1126/science.1175550.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉QTL Genomics Research Center, National Institute of Agrobiological Sciences, Kannondai 2-1-2, Tsukuba, Ibaraki 305-8602, Japan. fukusan@affrc.go.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19696351" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Amino Acid Motifs ; Amino Acid Sequence ; Chromosome Mapping ; Cloning, Molecular ; Genes, Plant ; Genetic Variation ; Haplotypes ; Immunity, Innate/*genetics ; Magnaporthe/*pathogenicity ; Molecular Sequence Data ; Oryza/*genetics/metabolism/*microbiology ; Phylogeny ; Plant Diseases/*microbiology ; Plant Proteins/chemistry/*genetics/*physiology ; Proline/analysis ; Protein Interaction Domains and Motifs ; Protein Structure, Tertiary ; Quantitative Trait Loci ; Sequence Deletion ; Transformation, 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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    Human induced pluripotent stem cells free of vector and transgene sequences (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-03-28
    Description: Reprogramming differentiated human cells to induced pluripotent stem (iPS) cells has applications in basic biology, drug development, and transplantation. Human iPS cell derivation previously required vectors that integrate into the genome, which can create mutations and limit the utility of the cells in both research and clinical applications. We describe the derivation of human iPS cells with the use of nonintegrating episomal vectors. After removal of the episome, iPS cells completely free of vector and transgene sequences are derived that are similar to human embryonic stem (ES) cells in proliferative and developmental potential. These results demonstrate that reprogramming human somatic cells does not require genomic integration or the continued presence of exogenous reprogramming factors and removes one obstacle to the clinical application of human iPS cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2758053/" 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/PMC2758053/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yu, Junying -- Hu, Kejin -- Smuga-Otto, Kim -- Tian, Shulan -- Stewart, Ron -- Slukvin, Igor I -- Thomson, James A -- P01 GM081629/GM/NIGMS NIH HHS/ -- P01 GM081629-01A1/GM/NIGMS NIH HHS/ -- P51 RR000167/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2009 May 8;324(5928):797-801. doi: 10.1126/science.1172482. Epub 2009 Mar 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Morgridge Institute for Research, Madison, WI 53707-7365, USA. jyyu2008@gmail.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19325077" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Differentiation ; Cell Shape ; *Cellular Reprogramming ; Clone Cells ; Embryonic Stem Cells/cytology ; Epstein-Barr Virus Nuclear Antigens/genetics ; Fibroblasts ; Gene Expression Profiling ; *Genetic Vectors ; Humans ; *Plasmids ; Pluripotent Stem Cells/*cytology/metabolism/transplantation ; Transcription Factors/genetics ; Transfection ; *Transgenes
    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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  • 20
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    Nuclear hormone receptor regulation of microRNAs controls developmental progression (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    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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    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
    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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    HIN-200 proteins regulate caspase activation in response to foreign cytoplasmic DNA (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    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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    Mutations in FUS, an RNA processing protein, cause familial amyotrophic lateral sclerosis type 6 (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    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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    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
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Comment on "Genetically determined differences in learning from errors" (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-07-16
    Description: Klein et al. (Reports, 7 December 2007, p. 1642) used individuals with a polymorphism adjacent to the dopamine receptor 2 gene as naturally occurring models for reduced brain dopamine receptor density in a probabilistic learning task. We raise the concern that this polymorphism resides in the gene for the kinase ANKK1, where it causes a nonconservative amino acid exchange.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lucht, Michael -- Rosskopf, Dieter -- New York, N.Y. -- Science. 2008 Jul 11;321(5886):200; author reply 200. doi: 10.1126/science.1155372.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Hospital for Psychiatry and Psychotherapy, Haus 30, Ernst-Moritz-Arndt University, Greifswald, Stralsund 18437, Germany. lucht@uni-greifswald.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18621654" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Brain/metabolism ; Cloning, Molecular ; Humans ; *Learning ; *Polymorphism, Genetic ; Protein-Serine-Threonine Kinases/*genetics/physiology ; Proteins/genetics/physiology ; Receptors, Dopamine D2/*genetics/metabolism ; Signal Transduction
    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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    Discovery of a cytokine and its receptor by functional screening of the extracellular proteome (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-05-10
    Description: To understand the system of secreted proteins and receptors involved in cell-cell signaling, we produced a comprehensive set of recombinant secreted proteins and the extracellular domains of transmembrane proteins, which constitute most of the protein components of the extracellular space. Each protein was tested in a suite of assays that measured metabolic, growth, or transcriptional responses in diverse cell types. The pattern of responses across assays was analyzed for the degree of functional selectivity of each protein. One of the highly selective proteins was a previously undescribed ligand, designated interleukin-34 (IL-34), which stimulates monocyte viability but does not affect responses in a wide spectrum of other assays. In a separate functional screen, we used a collection of extracellular domains of transmembrane proteins to discover the receptor for IL-34, which was a known cytokine receptor, colony-stimulating factor 1 (also called macrophage colony-stimulating factor) receptor. This systematic approach is thus useful for discovering new ligands and receptors and assessing the functional selectivity of extracellular regulatory proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lin, Haishan -- Lee, Ernestine -- Hestir, Kevin -- Leo, Cindy -- Huang, Minmei -- Bosch, Elizabeth -- Halenbeck, Robert -- Wu, Ge -- Zhou, Aileen -- Behrens, Dirk -- Hollenbaugh, Diane -- Linnemann, Thomas -- Qin, Minmin -- Wong, Justin -- Chu, Keting -- Doberstein, Stephen K -- Williams, Lewis T -- New York, N.Y. -- Science. 2008 May 9;320(5877):807-11. doi: 10.1126/science.1154370.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Five Prime Therapeutics, Inc., 1650 Owens Street, Suite 200, San Francisco, CA 94158, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18467591" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cloning, Molecular ; DNA, Complementary ; Extracellular Space/*chemistry ; Humans ; Interleukins/*isolation & purification/physiology/secretion ; Membrane Proteins/isolation & purification/physiology ; Protein Structure, Tertiary ; Proteome ; Receptors, Interleukin/*isolation & purification/physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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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
    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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  • 28
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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
    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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  • 29
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    Pyogenic bacterial infections in humans with MyD88 deficiency (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-08-02
    Description: MyD88 is a key downstream adapter for most Toll-like receptors (TLRs) and interleukin-1 receptors (IL-1Rs). MyD88 deficiency in mice leads to susceptibility to a broad range of pathogens in experimental settings of infection. We describe a distinct situation in a natural setting of human infection. Nine children with autosomal recessive MyD88 deficiency suffered from life-threatening, often recurrent pyogenic bacterial infections, including invasive pneumococcal disease. However, these patients were otherwise healthy, with normal resistance to other microbes. Their clinical status improved with age, but not due to any cellular leakiness in MyD88 deficiency. The MyD88-dependent TLRs and IL-1Rs are therefore essential for protective immunity to a small number of pyogenic bacteria, but redundant for host defense to most natural infections.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2688396/" 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/PMC2688396/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉von Bernuth, Horst -- Picard, Capucine -- Jin, Zhongbo -- Pankla, Rungnapa -- Xiao, Hui -- Ku, Cheng-Lung -- Chrabieh, Maya -- Mustapha, Imen Ben -- Ghandil, Pegah -- Camcioglu, Yildiz -- Vasconcelos, Julia -- Sirvent, Nicolas -- Guedes, Margarida -- Vitor, Artur Bonito -- Herrero-Mata, Maria Jose -- Arostegui, Juan Ignacio -- Rodrigo, Carlos -- Alsina, Laia -- Ruiz-Ortiz, Estibaliz -- Juan, Manel -- Fortuny, Claudia -- Yague, Jordi -- Anton, Jordi -- Pascal, Mariona -- Chang, Huey-Hsuan -- Janniere, Lucile -- Rose, Yoann -- Garty, Ben-Zion -- Chapel, Helen -- Issekutz, Andrew -- Marodi, Laszlo -- Rodriguez-Gallego, Carlos -- Banchereau, Jacques -- Abel, Laurent -- Li, Xiaoxia -- Chaussabel, Damien -- Puel, Anne -- Casanova, Jean-Laurent -- U19 AI057234/AI/NIAID NIH HHS/ -- U19 AI057234-02/AI/NIAID NIH HHS/ -- U19 AIO57234-02/PHS HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Aug 1;321(5889):691-6. doi: 10.1126/science.1158298.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Human Genetics of Infectious Diseases, INSERM U550, Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18669862" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Animals ; Bacterial Infections/*genetics/*immunology ; Cell Line, Transformed ; Child ; Child, Preschool ; Cytokines/metabolism ; Disease Susceptibility ; Female ; Gene Deletion ; Humans ; Immunity, Innate ; Male ; Mice ; Mutation, Missense ; Myeloid Differentiation Factor 88/*deficiency/genetics/metabolism ; Pneumococcal Infections/genetics/immunology ; Pseudomonas Infections/genetics/immunology ; Receptors, Interleukin-1/immunology/metabolism ; Signal Transduction ; Staphylococcal Infections/genetics/immunology ; Toll-Like Receptors/immunology/metabolism ; 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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    Genetic mapping in human disease (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-11-08
    Description: Genetic mapping provides a powerful approach to identify genes and biological processes underlying any trait influenced by inheritance, including human diseases. We discuss the intellectual foundations of genetic mapping of Mendelian and complex traits in humans, examine lessons emerging from linkage analysis of Mendelian diseases and genome-wide association studies of common diseases, and discuss questions and challenges that lie ahead.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2694957/" 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/PMC2694957/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Altshuler, David -- Daly, Mark J -- Lander, Eric S -- U54 HG003067/HG/NHGRI NIH HHS/ -- U54 HG003067-03/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2008 Nov 7;322(5903):881-8. doi: 10.1126/science.1156409.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Broad Institute of Harvard and MIT, Cambridge, MA 02142, USA. altshuler@molbio.mgh.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18988837" target="_blank"〉PubMed〈/a〉
    Keywords: *Chromosome Mapping ; Cloning, Molecular ; Disease/*genetics ; Genetic Linkage ; *Genome, Human ; *Genome-Wide Association Study ; Genotype ; Humans ; Linkage Disequilibrium ; Mutation ; Physical Chromosome Mapping ; Polymorphism, Single Nucleotide ; Quantitative Trait, Heritable ; Risk Factors ; Selection, Genetic
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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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
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    The serine protease TMPRSS6 is required to sense iron deficiency (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-05-03
    Description: Hepcidin, a liver-derived protein that restricts enteric iron absorption, is the key regulator of body iron content. Several proteins induce expression of the hepcidin-encoding gene Hamp in response to infection or high levels of iron. However, mechanism(s) of Hamp suppression during iron depletion are poorly understood. We describe mask: a recessive, chemically induced mutant mouse phenotype, characterized by progressive loss of body (but not facial) hair and microcytic anemia. The mask phenotype results from reduced absorption of dietary iron caused by high levels of hepcidin and is due to a splicing defect in the transmembrane serine protease 6 gene Tmprss6. Overexpression of normal TMPRSS6 protein suppresses activation of the Hamp promoter, and the TMPRSS6 cytoplasmic domain mediates Hamp suppression via proximal promoter element(s). TMPRSS6 is an essential component of a pathway that detects iron deficiency and blocks Hamp transcription, permitting enhanced dietary iron absorption.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2430097/" 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/PMC2430097/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Du, Xin -- She, Ellen -- Gelbart, Terri -- Truksa, Jaroslav -- Lee, Pauline -- Xia, Yu -- Khovananth, Kevin -- Mudd, Suzanne -- Mann, Navjiwan -- Moresco, Eva Marie Y -- Beutler, Ernest -- Beutler, Bruce -- AI054523/AI/NIAID NIH HHS/ -- DK53505-09/DK/NIDDK NIH HHS/ -- R01 DK053505-09/DK/NIDDK NIH HHS/ -- U54 AI054523/AI/NIAID NIH HHS/ -- U54 AI054523-019005/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2008 May 23;320(5879):1088-92. doi: 10.1126/science.1157121. Epub 2008 May 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Scripps Research Institute, 10550 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/18451267" target="_blank"〉PubMed〈/a〉
    Keywords: Anemia, Macrocytic/genetics/metabolism ; Animals ; Antimicrobial Cationic Peptides/*genetics/metabolism ; Cell Line, Tumor ; Gene Expression Regulation ; Hepcidins ; Humans ; Iron/blood/*deficiency/metabolism ; Membrane Proteins/chemistry/genetics/*metabolism ; Mice ; Mice, Mutant Strains ; Mice, Transgenic ; Models, Biological ; Mutation ; Phenotype ; Promoter Regions, Genetic ; Protein Structure, Tertiary ; Serine Endopeptidases/chemistry/genetics/*metabolism ; Signal Transduction ; 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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    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
    Print ISSN: 0036-8075
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  • 34
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    Generation of pluripotent stem cells from adult mouse liver and stomach cells (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-02-16
    Description: Induced pluripotent stem (iPS) cells have been generated from mouse and human fibroblasts by the retroviral transduction of four transcription factors. However, the cell origins and molecular mechanisms of iPS cell induction remain elusive. This report describes the generation of iPS cells from adult mouse hepatocytes and gastric epithelial cells. These iPS cell clones appear to be equivalent to embryonic stem cells in gene expression and are competent to generate germline chimeras. Genetic lineage tracings show that liver-derived iPS cells are derived from albumin-expressing cells. No common retroviral integration sites are found among multiple clones. These data suggest that iPS cells are generated by direct reprogramming of lineage-committed somatic cells and that retroviral integration into specific sites is not required.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Aoi, Takashi -- Yae, Kojiro -- Nakagawa, Masato -- Ichisaka, Tomoko -- Okita, Keisuke -- Takahashi, Kazutoshi -- Chiba, Tsutomu -- Yamanaka, Shinya -- New York, N.Y. -- Science. 2008 Aug 1;321(5889):699-702. doi: 10.1126/science.1154884. Epub 2008 Feb 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Stem Cell Biology, Institute for Frontier Medical Sciences, Kyoto University, Kyoto 606-8507, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18276851" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastocyst/cytology ; Cell Differentiation ; Cell Proliferation ; *Cellular Reprogramming ; Chimera ; Clone Cells ; Culture Media ; Embryonic Stem Cells/cytology/metabolism ; Epithelial Cells/*cytology ; Gastric Mucosa/*cytology ; Genetic Vectors ; Hepatocytes/*cytology ; Mice ; Mice, Nude ; Neoplasms/etiology ; Pluripotent Stem Cells/*cytology/metabolism ; Retroviridae/genetics ; Stem Cell Transplantation ; Transcription Factors/genetics ; Transfection ; Virus Integration
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Beta-arrestin-mediated localization of smoothened to the primary cilium (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-05-24
    Description: beta-Arrestins have important roles in the regulation of seven-transmembrane receptors (7TMRs). Smoothened (Smo) is a 7TMR that mediates effects of Hedgehog on developmental processes and whose dysregulation may cause tumorigenesis. beta-Arrestins are required for endocytosis of Smo and signaling to Gli transcription factors. In mammalian cells, Smo-dependent signaling requires translocation to primary cilia. We demonstrated that beta-arrestins mediate the activity-dependent interaction of Smo and the kinesin motor protein Kif3A. This multimeric complex localized to primary cilia and was disrupted in cells transfected with beta-arrestin small interfering RNA. beta-Arrestin 1 or beta-arrestin 2 depletion prevented the localization of Smo to primary cilia and the Smo-dependent activation of Gli. These results suggest roles for beta-arrestins in mediating the intracellular transport of a 7TMR to its obligate subcellular location for signaling.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2587210/" 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/PMC2587210/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kovacs, Jeffrey J -- Whalen, Erin J -- Liu, Renshui -- Xiao, Kunhong -- Kim, Jihee -- Chen, Minyong -- Wang, Jiangbo -- Chen, Wei -- Lefkowitz, Robert J -- 5R01 CA113656-02/CA/NCI NIH HHS/ -- 5T32 AI007217-25/AI/NIAID NIH HHS/ -- HL16037/HL/NHLBI NIH HHS/ -- HL70631/HL/NHLBI NIH HHS/ -- R01 CA113656/CA/NCI NIH HHS/ -- R01 CA113656-02/CA/NCI NIH HHS/ -- R01 CA113656-03/CA/NCI NIH HHS/ -- R01 HL016037/HL/NHLBI NIH HHS/ -- R01 HL016037-35/HL/NHLBI NIH HHS/ -- R01 HL070631/HL/NHLBI NIH HHS/ -- R01 HL070631-04/HL/NHLBI NIH HHS/ -- T32 AI007217/AI/NIAID NIH HHS/ -- T32 AI007217-25/AI/NIAID NIH HHS/ -- T32 AI007217-26/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Jun 27;320(5884):1777-81. doi: 10.1126/science.1157983. Epub 2008 May 22.〈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/18497258" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arrestins/genetics/*metabolism ; Cilia/*metabolism ; Hedgehog Proteins/metabolism ; Kinesin/*metabolism ; Mice ; Microscopy, Confocal ; Molecular Motor Proteins/*metabolism ; NIH 3T3 Cells ; Protein Transport ; RNA Interference ; Receptors, G-Protein-Coupled/*metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Transcription Factors/metabolism ; Transfection
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    Molecular biology. Secret weapon (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-08-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Young, Ryland F 3rd -- New York, N.Y. -- Science. 2008 Aug 15;321(5891):922-3. doi: 10.1126/science.1162910.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Biophysics, Texas A&M University, College Station, TX 77843-2128, USA. ryland@tamu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18703730" target="_blank"〉PubMed〈/a〉
    Keywords: Bacteriophage lambda/*genetics/*growth & development ; Cloning, Molecular ; DNA, Intergenic ; DNA, Viral ; Escherichia coli/*genetics/*virology ; Escherichia coli Proteins/genetics/*metabolism ; Genes, Bacterial ; Genome, Viral ; *Interspersed Repetitive Sequences ; RNA, Bacterial/*genetics/metabolism ; Ribonucleoproteins/metabolism ; Transcription, Genetic
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    Virus attenuation by genome-scale changes in codon pair bias (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-06-28
    Description: As a result of the redundancy of the genetic code, adjacent pairs of amino acids can be encoded by as many as 36 different pairs of synonymous codons. A species-specific "codon pair bias" provides that some synonymous codon pairs are used more or less frequently than statistically predicted. We synthesized de novo large DNA molecules using hundreds of over-or underrepresented synonymous codon pairs to encode the poliovirus capsid protein. Underrepresented codon pairs caused decreased rates of protein translation, and polioviruses containing such amino acid-independent changes were attenuated in mice. Polioviruses thus customized were used to immunize mice and provided protective immunity after challenge. This "death by a thousand cuts" strategy could be generally applicable to attenuating many kinds of viruses.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2754401/" 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/PMC2754401/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Coleman, J Robert -- Papamichail, Dimitris -- Skiena, Steven -- Futcher, Bruce -- Wimmer, Eckard -- Mueller, Steffen -- AI075219/AI/NIAID NIH HHS/ -- AI15122/AI/NIAID NIH HHS/ -- R01 AI075219/AI/NIAID NIH HHS/ -- R01 AI075219-01A1/AI/NIAID NIH HHS/ -- R37 AI015122/AI/NIAID NIH HHS/ -- R37 AI015122-34/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2008 Jun 27;320(5884):1784-7. doi: 10.1126/science.1155761.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics and Microbiology, Stony Brook University, Stony Brook, NY 11794, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18583614" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Animals ; Antibodies, Viral/biosynthesis ; Capsid Proteins/*genetics ; Cloning, Molecular ; *Codon ; Cytopathogenic Effect, Viral ; *Genome, Viral ; HeLa Cells ; Hot Temperature ; Humans ; Mice ; Mice, Transgenic ; Mutation ; Poliomyelitis/immunology/virology ; Poliovirus/*genetics/growth & development/immunology/*pathogenicity ; *Poliovirus Vaccines/genetics/immunology ; Protein Biosynthesis ; Vaccination ; Vaccines, Attenuated/genetics/immunology ; Viral Plaque Assay ; Virulence
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    Midbody targeting of the ESCRT machinery by a noncanonical coiled coil in CEP55 (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-10-25
    Description: The ESCRT (endosomal sorting complex required for transport) machinery is required for the scission of membrane necks in processes including the budding of HIV-1 and cytokinesis. An essential step in cytokinesis is recruitment of the ESCRT-I complex and the ESCRT-associated protein ALIX to the midbody (the structure that tethers two daughter cells) by the protein CEP55. Biochemical experiments show that peptides from ALIX and the ESCRT-I subunit TSG101 compete for binding to the ESCRT and ALIX-binding region (EABR) of CEP55. We solved the crystal structure of EABR bound to an ALIX peptide at a resolution of 2.0 angstroms. The structure shows that EABR forms an aberrant dimeric parallel coiled coil. Bulky and charged residues at the interface of the two central heptad repeats create asymmetry and a single binding site for an ALIX or TSG101 peptide. Both ALIX and ESCRT-I are required for cytokinesis, which suggests that multiple CEP55 dimers are required for function.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2720046/" 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/PMC2720046/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Hyung Ho -- Elia, Natalie -- Ghirlando, Rodolfo -- Lippincott-Schwartz, Jennifer -- Hurley, James H -- Z01 DK036125-01/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2008 Oct 24;322(5901):576-80. doi: 10.1126/science.1162042.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18948538" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Calcium-Binding Proteins/*chemistry/*metabolism ; Cell Cycle Proteins/*chemistry/*metabolism ; Cellular Structures/metabolism ; Crystallography, X-Ray ; *Cytokinesis ; DNA-Binding Proteins/chemistry/metabolism ; Dimerization ; Endosomal Sorting Complexes Required for Transport ; Endosomes/metabolism ; HeLa Cells ; Humans ; Hydrogen Bonding ; Hydrophobic and Hydrophilic Interactions ; Models, Biological ; Models, Molecular ; Nuclear Proteins/*chemistry/*metabolism ; Peptide Fragments/chemistry/metabolism ; Protein Binding ; Protein Conformation ; Transcription Factors/chemistry/metabolism ; Transfection
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    Apobec3 encodes Rfv3, a gene influencing neutralizing antibody control of retrovirus infection (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-09-06
    Description: Recovery from Friend virus 3 (Rfv3) is a single autosomal gene encoding a resistance trait that influences retroviral neutralizing antibody responses and viremia. Despite extensive research for 30 years, the molecular identity of Rfv3 has remained elusive. Here, we demonstrate that Rfv3 is encoded by Apobec3. Apobec3 maps to the same chromosome region as Rfv3 and has broad inhibitory activity against retroviruses, including HIV. Not only did genetic inactivation of Apobec3 convert Rfv3-resistant mice to a susceptible phenotype, but Apobec3 was also found to be naturally disabled by aberrant messenger RNA splicing in Rfv3-susceptible strains. The link between Apobec3 and neutralizing antibody responses highlights an Apobec3-dependent mechanism of host protection that might extend to HIV and other human retroviral infections.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2701658/" 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/PMC2701658/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Santiago, Mario L -- Montano, Mauricio -- Benitez, Robert -- Messer, Ronald J -- Yonemoto, Wes -- Chesebro, Bruce -- Hasenkrug, Kim J -- Greene, Warner C -- R01 AI065329/AI/NIAID NIH HHS/ -- R01 AI065329-04/AI/NIAID NIH HHS/ -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2008 Sep 5;321(5894):1343-6. doi: 10.1126/science.1161121.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gladstone Institute of Virology and Immunology, San Francisco, CA 94158, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18772436" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Viral/*biosynthesis/blood/immunology ; Chromosome Mapping ; Cloning, Molecular ; Cytidine Deaminase/*genetics/metabolism ; Friend murine leukemia virus/*immunology/physiology ; Immunity, Innate ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Molecular Sequence Data ; Neutralization Tests ; Retroviridae Infections/genetics/*immunology/virology ; Tumor Virus Infections/genetics/*immunology/virology ; Viremia
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    Widespread genetic incompatibility in C. elegans maintained by balancing selection (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-01-12
    Description: Natural selection is expected to eliminate genetic incompatibilities from interbreeding populations. We have discovered a globally distributed incompatibility in the primarily selfing species Caenorhabditis elegans that has been maintained despite its negative consequences for fitness. Embryos homozygous for a naturally occurring deletion of the zygotically acting gene zeel-1 arrest if their sperm parent carries an incompatible allele of a second, paternal-effect locus, peel-1. The two interacting loci are tightly linked, with incompatible alleles occurring in linkage disequilibrium in two common haplotypes. These haplotypes exhibit elevated sequence divergence, and population genetic analyses of this region indicate that natural selection is preserving both haplotypes in the population. Our data suggest that long-term maintenance of a balanced polymorphism has permitted the incompatibility to persist despite gene flow across the rest of the genome.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2421010/" 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/PMC2421010/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Seidel, Hannah S -- Rockman, Matthew V -- Kruglyak, Leonid -- GM071508/GM/NIGMS NIH HHS/ -- R01 HG004321/HG/NHGRI NIH HHS/ -- R01 HG004321-01/HG/NHGRI NIH HHS/ -- R37 MH059520/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2008 Feb 1;319(5863):589-94. doi: 10.1126/science.1151107. Epub 2008 Jan 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lewis-Sigler Institute for Integrative Genomics and Department of Ecology and Evolutionary Biology, Princeton University, Princeton, NJ 08544, USA. hseidel@princeton.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18187622" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Animals, Genetically Modified ; Caenorhabditis elegans/embryology/*genetics ; Cloning, Molecular ; Crosses, Genetic ; Disorders of Sex Development ; Embryo, Nonmammalian/physiology ; Embryonic Development ; Gene Flow ; Genes, Helminth ; Genetic Linkage ; Genome, Helminth ; Haplotypes ; Linkage Disequilibrium ; Male ; Molecular Sequence Data ; Penetrance ; Polymorphism, Single Nucleotide ; *Selection, Genetic
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    TMEM16A, a membrane protein associated with calcium-dependent chloride channel activity (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-09-06
    Description: Calcium-dependent chloride channels are required for normal electrolyte and fluid secretion, olfactory perception, and neuronal and smooth muscle excitability. The molecular identity of these membrane proteins is still unclear. Treatment of bronchial epithelial cells with interleukin-4 (IL-4) causes increased calcium-dependent chloride channel activity, presumably by regulating expression of the corresponding genes. We performed a global gene expression analysis to identify membrane proteins that are regulated by IL-4. Transfection of epithelial cells with specific small interfering RNA against each of these proteins shows that TMEM16A, a member of a family of putative plasma membrane proteins with unknown function, is associated with calcium-dependent chloride current, as measured with halide-sensitive fluorescent proteins, short-circuit current, and patch-clamp techniques. Our results indicate that TMEM16A is an intrinsic constituent of the calcium-dependent chloride channel. Identification of a previously unknown family of membrane proteins associated with chloride channel function will improve our understanding of chloride transport physiopathology and allow for the development of pharmacological tools useful for basic research and drug development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Caputo, Antonella -- Caci, Emanuela -- Ferrera, Loretta -- Pedemonte, Nicoletta -- Barsanti, Cristina -- Sondo, Elvira -- Pfeffer, Ulrich -- Ravazzolo, Roberto -- Zegarra-Moran, Olga -- Galietta, Luis J V -- GGP05103/Telethon/Italy -- New York, N.Y. -- Science. 2008 Oct 24;322(5901):590-4. doi: 10.1126/science.1163518. Epub 2008 Sep 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratorio di Genetica Molecolare, Istituto Giannina Gaslini, Genova 16148, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18772398" target="_blank"〉PubMed〈/a〉
    Keywords: Alternative Splicing ; Amino Acid Sequence ; Animals ; Bronchi/cytology/*metabolism ; Calcium/*metabolism ; Cell Line ; Cell Membrane/*metabolism ; Cells, Cultured ; Chloride Channels/*metabolism ; Chlorides/*metabolism ; Epithelial Cells/metabolism ; Humans ; Interleukin-4/metabolism ; Membrane Proteins/chemistry/genetics/*metabolism ; Molecular Sequence Data ; Neoplasm Proteins/chemistry/genetics/*metabolism ; Oligonucleotide Array Sequence Analysis ; Patch-Clamp Techniques ; RNA, Small Interfering ; Respiratory Mucosa/cytology/metabolism ; Transfection
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    Selective blockade of microRNA processing by Lin28 (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-02-23
    Description: MicroRNAs (miRNAs) play critical roles in development, and dysregulation of miRNA expression has been observed in human malignancies. Recent evidence suggests that the processing of several primary miRNA transcripts (pri-miRNAs) is blocked posttranscriptionally in embryonic stem cells, embryonal carcinoma cells, and primary tumors. Here we show that Lin28, a developmentally regulated RNA binding protein, selectively blocks the processing of pri-let-7 miRNAs in embryonic cells. Using in vitro and in vivo studies, we found that Lin28 is necessary and sufficient for blocking Microprocessor-mediated cleavage of pri-let-7 miRNAs. Our results identify Lin28 as a negative regulator of miRNA biogenesis and suggest that Lin28 may play a central role in blocking miRNA-mediated differentiation in stem cells and in certain cancers.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3368499/" 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/PMC3368499/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Viswanathan, Srinivas R -- Daley, George Q -- Gregory, Richard I -- DK70055/DK/NIDDK NIH HHS/ -- DP1 OD000256/OD/NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Apr 4;320(5872):97-100. doi: 10.1126/science.1154040. Epub 2008 Feb 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Stem Cell Program, Children's Hospital Boston, Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Harvard Stem Cell Institute, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18292307" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carcinoma, Embryonal ; Cell Differentiation ; Cell Line, Transformed ; Cell Line, Tumor ; Cellular Reprogramming ; DNA-Binding Proteins/metabolism ; Down-Regulation ; Embryonic Stem Cells/cytology/*metabolism ; Humans ; Mice ; MicroRNAs/*metabolism ; Pluripotent Stem Cells/cytology/metabolism ; Protein Binding ; RNA Interference ; *RNA Processing, Post-Transcriptional ; RNA-Binding Proteins/genetics/*metabolism ; Ribonuclease III/metabolism ; Transfection ; Up-Regulation
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    The spread of Ras activity triggered by activation of a single dendritic spine (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-06-17
    Description: In neurons, individual dendritic spines isolate N-methyl-d-aspartate (NMDA) receptor-mediated calcium ion (Ca2+) accumulations from the dendrite and other spines. However, the extent to which spines compartmentalize signaling events downstream of Ca2+ influx is not known. We combined two-photon fluorescence lifetime imaging with two-photon glutamate uncaging to image the activity of the small guanosine triphosphatase Ras after NMDA receptor activation at individual spines. Induction of long-term potentiation (LTP) triggered robust Ca2+-dependent Ras activation in single spines that decayed in approximately 5 minutes. Ras activity spread over approximately 10 micrometers of dendrite and invaded neighboring spines by diffusion. The spread of Ras-dependent signaling was necessary for the local regulation of the threshold for LTP induction. Thus, Ca2+-dependent synaptic signals can spread to couple multiple synapses on short stretches of dendrite.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2745709/" 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/PMC2745709/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Harvey, Christopher D -- Yasuda, Ryohei -- Zhong, Haining -- Svoboda, Karel -- AS1398/Autism Speaks/ -- R01 MH080047/MH/NIMH NIH HHS/ -- R01 MH080047-01/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Jul 4;321(5885):136-40. doi: 10.1126/science.1159675. Epub 2008 Jun 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Janelia Farm Research Campus, Howard Hughes Medical Institute, Ashburn, VA 20147, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18556515" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; Cell Membrane/metabolism ; Dendritic Spines/*physiology ; Diffusion ; Fluorescence Resonance Energy Transfer ; GTPase-Activating Proteins/metabolism ; Glutamic Acid/metabolism ; Guanine Nucleotide Exchange Factors/metabolism ; Hippocampus/cytology/physiology ; *Long-Term Potentiation ; Pyramidal Cells/*physiology ; Rats ; Receptors, N-Methyl-D-Aspartate/metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Synapses/*physiology ; Transfection ; ras Proteins/*metabolism
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    Field experiments with transformed plants reveal the sense of floral scents (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-08-30
    Description: Plants use many means to attract pollinators, including visual cues and odor. We investigated how nonpigment floral chemistry influences nectar removal, floral visitation, florivory, rates of outcrossing, and fitness through both male and female functions. We blocked expression of biosynthetic genes of the dominant floral attractant [benzyl acetone (Nachal1)] and nectar repellent [nicotine (Napmt1/2)] in all combinations in the native tobacco Nicotiana attenuata and measured their effects on plants in their native habitat. Both repellent and attractant were required to maximize capsule production and seed siring in emasculated flowers and flower visitation by native pollinators, whereas nicotine reduced florivory and nectar robbing.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kessler, Danny -- Gase, Klaus -- Baldwin, Ian T -- New York, N.Y. -- Science. 2008 Aug 29;321(5893):1200-2. doi: 10.1126/science.1160072.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Ecology, Max-Planck-Institute for Chemical Ecology, Hans-Knoll-Strasse 8, DE-07745 Jena, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18755975" target="_blank"〉PubMed〈/a〉
    Keywords: Acetone/*analogs & derivatives/metabolism ; Acyltransferases/genetics ; Animals ; Base Sequence ; Birds/*physiology ; Cloning, Molecular ; Flowers/chemistry/*physiology ; Methyltransferases/genetics ; Molecular Sequence Data ; Nicotine/*metabolism ; *Odors ; Plants, Genetically Modified ; Pollen/physiology ; RNA Interference ; Reproduction ; Seeds ; Tobacco/genetics/*physiology ; Transformation, Genetic
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    FBXW7 targets mTOR for degradation and cooperates with PTEN in tumor suppression (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-09-13
    Description: The enzyme mTOR (mammalian target of rapamycin) is a major target for therapeutic intervention to treat many human diseases, including cancer, but very little is known about the processes that control levels of mTOR protein. Here, we show that mTOR is targeted for ubiquitination and consequent degradation by binding to the tumor suppressor protein FBXW7. Human breast cancer cell lines and primary tumors showed a reciprocal relation between loss of FBXW7 and deletion or mutation of PTEN (phosphatase and tensin homolog), which also activates mTOR. Tumor cell lines harboring deletions or mutations in FBXW7 are particularly sensitive to rapamycin treatment, which suggests that loss of FBXW7 may be a biomarker for human cancers susceptible to treatment with inhibitors of the mTOR pathway.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2849753/" 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/PMC2849753/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mao, Jian-Hua -- Kim, Il-Jin -- Wu, Di -- Climent, Joan -- Kang, Hio Chung -- DelRosario, Reyno -- Balmain, Allan -- R01 CA116481/CA/NCI NIH HHS/ -- U01 CA084244/CA/NCI NIH HHS/ -- U01 CA084244-08/CA/NCI NIH HHS/ -- U01 CA084244-09/CA/NCI NIH HHS/ -- U01 CA084244-10/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2008 Sep 12;321(5895):1499-502. doi: 10.1126/science.1162981.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Research Institute, University of California at San Francisco, 2340 Sutter Street, San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18787170" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Breast Neoplasms/drug therapy/genetics/*metabolism/pathology ; Cell Cycle Proteins/genetics/*metabolism ; Cell Line ; Cell Line, Tumor ; F-Box Proteins/genetics/*metabolism ; Gene Deletion ; Gene Dosage ; Gene Silencing ; Genes, Tumor Suppressor ; Humans ; Mice ; Mice, Nude ; Mutation ; Neoplasm Transplantation ; PTEN Phosphohydrolase/genetics/*metabolism ; Phosphorylation ; Protein Binding ; Protein Kinases/*metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Signal Transduction ; Sirolimus/pharmacology/therapeutic use ; TOR Serine-Threonine Kinases ; Transfection ; Tumor Suppressor Proteins/*metabolism ; Ubiquitin-Protein Ligases/genetics/*metabolism ; Ubiquitination
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    Surface mobility of postsynaptic AMPARs tunes synaptic transmission (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-04-12
    Description: AMPA glutamate receptors (AMPARs) mediate fast excitatory synaptic transmission. Upon fast consecutive synaptic stimulation, transmission can be depressed. Recuperation from fast synaptic depression has been attributed solely to recovery of transmitter release and/or AMPAR desensitization. We show that AMPAR lateral diffusion, observed in both intact hippocampi and cultured neurons, allows fast exchange of desensitized receptors with naive functional ones within or near the postsynaptic density. Recovery from depression in the tens of millisecond time range can be explained in part by this fast receptor exchange. Preventing AMPAR surface movements through cross-linking, endogenous clustering, or calcium rise all slow recovery from depression. Physiological regulation of postsynaptic receptor mobility affects the fidelity of synaptic transmission by shaping the frequency dependence of synaptic responses.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2715948/" 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/PMC2715948/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heine, Martin -- Groc, Laurent -- Frischknecht, Renato -- Beique, Jean-Claude -- Lounis, Brahim -- Rumbaugh, Gavin -- Huganir, Richard L -- Cognet, Laurent -- Choquet, Daniel -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Apr 11;320(5873):201-5. doi: 10.1126/science.1152089.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉CNRS, UMR 5091, Universite Bordeaux, Bordeaux, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18403705" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Calcium/metabolism ; Cells, Cultured ; Diffusion ; Excitatory Amino Acid Antagonists/pharmacology ; Excitatory Postsynaptic Potentials ; Fluorescence Recovery After Photobleaching ; Glutamic Acid/metabolism ; Hippocampus/cytology/*physiology ; Kynurenic Acid/pharmacology ; Neuronal Plasticity ; Neurons/physiology ; Patch-Clamp Techniques ; Rats ; Rats, Sprague-Dawley ; Receptors, AMPA/*metabolism ; Recombinant Fusion Proteins/metabolism ; Synapses/drug effects/*physiology ; *Synaptic Transmission/drug effects ; Transfection
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    An alternative menaquinone biosynthetic pathway operating in microorganisms (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-09-20
    Description: In microorganisms, menaquinone is an obligatory component of the electron-transfer pathway. It is derived from chorismate by seven enzymes in Escherichia coli. However, a bioinformatic analysis of whole genome sequences has suggested that some microorganisms, including pathogenic species such as Helicobacter pylori and Campylobacter jejuni, do not have orthologs of the men genes, even though they synthesize menaquinone. We deduced the outline of this alternative pathway in a nonpathogenic strain of Streptomyces by bioinformatic screening, gene knockouts, shotgun cloning with isolated mutants, and in vitro studies with recombinant enzymes. As humans and commensal intestinal bacteria, including lactobacilli, lack this pathway, it represents an attractive target for the development of chemotherapeutics.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hiratsuka, Tomoshige -- Furihata, Kazuo -- Ishikawa, Jun -- Yamashita, Haruyuki -- Itoh, Nobuya -- Seto, Haruo -- Dairi, Tohru -- New York, N.Y. -- Science. 2008 Sep 19;321(5896):1670-3. doi: 10.1126/science.1160446.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biotechnology Research Center, Toyama Prefectural University, Toyama 939-0398, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18801996" target="_blank"〉PubMed〈/a〉
    Keywords: Archaea/enzymology/genetics/metabolism ; Bacteria/enzymology/genetics/*metabolism ; Biosynthetic Pathways/genetics ; Campylobacter jejuni/enzymology/genetics/metabolism ; Chorismic Acid/metabolism ; Cloning, Molecular ; Computational Biology ; Enzymes/genetics/metabolism ; *Genes, Bacterial ; Helicobacter pylori/enzymology/genetics/metabolism ; Molecular Sequence Data ; Mutagenesis ; Nucleosides/isolation & purification/*metabolism ; Recombinant Proteins/metabolism ; Streptomyces coelicolor/enzymology/genetics/*metabolism ; Thermus thermophilus/enzymology/genetics/metabolism ; Vitamin K 2/*metabolism
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    RNA exosome depletion reveals transcription upstream of active human promoters (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-12-06
    Description: Studies have shown that the bulk of eukaryotic genomes is transcribed. Transcriptome maps are frequently updated, but low-abundant transcripts have probably gone unnoticed. To eliminate RNA degradation, we depleted the exonucleolytic RNA exosome from human cells and then subjected the RNA to tiling microarray analysis. This revealed a class of short, polyadenylated and highly unstable RNAs. These promoter upstream transcripts (PROMPTs) are produced approximately 0.5 to 2.5 kilobases upstream of active transcription start sites. PROMPT transcription occurs in both sense and antisense directions with respect to the downstream gene. In addition, it requires the presence of the gene promoter and is positively correlated with gene activity. We propose that PROMPT transcription is a common characteristic of RNA polymerase II (RNAPII) transcribed genes with a possible regulatory potential.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Preker, Pascal -- Nielsen, Jesper -- Kammler, Susanne -- Lykke-Andersen, Soren -- Christensen, Marianne S -- Mapendano, Christophe K -- Schierup, Mikkel H -- Jensen, Torben Heick -- New York, N.Y. -- Science. 2008 Dec 19;322(5909):1851-4. doi: 10.1126/science.1164096. Epub 2008 Dec 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for mRNP Biogenesis and Metabolism, Department of Molecular Biology, C. F. Mollers Alle, Building 1130, Aarhus University, Denmark.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19056938" target="_blank"〉PubMed〈/a〉
    Keywords: DNA Methylation ; Exosomes/*metabolism ; HeLa Cells ; Humans ; Oligonucleotide Array Sequence Analysis ; *Promoter Regions, Genetic ; RNA Polymerase II/metabolism ; RNA Stability ; RNA, Antisense/*genetics/*metabolism ; RNA, Messenger/*genetics/*metabolism ; Transcription Factors/metabolism ; Transcription Initiation Site ; *Transcription, Genetic ; Transfection
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    Changes in regulation of a transcription factor lead to autogamy in cultivated tomatoes (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-10-27
    Description: We report the cloning of Style2.1, the major quantitative trait locus responsible for a key floral attribute (style length) associated with the evolution of self-pollination in cultivated tomatoes. The gene encodes a putative transcription factor that regulates cell elongation in developing styles. The transition from cross-pollination to self-pollination was accompanied, not by a change in the STYLE2.1 protein, but rather by a mutation in the Style2.1 promoter that results in a down-regulation of Style2.1 expression during flower development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Kai-Yi -- Cong, Bin -- Wing, Rod -- Vrebalov, Julia -- Tanksley, Steven D -- New York, N.Y. -- Science. 2007 Oct 26;318(5850):643-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Plant Breeding 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/17962563" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Biological Evolution ; Chromosome Mapping ; Cloning, Molecular ; Crosses, Genetic ; Down-Regulation ; Flowers/*anatomy & histology/genetics/growth & development ; Genes, Plant ; Genotype ; Helix-Loop-Helix Motifs ; Lycopersicon esculentum/anatomy & histology/*genetics/*physiology ; Molecular Sequence Data ; Plant Proteins/chemistry/*genetics/metabolism ; Pollen/physiology ; Promoter Regions, Genetic ; Quantitative Trait Loci ; Reproduction ; Sequence Deletion ; Transcription Factors/chemistry/*genetics/metabolism ; Transformation, Genetic
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    The slit receptor EVA-1 coactivates a SAX-3/Robo mediated guidance signal in C. elegans (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-09-29
    Description: The SAX-3/roundabout (Robo) receptor has SLT-1/Slit-dependent and -independent functions in guiding cell and axon migrations. We identified enhancer of ventral-axon guidance defects of unc-40 mutants (EVA-1) as a Caenorhabditis elegans transmembrane receptor for SLT-1. EVA-1 has two predicted galactose-binding ectodomains, acts cell-autonomously for SLT-1/Slit-dependent axon migration functions of SAX-3/Robo, binds to SLT-1 and SAX-3, colocalizes with SAX-3 on cells, and provides cell specificity to the activation of SAX-3 signaling by SLT-1. Double mutants of eva-1 or slt-1 with sax-3 mutations suggest that SAX-3 can (when slt-1 or eva-1 function is reduced) inhibit a parallel-acting guidance mechanism, which involves UNC-40/deleted in colorectal cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fujisawa, Kazuko -- Wrana, Jeffrey L -- Culotti, Joseph G -- NS41397/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2007 Sep 28;317(5846):1934-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Samuel Lunenfeld Research Institute of Mount Sinai Hospital, 600 University Avenue, Toronto, Ontario M5G 1X5, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17901337" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Animals, Genetically Modified ; Axons/*physiology ; Caenorhabditis elegans/cytology/genetics/growth & development/*physiology ; Caenorhabditis elegans Proteins/*chemistry/genetics/*metabolism ; Carrier Proteins/chemistry/genetics/*metabolism ; Cell Line ; Cell Movement ; Cloning, Molecular ; Humans ; Molecular Sequence Data ; Mutation ; Nerve Tissue Proteins/*metabolism ; Nervous System/growth & development/metabolism ; Neurons/physiology ; Protein Structure, Tertiary ; Receptors, Immunologic/*metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction
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    Genome-wide experimental determination of barriers to horizontal gene transfer (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-10-20
    Description: Horizontal gene transfer, in which genetic material is transferred from the genome of one organism to that of another, has been investigated in microbial species mainly through computational sequence analyses. To address the lack of experimental data, we studied the attempted movement of 246,045 genes from 79 prokaryotic genomes into Escherichia coli and identified genes that consistently fail to transfer. We studied the mechanisms underlying transfer inhibition by placing coding regions from different species under the control of inducible promoters. Our data suggest that toxicity to the host inhibited transfer regardless of the species of origin and that increased gene dosage and associated increased expression may be a predominant cause for transfer failure. Although these experimental studies examined transfer solely into E. coli, a computational analysis of gene-transfer rates across available bacterial and archaeal genomes supports that the barriers observed in our study are general across the tree of life.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sorek, Rotem -- Zhu, Yiwen -- Creevey, Christopher J -- Francino, M Pilar -- Bork, Peer -- Rubin, Edward M -- New York, N.Y. -- Science. 2007 Nov 30;318(5855):1449-52. Epub 2007 Oct 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Energy, Joint Genome Institute, 2800 Mitchell Drive, Walnut Creek, CA 94598, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17947550" target="_blank"〉PubMed〈/a〉
    Keywords: Archaea/classification/genetics ; Bacteria/classification/genetics ; Cloning, Molecular ; Computational Biology ; Escherichia coli/*genetics ; Gene Dosage ; *Gene Transfer, Horizontal ; *Genes, Archaeal ; *Genes, Bacterial ; Genetic Speciation ; Genome, Archaeal ; Genome, Bacterial ; Phylogeny
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    A membrane receptor for retinol binding protein mediates cellular uptake of vitamin A (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-01-27
    Description: Vitamin A has diverse biological functions. It is transported in the blood as a complex with retinol binding protein (RBP), but the molecular mechanism by which vitamin A is absorbed by cells from the vitamin A-RBP complex is not clearly understood. We identified in bovine retinal pigment epithelium cells STRA6, a multitransmembrane domain protein, as a specific membrane receptor for RBP. STRA6 binds to RBP with high affinity and has robust vitamin A uptake activity from the vitamin A-RBP complex. It is widely expressed in embryonic development and in adult organ systems. The RBP receptor represents a major physiological mediator of cellular vitamin A uptake.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kawaguchi, Riki -- Yu, Jiamei -- Honda, Jane -- Hu, Jane -- Whitelegge, Julian -- Ping, Peipei -- Wiita, Patrick -- Bok, Dean -- Sun, Hui -- 5T32EY07026/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 2007 Feb 9;315(5813):820-5. Epub 2007 Jan 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, David Geffen School of Medicine at UCLA, 650 Charles E. Young Drive South, Los Angeles, CA 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17255476" target="_blank"〉PubMed〈/a〉
    Keywords: Acyltransferases/metabolism ; Amino Acid Sequence ; Animals ; Blood-Retinal Barrier ; COS Cells ; Cattle ; Cell Line ; Cell Line, Tumor ; Cell Membrane/metabolism ; Cercopithecus aethiops ; Embryonic Development ; Endocytosis ; Humans ; Molecular Sequence Data ; Mutation, Missense ; Pigment Epithelium of Eye/*metabolism ; Placenta/metabolism ; Receptors, Cell Surface/*metabolism ; Retinal Vessels/metabolism ; Retinol-Binding Proteins/*metabolism ; Spleen/metabolism ; Transfection ; Vitamin A/*metabolism
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    Medicine. The yin-yang of sirtuins (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-07-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dillin, Andrew -- Kelly, Jeffery W -- New York, N.Y. -- Science. 2007 Jul 27;317(5837):461-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA. dillin@salk.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17656709" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Animals ; Autophagy ; Cell Line, Tumor ; Disease Models, Animal ; Drosophila melanogaster ; Humans ; Neurodegenerative Diseases/physiopathology ; Parkinson Disease/drug therapy/pathology/*physiopathology ; RNA Interference ; Rats ; Signal Transduction ; Sirtuin 1 ; Sirtuin 2 ; Sirtuins/*antagonists & inhibitors/genetics/metabolism/*physiology ; Transfection ; alpha-Synuclein/metabolism
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    Cysteine redox sensor in PKGIa enables oxidant-induced activation (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-08-25
    Description: Changes in the concentration of oxidants in cells can regulate biochemical signaling mechanisms that control cell function. We have found that guanosine 3',5'-monophosphate (cGMP)-dependent protein kinase (PKG) functions directly as a redox sensor. The Ialpha isoform, PKGIalpha, formed an interprotein disulfide linking its two subunits in cells exposed to exogenous hydrogen peroxide. This oxidation directly activated the kinase in vitro, and in rat cells and tissues. The affinity of the kinase for substrates it phosphorylates was enhanced by disulfide formation. This oxidation-induced activation represents an alternate mechanism for regulation along with the classical activation involving nitric oxide and cGMP. This mechanism underlies cGMP-independent vasorelaxation in response to oxidants in the cardiovascular system and provides a molecular explantion for how hydrogen peroxide can operate as an endothelium-derived hyperpolarizing factor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Burgoyne, Joseph R -- Madhani, Melanie -- Cuello, Friederike -- Charles, Rebecca L -- Brennan, Jonathan P -- Schroder, Ewald -- Browning, Darren D -- Eaton, Philip -- G0700320/Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2007 Sep 7;317(5843):1393-7. Epub 2007 Aug 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cardiology, Cardiovascular Division, King's College London, Rayne Institute, St. Thomas' Hospital, London SE1 7EH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17717153" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aorta ; Cell Line ; Cyclic GMP/metabolism ; Cyclic GMP-Dependent Protein Kinase Type I ; Cyclic GMP-Dependent Protein Kinases/genetics/*metabolism ; Cysteine/*metabolism ; Disulfides/metabolism ; Enzyme Activation ; Humans ; Hydrogen Peroxide/metabolism ; Male ; Nitric Oxide/metabolism ; Oxidants/*metabolism ; Oxidation-Reduction ; Oxidative Stress ; Rats ; Rats, Wistar ; Signal Transduction ; Tissue Culture Techniques ; Transfection ; Vasodilation/physiology
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    SCFFbxl3 controls the oscillation of the circadian clock by directing the degradation of cryptochrome proteins (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-04-28
    Description: One component of the circadian clock in mammals is the Clock-Bmal1 heterodimeric transcription factor. Among its downstream targets, two genes, Cry1 and Cry2, encode inhibitors of the Clock-Bmal1 complex that establish a negative-feedback loop. We found that both Cry1 and Cry2 proteins are ubiquitinated and degraded via the SCF(Fbxl3) ubiquitin ligase complex. This regulation by SCF(Fbxl3) is a prerequisite for the efficient and timely reactivation of Clock-Bmal1 and the consequent expression of Per1 and Per2, two regulators of the circadian clock that display tumor suppressor activity. Silencing of Fbxl3 produced no effect in Cry1-/-;Cry2-/- cells, which shows that Fbxl3 controls clock oscillations by mediating the degradation of CRY proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Busino, Luca -- Bassermann, Florian -- Maiolica, Alessio -- Lee, Choogon -- Nolan, Patrick M -- Godinho, Sofia I H -- Draetta, Giulio F -- Pagano, Michele -- MC_U142684172/Medical Research Council/United Kingdom -- MC_U142684173/Medical Research Council/United Kingdom -- MC_U142684175/Medical Research Council/United Kingdom -- R01-GM57587/GM/NIGMS NIH HHS/ -- R21-CA125173/CA/NCI NIH HHS/ -- R37-CA76584/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2007 May 11;316(5826):900-4. Epub 2007 Apr 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, NYU Cancer Institute, New York University School of Medicine, 550 First Avenue, MSB 599, New York, NY 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17463251" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors ; Animals ; Basic Helix-Loop-Helix Transcription Factors/metabolism ; CLOCK Proteins ; Cell Cycle Proteins/genetics/metabolism ; Cells, Cultured ; *Circadian Rhythm/genetics ; Cryptochromes ; F-Box Proteins/genetics/*metabolism ; Flavoproteins/genetics/*metabolism ; HeLa Cells ; Humans ; Mice ; NIH 3T3 Cells ; Nuclear Proteins/genetics/metabolism ; Period Circadian Proteins ; Promoter Regions, Genetic ; RNA Interference ; SKP Cullin F-Box Protein Ligases/*metabolism ; Trans-Activators/metabolism ; Transcription Factors/genetics/metabolism ; Transfection ; Ubiquitin/metabolism
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    Structural and regulatory genes required to make the gas dimethyl sulfide in bacteria (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-02-03
    Description: Dimethyl sulfide (DMS) is a key compound in global sulfur and carbon cycles. DMS oxidation products cause cloud nucleation and may affect weather and climate. DMS is generated largely by bacterial catabolism of dimethylsulfoniopropionate (DMSP), a secondary metabolite made by marine algae. We demonstrate that the bacterial gene dddD is required for this process and that its transcription is induced by the DMSP substrate. Cloned dddD from the marine bacterium Marinomonas and from two bacterial strains that associate with higher plants, the N(2)-fixing symbiont Rhizobium NGR234 and the root-colonizing Burkholderia cepacia AMMD, conferred to Escherichia coli the ability to make DMS from DMSP. The inferred enzymatic mechanism for DMS liberation involves an initial step in which DMSP is modified by addition of acyl coenzyme A, rather than the immediate release of DMS by a DMSP lyase, the previously suggested mechanism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Todd, Jonathan D -- Rogers, Rachel -- Li, You Guo -- Wexler, Margaret -- Bond, Philip L -- Sun, Lei -- Curson, Andrew R J -- Malin, Gill -- Steinke, Michael -- Johnston, Andrew W B -- New York, N.Y. -- Science. 2007 Feb 2;315(5812):666-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Biological Sciences, University of East Anglia, Norwich Research Park, Norwich NR4 7TJ, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17272727" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Bacterial Proteins/genetics/*metabolism ; Burkholderia cepacia/genetics/growth & development/metabolism ; Cloning, Molecular ; Coenzyme A-Transferases/genetics/*metabolism ; DNA Transposable Elements ; Escherichia coli/genetics/metabolism ; *Genes, Bacterial ; *Genes, Regulator ; Marinomonas/*genetics/growth & development/*metabolism ; Molecular Sequence Data ; Operon ; Oxidation-Reduction ; Phenotype ; Poaceae/microbiology ; Promoter Regions, Genetic ; Rhizobium/genetics/growth & development/metabolism ; Sulfides/*metabolism ; Sulfonium Compounds/metabolism ; Transformation, Bacterial
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    Switching from repression to activation: microRNAs can up-regulate translation (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-12-01
    Description: AU-rich elements (AREs) and microRNA target sites are conserved sequences in messenger RNA (mRNA) 3' untranslated regions (3'UTRs) that control gene expression posttranscriptionally. Upon cell cycle arrest, the ARE in tumor necrosis factor-alpha (TNFalpha) mRNA is transformed into a translation activation signal, recruiting Argonaute (AGO) and fragile X mental retardation-related protein 1 (FXR1), factors associated with micro-ribonucleoproteins (microRNPs). We show that human microRNA miR369-3 directs association of these proteins with the AREs to activate translation. Furthermore, we document that two well-studied microRNAs-Let-7 and the synthetic microRNA miRcxcr4-likewise induce translation up-regulation of target mRNAs on cell cycle arrest, yet they repress translation in proliferating cells. Thus, activation is a common function of microRNPs on cell cycle arrest. We propose that translation regulation by microRNPs oscillates between repression and activation during the cell cycle.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vasudevan, Shobha -- Tong, Yingchun -- Steitz, Joan A -- New York, N.Y. -- Science. 2007 Dec 21;318(5858):1931-4. Epub 2007 Nov 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biophysics and Biochemistry, Howard Hughes Medical Institute, Yale University School of Medicine, Boyer Center for Molecular Medicine, 295 Congress Avenue, New Haven, CT 06536, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18048652" target="_blank"〉PubMed〈/a〉
    Keywords: *3' Untranslated Regions ; Argonaute Proteins ; Base Pairing ; Cell Cycle ; Cell Line ; Cell Proliferation ; Computational Biology ; Eukaryotic Initiation Factor-2/genetics/metabolism ; *Gene Expression Regulation ; HMGA2 Protein/genetics ; HeLa Cells ; Humans ; Interphase ; MicroRNAs/*metabolism ; *Protein Biosynthesis ; RNA, Messenger/genetics/metabolism ; RNA-Binding Proteins/genetics/metabolism ; Ribonucleoproteins/metabolism ; Transfection ; Tumor Necrosis Factor-alpha/biosynthesis/*genetics ; *Up-Regulation
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    Disrupting the pairing between let-7 and Hmga2 enhances oncogenic transformation (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-02-27
    Description: MicroRNAs (miRNAs) are approximately 22-nucleotide RNAs that can pair to sites within messenger RNAs to specify posttranscriptional repression of these messages. Aberrant miRNA expression can contribute to tumorigenesis, but which of the many miRNA-target relationships are relevant to this process has been unclear. Here, we report that chromosomal translocations previously associated with human tumors disrupt repression of High Mobility Group A2 (Hmga2) by let-7 miRNA. This disrupted repression promotes anchorage-independent growth, a characteristic of oncogenic transformation. Thus, losing miRNA-directed repression of an oncogene provides a mechanism for tumorigenesis, and disrupting a single miRNA-target interaction can produce an observable phenotype in mammalian cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2556962/" 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/PMC2556962/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mayr, Christine -- Hemann, Michael T -- Bartel, David P -- R01 DK068348/DK/NIDDK NIH HHS/ -- R01 DK068348-01/DK/NIDDK NIH HHS/ -- R01 DK068348-02/DK/NIDDK NIH HHS/ -- R01 DK068348-03/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2007 Mar 16;315(5818):1576-9. Epub 2007 Feb 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Biology, Massachusetts Institute of Technology, and Whitehead Institute for Biomedical Research, 9 Cambridge Center, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17322030" target="_blank"〉PubMed〈/a〉
    Keywords: 3' Untranslated Regions ; Animals ; Cell Line, Tumor ; Cell Proliferation ; Cell Transformation, Neoplastic/*genetics ; Gene Expression Regulation ; Genes, Tumor Suppressor ; HMGA2 Protein/*genetics ; HeLa Cells ; Humans ; Mice ; Mice, Nude ; MicroRNAs/*genetics ; NIH 3T3 Cells ; Neoplasms, Experimental/etiology/genetics ; Oncogenes ; Transfection ; *Translocation, Genetic
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    Requirement of inositol pyrophosphates for full exocytotic capacity in pancreatic beta cells (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-11-24
    Description: Inositol pyrophosphates are recognized components of cellular processes that regulate vesicle trafficking, telomere length, and apoptosis. We observed that pancreatic beta cells maintain high basal concentrations of the pyrophosphate diphosphoinositol pentakisphosphate (InsP7 or IP7). Inositol hexakisphosphate kinases (IP6Ks) that can generate IP7 were overexpressed. This overexpression stimulated exocytosis of insulin-containing granules from the readily releasable pool. Exogenously applied IP7 dose-dependently enhanced exocytosis at physiological concentrations. We determined that IP6K1 and IP6K2 were present in beta cells. RNA silencing of IP6K1, but not IP6K2, inhibited exocytosis, which suggests that IP6K1 is the critical endogenous kinase. Maintenance of high concentrations of IP7 in the pancreatic beta cell may enhance the immediate exocytotic capacity and consequently allow rapid adjustment of insulin secretion in response to increased demand.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Illies, Christopher -- Gromada, Jesper -- Fiume, Roberta -- Leibiger, Barbara -- Yu, Jia -- Juhl, Kirstine -- Yang, Shao-Nian -- Barma, Deb K -- Falck, John R -- Saiardi, Adolfo -- Barker, Christopher J -- Berggren, Per-Olof -- GM31278/GM/NIGMS NIH HHS/ -- MC_U122680443/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2007 Nov 23;318(5854):1299-302.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rolf Luft Research Center for Diabetes and Endocrinology, Karolinska Institutet, SE-171 76, Stockholm, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18033884" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cricetinae ; Electric Capacitance ; *Exocytosis ; Inositol Phosphates/*metabolism ; Insulin/*secretion ; Insulin-Secreting Cells/*metabolism/secretion ; Islets of Langerhans/metabolism ; Mice ; Patch-Clamp Techniques ; Phosphotransferases (Phosphate Group Acceptor)/genetics/metabolism ; Phytic Acid/metabolism ; RNA Interference ; Rats ; Secretory Vesicles/*metabolism ; Transfection
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    Wnt induces LRP6 signalosomes and promotes dishevelled-dependent LRP6 phosphorylation (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-06-16
    Description: Multiple signaling pathways, including Wnt signaling, participate in animal development, stem cell biology, and human cancer. Although many components of the Wnt pathway have been identified, unresolved questions remain as to the mechanism by which Wnt binding to its receptors Frizzled and Low-density lipoprotein receptor-related protein 6 (LRP6) triggers downstream signaling events. With live imaging of vertebrate cells, we show that Wnt treatment quickly induces plasma membrane-associated LRP6 aggregates. LRP6 aggregates are phosphorylated and can be detergent-solubilized as ribosome-sized multiprotein complexes. Phospho-LRP6 aggregates contain Wnt-pathway components but no common vesicular traffic markers except caveolin. The scaffold protein Dishevelled (Dvl) is required for LRP6 phosphorylation and aggregation. We propose that Wnts induce coclustering of receptors and Dvl in LRP6-signalosomes, which in turn triggers LRP6 phosphorylation to promote Axin recruitment and beta-catenin stabilization.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bilic, Josipa -- Huang, Ya-Lin -- Davidson, Gary -- Zimmermann, Timo -- Cruciat, Cristina-Maria -- Bienz, Mariann -- Niehrs, Christof -- MC_U105192713/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2007 Jun 15;316(5831):1619-22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular Embryology, Deutsches Krebsforschungszentrum, Im Neuenheimer Feld 280, D-69120 Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17569865" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/*metabolism ; Animals ; Axin Protein ; Cell Line ; Cell Line, Tumor ; Cell Membrane/metabolism ; Centrifugation, Density Gradient ; Cytoplasm/metabolism ; Drosophila ; Glycogen Synthase Kinase 3/analysis/metabolism ; HeLa Cells ; Humans ; LDL-Receptor Related Proteins/analysis/genetics/*metabolism ; Low Density Lipoprotein Receptor-Related Protein-6 ; Mice ; Models, Biological ; Phosphoproteins/*metabolism ; Phosphorylation ; Repressor Proteins/analysis/metabolism ; *Signal Transduction ; Transfection ; Wnt Proteins/*metabolism ; Wnt3 Protein ; beta Catenin/metabolism
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    Patched1 regulates hedgehog signaling at the primary cilium (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-07-21
    Description: Primary cilia are essential for transduction of the Hedgehog (Hh) signal in mammals. We investigated the role of primary cilia in regulation of Patched1 (Ptc1), the receptor for Sonic Hedgehog (Shh). Ptc1 localized to cilia and inhibited Smoothened (Smo) by preventing its accumulation within cilia. When Shh bound to Ptc1, Ptc1 left the cilia, leading to accumulation of Smo and activation of signaling. Thus, primary cilia sense Shh and transduce signals that play critical roles in development, carcinogenesis, and stem cell function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rohatgi, Rajat -- Milenkovic, Ljiljana -- Scott, Matthew P -- R01 CA088060/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2007 Jul 20;317(5836):372-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Developmental Biology, Genetics, and Bioengineering and Howard Hughes Medical Institute, 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/17641202" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Membrane/metabolism ; Cells, Cultured ; Cilia/*metabolism ; Cyclohexylamines/pharmacology ; Embryo, Mammalian/metabolism ; Hedgehog Proteins/agonists/*metabolism ; Hydroxycholesterols/pharmacology ; Mesoderm/metabolism ; Mice ; NIH 3T3 Cells ; Protein Binding ; Receptors, Cell Surface/genetics/*metabolism ; Receptors, G-Protein-Coupled/metabolism ; *Signal Transduction ; Thiophenes/pharmacology ; Transcription, Genetic ; Transfection
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    5'-triphosphate-dependent activation of PKR by RNAs with short stem-loops (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-12-01
    Description: Molecular patterns in pathogenic RNAs can be recognized by the innate immune system, and a component of this response is the interferon-induced enzyme RNA-activated protein kinase (PKR). The major activators of PKR have been proposed to be long double-stranded RNAs. We report that RNAs with very limited secondary structures activate PKR in a 5'-triphosphate-dependent fashion in vitro and in vivo. Activation of PKR by 5'-triphosphate RNA is independent of RIG-I and is enhanced by treatment with type 1 interferon (IFN-alpha). Surveillance of molecular features at the 5' end of transcripts by PKR presents a means of allowing pathogenic RNA to be distinguished from self-RNA. The evidence presented here suggests that this form of RNA-based discrimination may be a critical step in mounting an early immune response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nallagatla, Subba Rao -- Hwang, Jungwook -- Toroney, Rebecca -- Zheng, Xiaofeng -- Cameron, Craig E -- Bevilacqua, Philip C -- GM58709/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2007 Nov 30;318(5855):1455-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, Pennsylvania State University, University Park, PA 16802, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18048689" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Line, Tumor ; Cercopithecus aethiops ; DEAD-box RNA Helicases/metabolism ; Enzyme Activation ; Eukaryotic Initiation Factor-2/metabolism ; Humans ; Immunity, Innate ; Interferon-alpha/immunology/metabolism ; Interferon-beta/metabolism ; Molecular Sequence Data ; *Nucleic Acid Conformation ; Phosphoric Monoester Hydrolases/metabolism ; Polyphosphates/metabolism ; RNA/chemistry/genetics/*metabolism ; RNA, Double-Stranded/chemistry/genetics/*metabolism ; Transfection ; Vero Cells ; eIF-2 Kinase/*metabolism
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    NOV (CCN3) functions as a regulator of human hematopoietic stem or progenitor cells (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-04-28
    Description: Clinically successful hematopoietic cell transplantation is dependent on hematopoietic stem and progenitor cells. Here we identify the matricellular protein Nephroblastoma Overexpressed (Nov, CCN3) as being essential for their functional integrity. Nov expression is restricted to the primitive (CD34) compartments of umbilical vein cord blood, and its knockdown in these cells by lentivirus-mediated RNA interference abrogates their function in vitro and in vivo. Conversely, forced expression of Nov and addition of recombinant Nov protein both enhance primitive stem and/or progenitor activity. Taken together, our results identify Nov (CCN3) as a regulator of human hematopoietic stem or progenitor cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gupta, Rajeev -- Hong, Dengli -- Iborra, Francisco -- Sarno, Samantha -- Enver, Tariq -- MC_U137961143/Medical Research Council/United Kingdom -- MC_U137973816/Medical Research Council/United Kingdom -- MC_U137973817/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2007 Apr 27;316(5824):590-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council Molecular Haematology Unit, Weatherall Institute of Molecular Medicine, University of Oxford, John Radcliffe Hospital, Headington, OX3 9DS, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17463287" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD34/analysis ; Cell Line ; Cells, Cultured ; Colony-Forming Units Assay ; Connective Tissue Growth Factor ; Genetic Vectors ; Hematopoiesis ; Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells/cytology/*physiology ; Humans ; Immediate-Early Proteins/genetics/*physiology ; Intercellular Signaling Peptides and Proteins/genetics/*physiology ; Lentivirus/genetics ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Nephroblastoma Overexpressed Protein ; RNA Interference ; Recombinant Proteins/metabolism ; Transfection ; Transplantation, Heterologous
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    Blue-light-activated histidine kinases: two-component sensors in bacteria (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-08-25
    Description: Histidine kinases, used for environmental sensing by bacterial two-component systems, are involved in regulation of bacterial gene expression, chemotaxis, phototaxis, and virulence. Flavin-containing domains function as light-sensory modules in plant and algal phototropins and in fungal blue-light receptors. We have discovered that the prokaryotes Brucella melitensis, Brucella abortus, Erythrobacter litoralis, and Pseudomonas syringae contain light-activated histidine kinases that bind a flavin chromophore and undergo photochemistry indicative of cysteinyl-flavin adduct formation. Infection of macrophages by B. abortus was stimulated by light in the wild type but was limited in photochemically inactive and null mutants, indicating that the flavin-containing histidine kinase functions as a photoreceptor regulating B. abortus virulence.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Swartz, Trevor E -- Tseng, Tong-Seung -- Frederickson, Marcus A -- Paris, Gaston -- Comerci, Diego J -- Rajashekara, Gireesh -- Kim, Jung-Gun -- Mudgett, Mary Beth -- Splitter, Gary A -- Ugalde, Rodolfo A -- Goldbaum, Fernando A -- Briggs, Winslow R -- Bogomolni, Roberto A -- 1.U54-AI-057153/AI/NIAID NIH HHS/ -- R01 GM068886/GM/NIGMS NIH HHS/ -- R01-GM068886/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2007 Aug 24;317(5841):1090-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry and Biochemistry, University of California, Santa Cruz, Santa Cruz, CA, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17717187" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Animals ; Brucella abortus/*enzymology/growth & development/pathogenicity ; Brucella melitensis/*enzymology ; Cell Line ; Cloning, Molecular ; Enzyme Activation ; Flavin Mononucleotide/metabolism ; *Light ; Macrophages/*microbiology ; Mice ; Molecular Sequence Data ; Mutation ; Phosphorylation ; Photochemistry ; Protein Kinases/chemistry/genetics/*metabolism ; Protein Structure, Tertiary ; Pseudomonas syringae/*enzymology ; Signal Transduction ; Sphingomonadaceae/*enzymology ; Virulence
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    Targeting of diacylglycerol degradation to M1 muscarinic receptors by beta-arrestins (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-02-03
    Description: Seven-transmembrane receptor (7TMR) signaling is transduced by second messengers such as diacylglycerol (DAG) generated in response to the heterotrimeric guanine nucleotide-binding protein Gq and is terminated by receptor desensitization and degradation of the second messengers. We show that beta-arrestins coordinate both processes for the Gq-coupled M1 muscarinic receptor. beta-Arrestins physically interact with diacylglycerol kinases (DGKs), enzymes that degrade DAG. Moreover, beta-arrestins are essential for conversion of DAG to phosphatidic acid after agonist stimulation, and this activity requires recruitment of the beta-arrestin-DGK complex to activated 7TMRs. The dual function of beta-arrestins, limiting production of diacylglycerol (by receptor desensitization) while enhancing its rate of degradation, is analogous to their ability to recruit adenosine 3',5'-monophosphate phosphodiesterases to Gs-coupled beta2-adrenergic receptors. Thus, beta-arrestins can serve similar regulatory functions for disparate classes of 7TMRs through structurally dissimilar enzymes that degrade chemically distinct second messengers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nelson, Christopher D -- Perry, Stephen J -- Regier, Debra S -- Prescott, Stephen M -- Topham, Matthew K -- Lefkowitz, Robert J -- CA95463/CA/NCI NIH HHS/ -- HL16037/HL/NHLBI NIH HHS/ -- HL70631/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2007 Feb 2;315(5812):663-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, 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/17272726" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arrestins/*metabolism ; COS Cells ; Carbachol/pharmacology ; Cell Line ; Cercopithecus aethiops ; Diacylglycerol Kinase/genetics/*metabolism ; Diglycerides/*metabolism ; Humans ; Mutation ; Phosphatidic Acids/metabolism ; Protein Binding ; RNA, Small Interfering ; Receptor, Muscarinic M1/*metabolism ; Recombinant Fusion Proteins/metabolism ; Second Messenger Systems ; *Signal Transduction ; Transfection
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    Coupling diurnal cytosolic Ca2+ oscillations to the CAS-IP3 pathway in Arabidopsis (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-03-10
    Description: Various signaling pathways rely on changes in cytosolic calcium ion concentration ([Ca2+]i). In plants, resting [Ca2+]i oscillates diurnally. We show that in Arabidopsis thaliana, [Ca2+]i oscillations are synchronized to extracellular Ca2+ concentration ([Ca2+]o) oscillations largely through the Ca2+-sensing receptor CAS. CAS regulates concentrations of inositol 1,4,5-trisphosphate (IP3), which in turn directs release of Ca2+ from internal stores. The oscillating amplitudes of [Ca2+]o and [Ca2+]i are controlled by soil Ca2+ concentrations and transpiration rates. The phase and period of oscillations are likely determined by stomatal conductance. Thus, the internal concentration of Ca2+ in plant cells is constantly being actively revised.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tang, Ru-Hang -- Han, Shengcheng -- Zheng, Hailei -- Cook, Charles W -- Choi, Christopher S -- Woerner, Todd E -- Jackson, Robert B -- Pei, Zhen-Ming -- New York, N.Y. -- Science. 2007 Mar 9;315(5817):1423-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Duke University, Durham, NC 27708, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17347443" target="_blank"〉PubMed〈/a〉
    Keywords: Aequorin/metabolism ; Arabidopsis/cytology/genetics/growth & development/*metabolism ; Arabidopsis Proteins/genetics/*metabolism ; Calcium/*metabolism ; *Calcium Signaling ; *Circadian Rhythm ; Cloning, Molecular ; Humans ; Inositol 1,4,5-Trisphosphate/*metabolism ; Ion Transport ; Luminescence ; Plant Shoots/metabolism ; Plant Transpiration ; Receptors, Calcium-Sensing/genetics/*metabolism ; Soil/analysis
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    Suppression of microRNA-silencing pathway by HIV-1 during virus replication (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-02-27
    Description: MicroRNAs (miRNAs) are single-stranded noncoding RNAs of 19 to 25 nucleotides that function as gene regulators and as a host cell defense against both RNA and DNA viruses. We provide evidence for a physiological role of the miRNA-silencing machinery in controlling HIV-1 replication. Type III RNAses Dicer and Drosha, responsible for miRNA processing, inhibited virus replication both in peripheral blood mononuclear cells from HIV-1-infected donors and in latently infected cells. In turn, HIV-1 actively suppressed the expression of the polycistronic miRNA cluster miR-17/92. This suppression was found to be required for efficient viral replication and was dependent on the histone acetyltransferase Tat cofactor PCAF. Our results highlight the involvement of the miRNA-silencing pathway in HIV-1 replication and latency.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Triboulet, Robinson -- Mari, Bernard -- Lin, Yea-Lih -- Chable-Bessia, Christine -- Bennasser, Yamina -- Lebrigand, Kevin -- Cardinaud, Bruno -- Maurin, Thomas -- Barbry, Pascal -- Baillat, Vincent -- Reynes, Jacques -- Corbeau, Pierre -- Jeang, Kuan-Teh -- Benkirane, Monsef -- New York, N.Y. -- Science. 2007 Mar 16;315(5818):1579-82. Epub 2007 Feb 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire de Virologie Moleculaire, Institut de Genetique Humaine, Montpellier, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17322031" target="_blank"〉PubMed〈/a〉
    Keywords: 3' Untranslated Regions ; Cell Cycle Proteins/genetics/metabolism ; Cell Line ; Gene Expression Regulation ; Gene Products, tat/metabolism ; HIV-1/genetics/*physiology ; HeLa Cells ; Histone Acetyltransferases/genetics/metabolism ; Humans ; Jurkat Cells ; Leukocytes, Mononuclear/enzymology/*virology ; MicroRNAs/*genetics ; Oligonucleotide Array Sequence Analysis ; *RNA Interference ; RNA, Small Interfering/genetics ; Ribonuclease III/genetics/metabolism ; Transcription Factors/genetics/metabolism ; Transfection ; Virus Latency ; *Virus Replication ; p300-CBP Transcription Factors ; tat Gene Products, Human Immunodeficiency Virus
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    Parallels between cytokinesis and retroviral budding: a role for the ESCRT machinery (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-06-09
    Description: During cytokinesis, as dividing animal cells pull apart into two daughter cells, the final stage, termed abscission, requires breakage of the midbody, a thin membranous stalk connecting the daughter cells. This membrane fission event topologically resembles the budding of viruses, such as HIV-1, from infected cells. We found that two proteins involved in HIV-1 budding-tumor susceptibility gene 101 (Tsg101), a subunit of the endosomal sorting complex required for transport I (ESCRT-I), and Alix, an ESCRT-associated protein-were recruited to the midbody during cytokinesis by interaction with centrosome protein 55 (Cep55), a centrosome and midbody protein essential for abscission. Tsg101, Alix, and possibly other components of ESCRT-I were required for the completion of cytokinesis. Thus, HIV-1 budding and cytokinesis use a similar subset of cellular components to carry out topologically similar membrane fission events.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carlton, Jez G -- Martin-Serrano, Juan -- G0400207/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2007 Jun 29;316(5833):1908-12. Epub 2007 Jun 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Infectious Diseases, King's College London School of Medicine, London, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17556548" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphatases/metabolism ; Amino Acid Motifs ; Calcium-Binding Proteins/*metabolism ; Carrier Proteins/*metabolism ; Cell Cycle Proteins/*metabolism ; *Cytokinesis ; DNA-Binding Proteins/*metabolism ; Endosomal Sorting Complexes Required for Transport ; Endosomes/metabolism ; HIV-1/*physiology ; HeLa Cells ; Humans ; Microtubules/metabolism ; Nuclear Proteins/*metabolism ; Protein Binding ; Protein Structure, Tertiary ; R-SNARE Proteins/metabolism ; RNA Interference ; Recombinant Fusion Proteins/metabolism ; Syntaxin 1/metabolism ; Transcription Factors/*metabolism ; Transfection ; Vesicular Transport Proteins/metabolism
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    Sirtuin 2 inhibitors rescue alpha-synuclein-mediated toxicity in models of Parkinson's disease (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-06-26
    Description: The sirtuins are members of the histone deacetylase family of proteins that participate in a variety of cellular functions and play a role in aging. We identified a potent inhibitor of sirtuin 2 (SIRT2) and found that inhibition of SIRT2 rescued alpha-synuclein toxicity and modified inclusion morphology in a cellular model of Parkinson's disease. Genetic inhibition of SIRT2 via small interfering RNA similarly rescued alpha-synuclein toxicity. Furthermore, the inhibitors protected against dopaminergic cell death both in vitro and in a Drosophila model of Parkinson's disease. The results suggest a link between neurodegeneration and aging.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Outeiro, Tiago Fleming -- Kontopoulos, Eirene -- Altmann, Stephen M -- Kufareva, Irina -- Strathearn, Katherine E -- Amore, Allison M -- Volk, Catherine B -- Maxwell, Michele M -- Rochet, Jean-Christophe -- McLean, Pamela J -- Young, Anne B -- Abagyan, Ruben -- Feany, Mel B -- Hyman, Bradley T -- Kazantsev, Aleksey G -- 5P50-NS38372A-06/NS/NINDS NIH HHS/ -- R01-NS049221/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2007 Jul 27;317(5837):516-9. Epub 2007 Jun 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Alzheimer's Research Unit, MGH, Harvard Medical School, CNY 114, 16th Street, Charlestown, MA 02129, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17588900" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Animals ; Animals, Genetically Modified ; Cell Death/drug effects ; Cell Line, Tumor ; Cells, Cultured ; Disease Models, Animal ; Dopamine/physiology ; Dose-Response Relationship, Drug ; Drosophila melanogaster ; Furans/*pharmacology ; Humans ; Models, Molecular ; Neurons/cytology/drug effects ; Parkinson Disease/*drug therapy/metabolism/pathology/*physiopathology ; Protein Conformation ; Quinolines/*pharmacology ; RNA, Small Interfering/genetics ; Rats ; Sirtuin 1 ; Sirtuin 2 ; Sirtuins/*antagonists & inhibitors/chemistry/genetics/*metabolism ; Transfection ; Tubulin/metabolism ; alpha-Synuclein/genetics/*metabolism
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    Comment on "Obestatin, a peptide encoded by the ghrelin gene, opposes ghrelin's effects on food intake" (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-02-10
    Description: Zhang et al. (Research Articles, 11 November 2005, p. 996) reported that obestatin, a peptide derived from the ghrelin precursor, activated the orphan G protein-coupled receptor GPR39. However, we found that I125-obestatin does not bind GPR39 and observed no effects of obestatin on GPR39-transfected cells in various functional assays (cyclic adenosine monophosphate production, calcium mobilization, and GPR39 internalization). Our results indicate that obestatin is not the cognate ligand for GPR39.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chartrel, N -- Alvear-Perez, R -- Leprince, J -- Iturrioz, X -- Reaux-Le Goazigo, A -- Audinot, V -- Chomarat, P -- Coge, F -- Nosjean, O -- Rodriguez, M -- Galizzi, J P -- Boutin, J A -- Vaudry, H -- Llorens-Cortes, C -- New York, N.Y. -- Science. 2007 Feb 9;315(5813):766; author reply 766.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut National de la Sante et de la Recherche Medicale (INSERM), U413, Laboratory of Cellular and Molecular Neuroendocrinology, and European Institute for Peptide Research (IFRMP 23), University of Rouen, 76821 Mont-Saint-Aignan, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17289961" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; CHO Cells ; Calcium/metabolism ; Cell Membrane/metabolism ; Colforsin/pharmacology ; Cricetinae ; Cricetulus ; Cyclic AMP/metabolism ; Ghrelin ; Humans ; Ligands ; Molecular Sequence Data ; Peptide Hormones/genetics/*metabolism/pharmacology ; Pituitary Gland/cytology/metabolism ; Protein Binding ; Receptors, G-Protein-Coupled/genetics/*metabolism ; Transfection
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    Sensing X chromosome pairs before X inactivation via a novel X-pairing region of the Xic (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-12-08
    Description: Mammalian dosage compensation involves silencing of one of the two X chromosomes in females and is controlled by the X-inactivation center (Xic). The Xic, which includes Xist and its antisense transcription unit Tsix/Xite, somehow senses the number of X chromosomes and triggers Xist up-regulation from one of the two X chromosomes in females. We found that a segment of the mouse Xic lying several hundred kilobases upstream of Xist brings the two Xics together before the onset of X inactivation. This region can autonomously drive Xic trans-interactions even as an ectopic single-copy transgene. Its introduction into male embryonic stem cells is strongly selected against, consistent with a possible role in trans-activating Xist. We propose that homologous associations driven by this novel X-pairing region (Xpr) of the Xic enable a cell to sense that more than one X chromosome is present and coordinate reciprocal Xist/Tsix expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Augui, S -- Filion, G J -- Huart, S -- Nora, E -- Guggiari, M -- Maresca, M -- Stewart, A F -- Heard, E -- New York, N.Y. -- Science. 2007 Dec 7;318(5856):1632-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉CNRS UMR218, Curie Institute, 26 rue d'Ulm, Paris 75005, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18063799" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Cell Differentiation ; Cell Line ; *Chromosome Pairing ; Chromosomes, Artificial, Bacterial ; Down-Regulation ; Embryonic Stem Cells ; Female ; Mice ; Mice, Transgenic ; RNA, Long Noncoding ; RNA, Untranslated/genetics/metabolism ; S Phase ; Transfection ; Transgenes ; Up-Regulation ; X Chromosome/*genetics/physiology ; *X Chromosome Inactivation
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    Ca2+ entry through plasma membrane IP3 receptors (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-07-15
    Description: Inositol 1,4,5-trisphosphate receptors (IP3Rs) release calcium ions, Ca2+, from intracellular stores, but their roles in mediating Ca2+ entry are unclear. IP3 stimulated opening of very few (1.9 +/- 0.2 per cell) Ca2+-permeable channels in whole-cell patch-clamp recording of DT40 chicken or mouse B cells. Activation of the B cell receptor (BCR) in perforated-patch recordings evoked the same response. IP3 failed to stimulate intracellular or plasma membrane (PM) channels in cells lacking IP3R. Expression of IP3R restored both responses. Mutations within the pore affected the conductances of IP3-activated PM and intracellular channels similarly. An impermeant pore mutant abolished BCR-evoked Ca2+ signals, and PM IP3Rs were undetectable. After introduction of an alpha-bungarotoxin binding site near the pore, PM IP3Rs were modulated by extracellular alpha-bungarotoxin. IP(3)Rs are unusual among endoplasmic reticulum proteins in being also functionally expressed at the PM, where very few IP3Rs contribute substantially to the Ca2+ entry evoked by the BCR.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dellis, Olivier -- Dedos, Skarlatos G -- Tovey, Stephen C -- Taufiq-Ur-Rahman -- Dubel, Stefan J -- Taylor, Colin W -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2006 Jul 14;313(5784):229-33.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Tennis Court Road, Cambridge, CB2 1PD, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16840702" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/metabolism ; Bungarotoxins/metabolism/pharmacology ; Calcium/*metabolism ; Calcium Channels/genetics/*metabolism ; *Calcium Signaling ; Cell Membrane/*metabolism ; Cells, Cultured ; Chickens ; Electric Conductivity ; Endoplasmic Reticulum/metabolism ; Inositol 1,4,5-Trisphosphate/metabolism ; Inositol 1,4,5-Trisphosphate Receptors ; *Ion Channel Gating ; Mice ; Nuclear Envelope/metabolism ; Patch-Clamp Techniques ; Point Mutation ; Rats ; Receptors, Antigen, B-Cell/metabolism ; Receptors, Cytoplasmic and Nuclear/antagonists & inhibitors/genetics/*metabolism ; Transfection
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    Sequential interplay of nicotinic and GABAergic signaling guides neuronal development (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-12-13
    Description: GABA (gamma-aminobutyric acid), the major inhibitory transmitter in the brain, goes through a transitory phase of excitation during development. The excitatory phase promotes neuronal growth and integration into circuits. We show here that spontaneous nicotinic cholinergic activity is responsible for terminating GABAergic excitation and initiating inhibition. It does so by changing chloride transporter levels, shifting the driving force on GABA-induced currents. The timing of the transition is critical, because the two phases of GABAergic signaling provide contrasting developmental instructions. Synergistic with nicotinic excitation, GABAergic inhibition constrains neuronal morphology and innervation. The results reveal a multitiered activity-dependent strategy controlling neuronal development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, Zhaoping -- Neff, Robert A -- Berg, Darwin K -- NS012601/NS/NINDS NIH HHS/ -- NS035469/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2006 Dec 8;314(5805):1610-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biological Sciences, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0357, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17158331" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cadmium/pharmacology ; Calcium/metabolism ; Chick Embryo ; Chlorides/metabolism ; Ganglia, Parasympathetic/cytology/embryology ; Hippocampus/cytology/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Neurons/cytology/*physiology ; Nicotine/metabolism/pharmacology ; Nicotinic Antagonists/pharmacology ; Patch-Clamp Techniques ; Receptors, Nicotinic/*metabolism ; Recombinant Fusion Proteins/metabolism ; *Signal Transduction ; Sodium-Potassium-Chloride Symporters/metabolism ; Solute Carrier Family 12, Member 2 ; Symporters/genetics/metabolism ; Synaptic Transmission ; Transfection ; alpha7 Nicotinic Acetylcholine Receptor ; gamma-Aminobutyric Acid/*metabolism
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    A bacterial protein enhances the release and efficacy of liposomal cancer drugs (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-11-25
    Description: Clostridium novyi-NT is an anaerobic bacterium that can infect hypoxic regions within experimental tumors. Because C. novyi-NT lyses red blood cells, we hypothesized that its membrane-disrupting properties could be exploited to enhance the release of liposome-encapsulated drugs within tumors. Here, we show that treatment of mice bearing large, established tumors with C. novyi-NT plus a single dose of liposomal doxorubicin often led to eradication of the tumors. The bacterial factor responsible for the enhanced drug release was identified as a previously unrecognized protein termed liposomase. This protein could potentially be incorporated into diverse experimental approaches for the specific delivery of chemotherapeutic agents to tumors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cheong, Ian -- Huang, Xin -- Bettegowda, Chetan -- Diaz, Luis A Jr -- Kinzler, Kenneth W -- Zhou, Shibin -- Vogelstein, Bert -- CA062924/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2006 Nov 24;314(5803):1308-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and the Ludwig Center for Cancer Genetics and Therapeutics, Johns Hopkins Kimmel Comprehensive Cancer Center, Baltimore, MD 21231, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17124324" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antineoplastic Agents/*administration & dosage/pharmacokinetics/therapeutic use ; Bacterial Proteins/chemistry/genetics/*metabolism ; Base Sequence ; Camptothecin/administration & dosage/analogs & ; derivatives/pharmacokinetics/therapeutic use ; Cell Line, Tumor ; Cloning, Molecular ; Clostridium/*chemistry/genetics ; Colorectal Neoplasms/*drug therapy ; Doxorubicin/*administration & dosage/pharmacokinetics/therapeutic use ; Drug Carriers ; Humans ; Lipase/chemistry/genetics/*metabolism ; Lipid Bilayers/chemistry ; Liposomes/chemistry/*metabolism ; Mice ; Molecular Sequence Data ; Mutation ; Neoplasm Transplantation ; Protein Structure, Tertiary
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    ATM engages autodegradation of the E3 ubiquitin ligase COP1 after DNA damage (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-08-26
    Description: The ataxia telangiectasia mutated (ATM) protein kinase is a critical component of a DNA-damage response network configured to maintain genomic integrity. The abundance of an essential downstream effecter of this pathway, the tumor suppressor protein p53, is tightly regulated by controlled degradation through COP1 and other E3 ubiquitin ligases, such as MDM2 and Pirh2; however, the signal transduction pathway that regulates the COP1-p53 axis following DNA damage remains enigmatic. We observed that in response to DNA damage, ATM phosphorylated COP1 on Ser(387) and stimulated a rapid autodegradation mechanism. Ionizing radiation triggered an ATM-dependent movement of COP1 from the nucleus to the cytoplasm, and ATM-dependent phosphorylation of COP1 on Ser(387) was both necessary and sufficient to disrupt the COP1-p53 complex and subsequently to abrogate the ubiquitination and degradation of p53. Furthermore, phosphorylation of COP1 on Ser(387) was required to permit p53 to become stabilized and to exert its tumor suppressor properties in response to DNA damage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dornan, David -- Shimizu, Harumi -- Mah, Angie -- Dudhela, Tanay -- Eby, Michael -- O'rourke, Karen -- Seshagiri, Somasekar -- Dixit, Vishva M -- New York, N.Y. -- Science. 2006 Aug 25;313(5790):1122-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiological Chemistry, Genentech, Inc., 1 DNA Way, South San Francisco, CA 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16931761" target="_blank"〉PubMed〈/a〉
    Keywords: Ataxia Telangiectasia Mutated Proteins ; Cell Cycle Proteins/genetics/*metabolism ; Cell Line ; Cell Line, Tumor ; Cell Nucleus/metabolism ; Cytoplasm/metabolism ; *DNA Damage ; DNA-Binding Proteins/genetics/*metabolism ; Escherichia coli/genetics/metabolism ; Etoposide/pharmacology ; Humans ; Mutation ; Nuclear Proteins/genetics/*metabolism ; Phosphorylation ; Phosphoserine/metabolism ; Proteasome Endopeptidase Complex/metabolism ; Protein-Serine-Threonine Kinases/genetics/*metabolism ; RNA, Small Interfering ; Radiation, Ionizing ; Recombinant Fusion Proteins/metabolism ; Transfection ; Tumor Suppressor Protein p53/genetics/metabolism ; Tumor Suppressor Proteins/genetics/*metabolism ; Ubiquitin/metabolism ; Ubiquitin-Protein Ligases/genetics/*metabolism
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    Chemistry. Dendrimers at work (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-08-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Helms, Brett -- Meijer, E W -- New York, N.Y. -- Science. 2006 Aug 18;313(5789):929-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Macromolecular and Organic Chemistry and Department of Biomedical Engineering, Eindhoven University of Technology, 5600 MB Eindhoven, Netherlands. e.w.meijer@tue.nl〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16917051" target="_blank"〉PubMed〈/a〉
    Keywords: Chemistry, Pharmaceutical ; Contrast Media ; *Dendrimers/chemical synthesis/chemistry/therapeutic use ; Drug Approval ; Drug Carriers ; Drug Design ; Humans ; Magnetic Resonance Imaging ; Molecular Structure ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Cytokinin signaling and its inhibitor AHP6 regulate cell fate during vascular development (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-01-10
    Description: The cell lineages that form the transporting tissues (xylem and phloem) and the intervening pluripotent procambial tissue originate from stem cells near the root tip. We demonstrate that in Arabidopsis, cytokinin phytohormones negatively regulate protoxylem specification. AHP6, an inhibitory pseudophosphotransfer protein, counteracts cytokinin signaling, allowing protoxylem formation. Conversely, cytokinin signaling negatively regulates the spatial domain of AHP6 expression. Thus, by controlling the identity of cell lineages, the reciprocal interaction of cytokinin signaling and its spatially specific modulator regulates proliferation and differentiation of cell lineages during vascular development, demonstrating a previously unrecognized regulatory circuit underlying meristem organization.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mahonen, Ari Pekka -- Bishopp, Anthony -- Higuchi, Masayuki -- Nieminen, Kaisa M -- Kinoshita, Kaori -- Tormakangas, Kirsi -- Ikeda, Yoshihisa -- Oka, Atsuhiro -- Kakimoto, Tatsuo -- Helariutta, Yka -- New York, N.Y. -- Science. 2006 Jan 6;311(5757):94-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Plant Molecular Biology Laboratory, Institute of Biotechnology, POB 56, FI-00014, University of Helsinki, Finland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16400151" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Alleles ; Arabidopsis/*cytology/genetics/growth & development/*metabolism ; Arabidopsis Proteins/genetics/*metabolism/physiology ; Cell Differentiation ; Cell Division ; Cell Lineage ; Cloning, Molecular ; Cytokinins/*metabolism ; Genes, Plant ; Kinetin/metabolism/pharmacology ; Meristem/cytology/growth & development/metabolism ; Morphogenesis ; Phenotype ; Phosphorylation ; Plant Growth Regulators/*metabolism ; Plant Roots/*cytology/growth & development/metabolism ; Plant Shoots/metabolism ; Plants, Genetically Modified ; *Signal Transduction ; Suppression, Genetic ; Zeatin/metabolism/pharmacology
    Print ISSN: 0036-8075
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    CDK2-dependent phosphorylation of FOXO1 as an apoptotic response to DNA damage (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-10-14
    Description: The function of cyclin-dependent kinase 2 (CDK2) is often abolished after DNA damage. The inhibition of CDK2 plays a central role in DNA damage-induced cell cycle arrest and DNA repair. However, whether CDK2 also influences the survival of cells under genotoxic stress is unknown. Forkhead box O (FOXO) transcription factors are emerging as key regulators of cell survival. CDK2 specifically phosphorylated FOXO1 at serine-249 (Ser249) in vitro and in vivo. Phosphorylation of Ser249 resulted in cytoplasmic localization and inhibition of FOXO1. This phosphorylation was abrogated upon DNA damage through the cell cycle checkpoint pathway that is dependent on the protein kinases Chk1 and Chk2. Moreover, silencing of FOXO1 by small interfering RNA diminished DNA damage-induced death in both p53-deficient and p53-proficient cells. This effect was reversed by restored expression of FOXO1 in a manner depending on phosphorylation of Ser249. Functional interaction between CDK2 and FOXO1 provides a mechanism that regulates apoptotic cell death after DNA strand breakage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, Haojie -- Regan, Kevin M -- Lou, Zhenkun -- Chen, Junjie -- Tindall, Donald J -- CA91956/CA/NCI NIH HHS/ -- DK60920/DK/NIDDK NIH HHS/ -- DK65236/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2006 Oct 13;314(5797):294-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biology, Mayo Clinic College of Medicine, Rochester, MN 55905, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17038621" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Camptothecin/pharmacology ; Cell Line, Tumor ; Cell Nucleus/metabolism ; Checkpoint Kinase 2 ; Cyclin-Dependent Kinase 2/antagonists & inhibitors/genetics/*metabolism ; Cytoplasm/metabolism ; *DNA Damage ; Forkhead Transcription Factors/antagonists & inhibitors/*metabolism ; Humans ; Mice ; Phosphorylation ; Phosphoserine/metabolism ; Protein Kinases/metabolism ; Protein-Serine-Threonine Kinases/metabolism ; RNA, Small Interfering ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Transcription, Genetic ; Transfection ; Tumor Suppressor Protein p53/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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    Activity-dependent regulation of MEF2 transcription factors suppresses excitatory synapse number (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-02-18
    Description: In the mammalian nervous system, neuronal activity regulates the strength and number of synapses formed. The genetic program that coordinates this process is poorly understood. We show that myocyte enhancer factor 2 (MEF2) transcription factors suppressed excitatory synapse number in a neuronal activity- and calcineurin-dependent manner as hippocampal neurons formed synapses. In response to increased neuronal activity, calcium influx into neurons induced the activation of the calcium/calmodulin-regulated phosphatase calcineurin, which dephosphorylated and activated MEF2. When activated, MEF2 promoted the transcription of a set of genes, including arc and synGAP, that restrict synapse number. These findings define an activity-dependent transcriptional program that may control synapse number during development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Flavell, Steven W -- Cowan, Christopher W -- Kim, Tae-Kyung -- Greer, Paul L -- Lin, Yingxi -- Paradis, Suzanne -- Griffith, Eric C -- Hu, Linda S -- Chen, Chinfei -- Greenberg, Michael E -- AG05870/AG/NIA NIH HHS/ -- HD18655/HD/NICHD NIH HHS/ -- NS28829/NS/NINDS NIH HHS/ -- R01 EY013613/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 2006 Feb 17;311(5763):1008-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neurobiology Program, Children's Hospital, and Departments of Neurology and Neurobiology, Harvard Medical School, 300 Longwood Avenue, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16484497" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcineurin/metabolism ; Calcium/metabolism ; Cells, Cultured ; Cytoskeletal Proteins/genetics ; Dendrites/physiology/ultrastructure ; Excitatory Postsynaptic Potentials ; GTPase-Activating Proteins/genetics ; Gene Expression Regulation ; Glutamic Acid/metabolism ; Hippocampus/cytology/*physiology ; MEF2 Transcription Factors ; Mutation ; Myogenic Regulatory Factors/genetics/*physiology ; Nerve Tissue Proteins/genetics ; Neurons/*physiology ; Oligonucleotide Array Sequence Analysis ; Phosphorylation ; RNA Interference ; Rats ; Rats, Long-Evans ; Recombinant Fusion Proteins/metabolism ; Synapses/*physiology ; Synaptic Transmission ; Transcription, Genetic ; Transfection
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    BKCa-Cav channel complexes mediate rapid and localized Ca2+-activated K+ signaling (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-10-28
    Description: Large-conductance calcium- and voltage-activated potassium channels (BKCa) are dually activated by membrane depolarization and elevation of cytosolic calcium ions (Ca2+). Under normal cellular conditions, BKCa channel activation requires Ca2+ concentrations that typically occur in close proximity to Ca2+ sources. We show that BKCa channels affinity-purified from rat brain are assembled into macromolecular complexes with the voltage-gated calcium channels Cav1.2 (L-type), Cav2.1 (P/Q-type), and Cav2.2 (N-type). Heterologously expressed BKCa-Cav complexes reconstitute a functional "Ca2+ nanodomain" where Ca2+ influx through the Cav channel activates BKCa in the physiological voltage range with submillisecond kinetics. Complex formation with distinct Cav channels enables BKCa-mediated membrane hyperpolarization that controls neuronal firing pattern and release of hormones and transmitters in the central nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Berkefeld, Henrike -- Sailer, Claudia A -- Bildl, Wolfgang -- Rohde, Volker -- Thumfart, Jorg-Oliver -- Eble, Silke -- Klugbauer, Norbert -- Reisinger, Ellen -- Bischofberger, Josef -- Oliver, Dominik -- Knaus, Hans-Gunther -- Schulte, Uwe -- Fakler, Bernd -- New York, N.Y. -- Science. 2006 Oct 27;314(5799):615-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Physiology, University of Freiburg, Hermann-Herder-Strasse 7, 79104 Freiburg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17068255" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Brain Chemistry ; CHO Cells ; Calcium/*metabolism ; Calcium Channels, L-Type/drug effects/isolation & purification/*metabolism ; Calcium Channels, N-Type/drug effects/isolation & purification/*metabolism ; Calcium Signaling ; Chromaffin Cells/drug effects/metabolism ; Cricetinae ; Cricetulus ; Egtazic Acid/analogs & derivatives/pharmacology ; Large-Conductance Calcium-Activated Potassium Channels/drug effects/isolation & ; purification/*metabolism ; Membrane Potentials/drug effects ; Molecular Sequence Data ; Patch-Clamp Techniques ; Potassium/*metabolism ; Rats ; *Signal Transduction ; Transfection ; Xenopus
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    A "silent" polymorphism in the MDR1 gene changes substrate specificity (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-12-23
    Description: Synonymous single-nucleotide polymorphisms (SNPs) do not produce altered coding sequences, and therefore they are not expected to change the function of the protein in which they occur. We report that a synonymous SNP in the Multidrug Resistance 1 (MDR1) gene, part of a haplotype previously linked to altered function of the MDR1 gene product P-glycoprotein (P-gp), nonetheless results in P-gp with altered drug and inhibitor interactions. Similar mRNA and protein levels, but altered conformations, were found for wild-type and polymorphic P-gp. We hypothesize that the presence of a rare codon, marked by the synonymous polymorphism, affects the timing of cotranslational folding and insertion of P-gp into the membrane, thereby altering the structure of substrate and inhibitor interaction sites.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kimchi-Sarfaty, Chava -- Oh, Jung Mi -- Kim, In-Wha -- Sauna, Zuben E -- Calcagno, Anna Maria -- Ambudkar, Suresh V -- Gottesman, Michael M -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2007 Jan 26;315(5811):525-8. Epub 2006 Dec 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA. kimchi@cber.fda.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17185560" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Membrane/metabolism ; Cercopithecus aethiops ; Codon ; Cyclosporine/pharmacology ; *Genes, MDR ; Haplotypes ; HeLa Cells ; Humans ; Mutagenesis, Site-Directed ; P-Glycoprotein/antagonists & inhibitors/*chemistry/genetics/*metabolism ; *Polymorphism, Single Nucleotide ; Protein Biosynthesis ; Protein Conformation ; *Protein Folding ; Protein Structure, Tertiary ; RNA, Messenger/genetics/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Rhodamine 123/metabolism/pharmacology ; Sirolimus/pharmacology ; Substrate Specificity ; Transfection ; Verapamil/metabolism/pharmacology
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    PIN proteins perform a rate-limiting function in cellular auxin efflux (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-04-08
    Description: Intercellular flow of the phytohormone auxin underpins multiple developmental processes in plants. Plant-specific pin-formed (PIN) proteins and several phosphoglycoprotein (PGP) transporters are crucial factors in auxin transport-related development, yet the molecular function of PINs remains unknown. Here, we show that PINs mediate auxin efflux from mammalian and yeast cells without needing additional plant-specific factors. Conditional gain-of-function alleles and quantitative measurements of auxin accumulation in Arabidopsis and tobacco cultured cells revealed that the action of PINs in auxin efflux is distinct from PGP, rate-limiting, specific to auxins, and sensitive to auxin transport inhibitors. This suggests a direct involvement of PINs in catalyzing cellular auxin efflux.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Petrasek, Jan -- Mravec, Jozef -- Bouchard, Rodolphe -- Blakeslee, Joshua J -- Abas, Melinda -- Seifertova, Daniela -- Wisniewska, Justyna -- Tadele, Zerihun -- Kubes, Martin -- Covanova, Milada -- Dhonukshe, Pankaj -- Skupa, Petr -- Benkova, Eva -- Perry, Lucie -- Krecek, Pavel -- Lee, Ok Ran -- Fink, Gerald R -- Geisler, Markus -- Murphy, Angus S -- Luschnig, Christian -- Zazimalova, Eva -- Friml, Jiri -- New York, N.Y. -- Science. 2006 May 12;312(5775):914-8. Epub 2006 Apr 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Experimental Botany, the Academy of Sciences of the Czech Republic, 165 02 Prague 6, Czech Republic.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16601150" target="_blank"〉PubMed〈/a〉
    Keywords: ATP-Binding Cassette Transporters/genetics/metabolism ; Arabidopsis/cytology/growth & development/*metabolism/physiology ; Arabidopsis Proteins/genetics/*metabolism ; Biological Transport ; Cell Membrane/metabolism ; Cells, Cultured ; Gravitropism ; HeLa Cells ; Humans ; Indoleacetic Acids/*metabolism ; Kinetics ; Membrane Transport Proteins/genetics/*metabolism ; Mutation ; Naphthaleneacetic Acids/metabolism ; Phthalimides/pharmacology ; Plant Roots/physiology ; Saccharomyces cerevisiae/genetics ; Tobacco ; Transfection ; Transformation, Genetic
    Print ISSN: 0036-8075
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    RNA interference directs innate immunity against viruses in adult Drosophila (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-03-25
    Description: Innate immunity against bacterial and fungal pathogens is mediated by Toll and immune deficiency (Imd) pathways, but little is known about the antiviral response in Drosophila. Here, we demonstrate that an RNA interference pathway protects adult flies from infection by two evolutionarily diverse viruses. Our work also describes a molecular framework for the viral immunity, in which viral double-stranded RNA produced during infection acts as the pathogen trigger whereas Drosophila Dicer-2 and Argonaute-2 act as host sensor and effector, respectively. These findings establish a Drosophila model for studying the innate immunity against viruses in animals.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1509097/" 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/PMC1509097/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Xiao-Hong -- Aliyari, Roghiyh -- Li, Wan-Xiang -- Li, Hong-Wei -- Kim, Kevin -- Carthew, Richard -- Atkinson, Peter -- Ding, Shou-Wei -- AI052447/AI/NIAID NIH HHS/ -- R01 AI052447/AI/NIAID NIH HHS/ -- R01 GM068743/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Apr 21;312(5772):452-4. Epub 2006 Mar 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Graduate Program for Microbiology, University of California, Riverside, CA 92521, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16556799" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Argonaute Proteins ; Cell Line ; Drosophila Proteins/genetics/metabolism/physiology ; Drosophila melanogaster/embryology/genetics/*immunology/*virology ; Embryo, Nonmammalian/immunology/virology ; Escherichia coli/physiology ; *Immunity, Innate ; Insect Viruses/genetics/*physiology ; Micrococcus luteus/physiology ; Mutation ; Nodaviridae/*physiology ; RNA Helicases/genetics/metabolism ; *RNA Interference ; RNA Viruses/genetics/physiology ; RNA, Double-Stranded/metabolism ; RNA, Small Interfering/metabolism ; RNA, Viral/genetics/metabolism ; RNA-Binding Proteins/genetics/physiology ; RNA-Induced Silencing Complex/genetics/physiology ; Ribonuclease III ; Signal Transduction ; Toll-Like Receptors/physiology ; Transfection ; Virus Replication
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    The Neurospora checkpoint kinase 2: a regulatory link between the circadian and cell cycles (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-07-01
    Description: The clock gene period-4 (prd-4) in Neurospora was identified by a single allele displaying shortened circadian period and altered temperature compensation. Positional cloning followed by functional tests show that PRD-4 is an ortholog of mammalian checkpoint kinase 2 (Chk2). Expression of prd-4 is regulated by the circadian clock and, reciprocally, PRD-4 physically interacts with the clock component FRQ, promoting its phosphorylation. DNA-damaging agents can reset the clock in a manner that depends on time of day, and this resetting is dependent on PRD-4. Thus, prd-4, the Neurospora Chk2, identifies a molecular link that feeds back conditionally from circadian output to input and the cell cycle.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pregueiro, Antonio M -- Liu, Qiuyun -- Baker, Christopher L -- Dunlap, Jay C -- Loros, Jennifer J -- MH44651/MH/NIMH NIH HHS/ -- P01 GM068087/GM/NIGMS NIH HHS/ -- R01 GM034985/GM/NIGMS NIH HHS/ -- R37GM34985/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Aug 4;313(5787):644-9. Epub 2006 Jun 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Dartmouth Medical School, Hanover, NH 03755, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16809488" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; *Cell Cycle ; Checkpoint Kinase 2 ; *Circadian Rhythm ; Cloning, Molecular ; DNA Damage ; Feedback, Physiological ; Fungal Proteins/chemistry/genetics/metabolism ; Gene Expression Regulation, Fungal ; Genes, Fungal ; Methyl Methanesulfonate/pharmacology ; Molecular Sequence Data ; Mutation ; Neurospora/*enzymology/genetics ; Neurospora crassa/cytology/*enzymology/*physiology ; Phosphorylation ; Protein-Serine-Threonine Kinases/chemistry/*genetics/*metabolism
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    A topoisomerase IIbeta-mediated dsDNA break required for regulated transcription (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-06-24
    Description: Multiple enzymatic activities are required for transcriptional initiation. The enzyme DNA topoisomerase II associates with gene promoter regions and can generate breaks in double-stranded DNA (dsDNA). Therefore, it is of interest to know whether this enzyme is critical for regulated gene activation. We report that the signal-dependent activation of gene transcription by nuclear receptors and other classes of DNA binding transcription factors, including activating protein 1, requires DNA topoisomerase IIbeta-dependent, transient, site-specific dsDNA break formation. Subsequent to the break, poly(adenosine diphosphate-ribose) polymerase-1 enzymatic activity is induced, which is required for a nucleosome-specific histone H1-high-mobility group B exchange event and for local changes of chromatin architecture. Our data mechanistically link DNA topoisomerase IIbeta-dependent dsDNA breaks and the components of the DNA damage and repair machinery in regulated gene transcription.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ju, Bong-Gun -- Lunyak, Victoria V -- Perissi, Valentina -- Garcia-Bassets, Ivan -- Rose, David W -- Glass, Christopher K -- Rosenfeld, Michael G -- New York, N.Y. -- Science. 2006 Jun 23;312(5781):1798-802.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Medicine, School of Medicine, 9500 Gilman Drive, University of California, San Diego, La Jolla, CA 92093-0648, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16794079" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line, Tumor ; Chromatin/metabolism ; Chromatin Immunoprecipitation ; DNA/*metabolism ; DNA Damage ; DNA Repair ; DNA Topoisomerases, Type II/*metabolism ; DNA-Binding Proteins/antagonists & inhibitors/*metabolism ; Enzyme Inhibitors/pharmacology ; Estradiol/pharmacology ; Estrogen Receptor alpha/metabolism ; Histones/metabolism ; Humans ; Membrane Proteins/genetics ; Nucleosomes/metabolism ; Poly(ADP-ribose) Polymerases/metabolism ; Presenilin-2 ; Promoter Regions, Genetic ; Response Elements ; Thiobarbiturates/pharmacology ; Topoisomerase II Inhibitors ; Transcription Factors/metabolism ; *Transcription, Genetic ; *Transcriptional Activation ; Transfection
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    Epilepsy-related ligand/receptor complex LGI1 and ADAM22 regulate synaptic transmission (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-09-23
    Description: Abnormally synchronized synaptic transmission in the brain causes epilepsy. Most inherited forms of epilepsy result from mutations in ion channels. However, one form of epilepsy, autosomal dominant partial epilepsy with auditory features (ADPEAF), is characterized by mutations in a secreted neuronal protein, LGI1. We show that ADAM22, a transmembrane protein that when mutated itself causes seizure, serves as a receptor for LGI1. LGI1 enhances AMPA receptor-mediated synaptic transmission in hippocampal slices. The mutated form of LGI1 fails to bind to ADAM22. ADAM22 is anchored to the postsynaptic density by cytoskeletal scaffolds containing stargazin. These studies in rat brain indicate possible avenues for understanding human epilepsy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fukata, Yuko -- Adesnik, Hillel -- Iwanaga, Tsuyoshi -- Bredt, David S -- Nicoll, Roger A -- Fukata, Masaki -- New York, N.Y. -- Science. 2006 Sep 22;313(5794):1792-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Genomics and Proteomics, National Institute for Longevity Sciences, National Center for Geriatrics and Gerontology, Obu, Aichi 474-8522, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16990550" target="_blank"〉PubMed〈/a〉
    Keywords: ADAM Proteins/chemistry/genetics/*metabolism ; Animals ; Calcium Channels/metabolism ; Cell Line ; Cerebellar Cortex/metabolism ; Cerebral Cortex/metabolism ; Epilepsies, Partial/physiopathology ; Hippocampus/metabolism/*physiology ; Humans ; Intracellular Signaling Peptides and Proteins/metabolism ; Ligands ; Membrane Proteins/metabolism ; Mice ; N-Methylaspartate/metabolism ; Nerve Tissue Proteins/genetics/metabolism ; Protein Binding ; Protein Structure, Tertiary ; Proteins/*metabolism ; Rats ; Receptors, AMPA/*metabolism ; Recombinant Fusion Proteins/metabolism ; Synapses/metabolism ; *Synaptic Transmission ; Transfection ; alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid/metabolism
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    Human IRGM induces autophagy to eliminate intracellular mycobacteria (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-08-05
    Description: Immunity-related p47 guanosine triphosphatases (IRG) play a role in defense against intracellular pathogens. We found that the murine Irgm1 (LRG-47) guanosine triphosphatase induced autophagy and generated large autolysosomal organelles as a mechanism for the elimination of intracellular Mycobacterium tuberculosis. We also identified a function for a human IRG protein in the control of intracellular pathogens and report that the human Irgm1 ortholog, IRGM, plays a role in autophagy and in the reduction of intracellular bacillary load.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Singh, Sudha B -- Davis, Alexander S -- Taylor, Gregory A -- Deretic, Vojo -- AI42999/AI/NIAID NIH HHS/ -- AI45148/AI/NIAID NIH HHS/ -- AI57831/AI/NIAID NIH HHS/ -- R01 AI057831/AI/NIAID NIH HHS/ -- T32 AI007538/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2006 Sep 8;313(5792):1438-41. Epub 2006 Aug 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics and Microbiology, University of New Mexico School of Medicine, Albuquerque, NM 87131, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16888103" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Autophagy ; Cell Line ; Cytosol/metabolism ; GTP-Binding Proteins/genetics/*physiology ; HeLa Cells ; Humans ; Interferon-gamma/immunology ; Lysosomes/metabolism/microbiology/ultrastructure ; Macrophages/*immunology/*microbiology ; Mice ; Microbial Viability ; Microtubule-Associated Proteins/metabolism ; Mycobacterium bovis/*immunology/physiology ; Phagosomes/metabolism/microbiology/*ultrastructure ; RNA, Small Interfering ; Transfection ; Vacuoles/metabolism/ultrastructure
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  • 88
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    Regulation of adult bone mass by the zinc finger adapter protein Schnurri-3 (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-05-27
    Description: Genetic mutations that disrupt osteoblast function can result in skeletal dysmorphogenesis or, more rarely, in increased postnatal bone formation. Here we show that Schnurri-3 (Shn3), a mammalian homolog of the Drosophila zinc finger adapter protein Shn, is an essential regulator of adult bone formation. Mice lacking Shn3 display adult-onset osteosclerosis with increased bone mass due to augmented osteoblast activity. Shn3 was found to control protein levels of Runx2, the principal transcriptional regulator of osteoblast differentiation, by promoting its degradation through recruitment of the E3 ubiquitin ligase WWP1 to Runx2. By this means, Runx2-mediated extracellular matrix mineralization was antagonized, revealing an essential role for Shn3 as a central regulator of postnatal bone mass.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jones, Dallas C -- Wein, Marc N -- Oukka, Mohamed -- Hofstaetter, Jochen G -- Glimcher, Melvin J -- Glimcher, Laurie H -- AI29673/AI/NIAID NIH HHS/ -- AR46983/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 2006 May 26;312(5777):1223-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16728642" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; *Bone Density ; Bone and Bones/*anatomy & histology/chemistry/physiology ; Cell Line ; Cells, Cultured ; Core Binding Factor Alpha 1 Subunit/genetics/metabolism ; DNA-Binding Proteins/analysis/genetics/*metabolism ; Gene Expression Regulation ; Immunoprecipitation ; Mice ; Osteoblasts/chemistry/physiology ; Osteoclasts/physiology ; Osteogenesis ; Protein Binding ; Protein Structure, Tertiary ; RNA Interference ; RNA, Messenger/genetics/metabolism ; Transcriptional Activation ; Transfection ; Ubiquitin/metabolism ; Ubiquitin-Protein Ligases/chemistry/metabolism ; Zinc Fingers
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  • 89
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    Chemical rescue of a mutant enzyme in living cells (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-03-04
    Description: The restoration of catalytic activity to mutant enzymes by small molecules is well established for in vitro systems. Here, we show that the protein tyrosine kinase Src arginine-388--〉alanine (R388A) mutant can be rescued in live cells with the use of the small molecule imidazole. Cellular rescue of a viral Src homolog was rapid and reversible and conferred predicted oncogenic properties. Using chemical rescue in combination with mass spectrometry, we confirmed six known Src kinase substrates and identified several new protein targets. Chemical rescue data suggest that cellular Src is active under basal conditions. Rescue of R388A cellular Src provided insights into the mitogen-activated protein kinase pathway. This chemical rescue approach will likely have many applications in cell signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Qiao, Yingfeng -- Molina, Henrik -- Pandey, Akhilesh -- Zhang, Jin -- Cole, Philip A -- New York, N.Y. -- Science. 2006 Mar 3;311(5765):1293-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16513984" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Cell Line ; Cell Transformation, Neoplastic ; Fluorescence Resonance Energy Transfer ; Gene Expression Profiling ; Gene Expression Regulation ; Growth Substances/metabolism/pharmacology ; Humans ; Imidazoles/*metabolism/pharmacology ; Kinetics ; Mice ; Mitogen-Activated Protein Kinases/metabolism ; Mutation ; Nuclear Proteins/metabolism ; Oligonucleotide Array Sequence Analysis ; Phenotype ; Phosphorylation ; Phosphotyrosine/metabolism ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins pp60(c-src)/*genetics/*metabolism ; Recombinant Proteins/metabolism ; Transfection ; src Homology Domains
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  • 90
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    RIG-I-mediated antiviral responses to single-stranded RNA bearing 5'-phosphates (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-10-14
    Description: Double-stranded RNA (dsRNA) produced during viral replication is believed to be the critical trigger for activation of antiviral immunity mediated by the RNA helicase enzymes retinoic acid-inducible gene I (RIG-I) and melanoma differentiation-associated gene 5 (MDA5). We showed that influenza A virus infection does not generate dsRNA and that RIG-I is activated by viral genomic single-stranded RNA (ssRNA) bearing 5'-phosphates. This is blocked by the influenza protein nonstructured protein 1 (NS1), which is found in a complex with RIG-I in infected cells. These results identify RIG-I as a ssRNA sensor and potential target of viral immune evasion and suggest that its ability to sense 5'-phosphorylated RNA evolved in the innate immune system as a means of discriminating between self and nonself.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pichlmair, Andreas -- Schulz, Oliver -- Tan, Choon Ping -- Naslund, Tanja I -- Liljestrom, Peter -- Weber, Friedemann -- Reis e Sousa, Caetano -- New York, N.Y. -- Science. 2006 Nov 10;314(5801):997-1001. Epub 2006 Oct 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunobiology Laboratory, Cancer Research UK, London Research Institute, London WC2A 3PX, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17038589" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cells, Cultured ; Cytoplasm/metabolism/virology ; DEAD-box RNA Helicases/genetics/*metabolism ; Dendritic Cells/virology ; Encephalomyocarditis virus/genetics/immunology/metabolism ; Genome, Viral ; Humans ; *Immunity, Innate ; Influenza A virus/*genetics/*immunology/metabolism/physiology ; Interferon-alpha/biosynthesis ; Interferon-beta/biosynthesis ; Mice ; Mice, Inbred C57BL ; Phosphates/metabolism ; Phosphorylation ; RNA Caps/metabolism ; RNA, Double-Stranded/metabolism ; RNA, Viral/chemistry/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Transfection ; Vesicular stomatitis Indiana virus/genetics/immunology/metabolism ; Viral Nonstructural Proteins/genetics/metabolism ; Virus Replication
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  • 91
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    Kaposi's sarcoma-associated herpesvirus fusion-entry receptor: cystine transporter xCT (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-04-01
    Description: Kaposi's sarcoma-associated herpesvirus (KSHV, human herpesvirus 8) is the causative agent of Kaposi's sarcoma and other lymphoproliferative syndromes often associated with HIV/AIDS. Functional complementary DNA selection for a receptor mediating KSHV cell fusion identified xCT, the 12-transmembrane light chain of the human cystine/glutamate exchange transporter system x-c. Expression of recombinant xCT rendered otherwise not susceptible target cells permissive for both KSHV cell fusion and virion entry. Antibodies against xCT blocked KSHV fusion and entry with naturally permissive target cells. KSHV target cell permissiveness correlated closely with endogenous expression of xCT messenger RNA and protein in diverse human and nonhuman cell types.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaleeba, Johnan A R -- Berger, Edward A -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2006 Mar 31;311(5769):1921-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16574866" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Transport System y+/genetics/immunology/*metabolism ; Animals ; Cell Fusion ; Cell Line ; Cell Line, Tumor ; DNA, Complementary ; Herpesvirus 8, Human/*metabolism ; Humans ; Immune Sera ; Mice ; RNA, Messenger/analysis/genetics ; Receptors, Virus/genetics/immunology/*metabolism ; Recombinant Proteins/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Transfection
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  • 92
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    Regulation of B cell tolerance by the lupus susceptibility gene Ly108 (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-06-17
    Description: The susceptibility locus for the autoimmune disease lupus on murine chromosome 1, Sle1z/Sle1bz, and the orthologous human locus are associated with production of autoantibody to chromatin. We report that the presence of Sle1z/Sle1bz impairs B cell anergy, receptor revision, and deletion. Members of the SLAM costimulatory molecule family constitute prime candidates for Sle1bz, among which the Ly108.1 isoform of the Ly108 gene was most highly expressed in immature B cells from lupus-prone B6.Sle1z mice. The normal Ly108.2 allele, but not the lupus-associated Ly108.1 allele, was found to sensitize immature B cells to deletion and RAG reexpression. As a potential regulator of tolerance checkpoints, Ly108 may censor self-reactive B cells, hence safeguarding against autoimmunity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kumar, Kirthi Raman -- Li, Liunan -- Yan, Mei -- Bhaskarabhatla, Madhavi -- Mobley, Angela B -- Nguyen, Charles -- Mooney, Jill M -- Schatzle, John D -- Wakeland, Edward K -- Mohan, Chandra -- AI54902/AI/NIAID NIH HHS/ -- NIH RO1 AR44894/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Jun 16;312(5780):1665-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine (Rheumatology), 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/16778059" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Ly/*genetics ; Autoantigens/immunology ; B-Lymphocytes/*immunology ; Bone Marrow Cells/immunology ; Cell Death ; Cell Line, Tumor ; Cells, Cultured ; Clonal Anergy ; Clonal Deletion ; *Genetic Predisposition to Disease ; *Immune Tolerance ; Lupus Erythematosus, Systemic/*genetics/immunology ; Mice ; Mice, Transgenic ; Multifactorial Inheritance ; Muramidase/immunology ; Receptors, Antigen, B-Cell/immunology ; Spleen/immunology ; Transfection
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  • 93
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    Structure and receptor specificity of the hemagglutinin from an H5N1 influenza virus (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-03-18
    Description: The hemagglutinin (HA) structure at 2.9 angstrom resolution, from a highly pathogenic Vietnamese H5N1 influenza virus, is more related to the 1918 and other human H1 HAs than to a 1997 duck H5 HA. Glycan microarray analysis of this Viet04 HA reveals an avian alpha2-3 sialic acid receptor binding preference. Introduction of mutations that can convert H1 serotype HAs to human alpha2-6 receptor specificity only enhanced or reduced affinity for avian-type receptors. However, mutations that can convert avian H2 and H3 HAs to human receptor specificity, when inserted onto the Viet04 H5 HA framework, permitted binding to a natural human alpha2-6 glycan, which suggests a path for this H5N1 virus to gain a foothold in the human population.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stevens, James -- Blixt, Ola -- Tumpey, Terrence M -- Taubenberger, Jeffery K -- Paulson, James C -- Wilson, Ian A -- AI058113/AI/NIAID NIH HHS/ -- AI42266/AI/NIAID NIH HHS/ -- CA55896/CA/NCI NIH HHS/ -- GM060938/GM/NIGMS NIH HHS/ -- GM062116/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Apr 21;312(5772):404-10. Epub 2006 Mar 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA. jstevens@scripps.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16543414" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amino Acid Substitution ; Animals ; Antigenic Variation ; Binding Sites ; Birds ; Carbohydrate Conformation ; Cloning, Molecular ; Crystallography, X-Ray ; Glycosylation ; Hemagglutinin Glycoproteins, Influenza ; Virus/*chemistry/genetics/immunology/*metabolism ; Humans ; Influenza A Virus, H5N1 Subtype/*chemistry/genetics/metabolism/*pathogenicity ; Lung/virology ; Models, Molecular ; Molecular Sequence Data ; Mutation ; Polysaccharides/metabolism ; Protein Conformation ; Protein Folding ; Protein Structure, Tertiary ; Receptors, Virus/chemistry/*metabolism ; Respiratory Mucosa/virology ; Sialic Acids/chemistry/metabolism ; Species Specificity ; Virulence
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  • 94
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    Dynamic nuclear actin assembly by Arp2/3 complex and a baculovirus WASP-like protein (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-10-21
    Description: Diverse bacterial and viral pathogens induce actin polymerization in the cytoplasm of host cells to facilitate infection. Here, we describe a pathogenic mechanism for promoting dynamic actin assembly in the nucleus to enable viral replication. The baculovirus Autographa californica multiple nucleopolyhedrovirus induced nuclear actin polymerization by translocating the host actin-nucleating Arp2/3 complex into the nucleus, where it was activated by p78/83, a viral Wiskott-Aldrich syndrome protein (WASP)-like protein. Nuclear actin assembly by p78/83 and Arp2/3 complex was essential for viral progeny production. Recompartmentalizing dynamic host actin may represent a conserved mode of pathogenesis and reflect viral manipulation of normal functions of nuclear actin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goley, Erin D -- Ohkawa, Taro -- Mancuso, Joel -- Woodruff, Jeffrey B -- D'Alessio, Joseph A -- Cande, W Zacheus -- Volkman, Loy E -- Welch, Matthew D -- AI054693/AI/NIAID NIH HHS/ -- GM59609/GM/NIGMS NIH HHS/ -- R01 GM059609/GM/NIGMS NIH HHS/ -- R01 GM059609-07/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Oct 20;314(5798):464-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17053146" target="_blank"〉PubMed〈/a〉
    Keywords: Actin-Related Protein 2-3 Complex/*metabolism ; Actins/*metabolism ; Animals ; Biopolymers/metabolism ; Cell Line ; Cell Nucleus/*metabolism ; Fluorescence Recovery After Photobleaching ; Moths ; Mutation ; Nucleocapsid/metabolism/ultrastructure ; Nucleopolyhedrovirus/genetics/*physiology ; Transfection ; Viral Proteins/chemistry/genetics/isolation & purification/*metabolism ; Virion/ultrastructure ; Virus Replication ; Wiskott-Aldrich Syndrome Protein/chemistry
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  • 95
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    Methylation of tRNAAsp by the DNA methyltransferase homolog Dnmt2 (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-01-21
    Description: The sequence and the structure of DNA methyltransferase-2 (Dnmt2) bear close affinities to authentic DNA cytosine methyltransferases. A combined genetic and biochemical approach revealed that human DNMT2 did not methylate DNA but instead methylated a small RNA; mass spectrometry showed that this RNA is aspartic acid transfer RNA (tRNA(Asp)) and that DNMT2 specifically methylated cytosine 38 in the anticodon loop. The function of DNMT2 is highly conserved, and human DNMT2 protein restored methylation in vitro to tRNA(Asp) from Dnmt2-deficient strains of mouse, Arabidopsis thaliana, and Drosophila melanogaster in a manner that was dependent on preexisting patterns of modified nucleosides. Indirect sequence recognition is also a feature of eukaryotic DNA methyltransferases, which may have arisen from a Dnmt2-like RNA methyltransferase.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goll, Mary Grace -- Kirpekar, Finn -- Maggert, Keith A -- Yoder, Jeffrey A -- Hsieh, Chih-Lin -- Zhang, Xiaoyu -- Golic, Kent G -- Jacobsen, Steven E -- Bestor, Timothy H -- New York, N.Y. -- Science. 2006 Jan 20;311(5759):395-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics and Development, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16424344" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anticodon ; Arabidopsis/genetics/physiology ; Arabidopsis Proteins/genetics ; Catalytic Domain ; Cytosine/metabolism ; DNA (Cytosine-5-)-Methyltransferase/chemistry/genetics/*metabolism ; Drosophila Proteins/genetics ; Drosophila melanogaster/genetics/physiology ; Evolution, Molecular ; Humans ; Mass Spectrometry ; Methylation ; Mice ; Mutation ; NIH 3T3 Cells ; RNA, Plant/metabolism ; RNA, Transfer, Asp/chemistry/*metabolism ; Transfection
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    Human catechol-O-methyltransferase haplotypes modulate protein expression by altering mRNA secondary structure (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-12-23
    Description: Catechol-O-methyltransferase (COMT) is a key regulator of pain perception, cognitive function, and affective mood. Three common haplotypes of the human COMT gene, divergent in two synonymous and one nonsynonymous position, code for differences in COMT enzymatic activity and are associated with pain sensitivity. Haplotypes divergent in synonymous changes exhibited the largest difference in COMT enzymatic activity, due to a reduced amount of translated protein. The major COMT haplotypes varied with respect to messenger RNA local stem-loop structures, such that the most stable structure was associated with the lowest protein levels and enzymatic activity. Site-directed mutagenesis that eliminated the stable structure restored the amount of translated protein. These data highlight the functional significance of synonymous variations and suggest the importance of haplotypes over single-nucleotide polymorphisms for analysis of genetic variations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nackley, A G -- Shabalina, S A -- Tchivileva, I E -- Satterfield, K -- Korchynskyi, O -- Makarov, S S -- Maixner, W -- Diatchenko, L -- New York, N.Y. -- Science. 2006 Dec 22;314(5807):1930-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Neurosensory Disorders, University of North Carolina, Chapel Hill, NC 27599, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17185601" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Amino Acid Substitution ; Animals ; Base Pairing ; Base Sequence ; Catechol O-Methyltransferase/*biosynthesis/*genetics/metabolism ; *Haplotypes ; Humans ; Molecular Sequence Data ; Mutagenesis, Site-Directed ; *Nucleic Acid Conformation ; PC12 Cells ; Pain/genetics ; Phenotype ; Polymorphism, Single Nucleotide ; RNA Stability ; RNA, Messenger/*chemistry/genetics/metabolism ; Rats ; Transfection
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  • 97
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    Community genomics among stratified microbial assemblages in the ocean's interior (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-01-28
    Description: Microbial life predominates in the ocean, yet little is known about its genomic variability, especially along the depth continuum. We report here genomic analyses of planktonic microbial communities in the North Pacific Subtropical Gyre, from the ocean's surface to near-sea floor depths. Sequence variation in microbial community genes reflected vertical zonation of taxonomic groups, functional gene repertoires, and metabolic potential. The distributional patterns of microbial genes suggested depth-variable community trends in carbon and energy metabolism, attachment and motility, gene mobility, and host-viral interactions. Comparative genomic analyses of stratified microbial communities have the potential to provide significant insight into higher-order community organization and dynamics.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉DeLong, Edward F -- Preston, Christina M -- Mincer, Tracy -- Rich, Virginia -- Hallam, Steven J -- Frigaard, Niels-Ulrik -- Martinez, Asuncion -- Sullivan, Matthew B -- Edwards, Robert -- Brito, Beltran Rodriguez -- Chisholm, Sallie W -- Karl, David M -- New York, N.Y. -- Science. 2006 Jan 27;311(5760):496-503.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Massachusetts Institute of Technology, Cambridge, MA 02139, USA. delong@mit.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16439655" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Archaea/classification/*genetics/metabolism ; Archaeal Proteins/chemistry/genetics/metabolism ; Bacteria/classification/*genetics/metabolism ; Bacterial Proteins/chemistry/genetics/metabolism ; Bacteriophages/genetics ; Base Sequence ; Cloning, Molecular ; Cluster Analysis ; Computational Biology ; Cosmids ; DNA, Viral/chemistry/genetics ; Ecosystem ; Gene Library ; *Genes, Archaeal ; *Genes, Bacterial ; Genes, rRNA ; *Genomics ; Molecular Sequence Data ; Pacific Ocean ; Seawater/*microbiology ; Sequence Analysis, DNA ; Water Microbiology
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    Germline mutations in genes within the MAPK pathway cause cardio-facio-cutaneous syndrome (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-01-28
    Description: Cardio-facio-cutaneous (CFC) syndrome is a sporadic developmental disorder involving characteristic craniofacial features, cardiac defects, ectodermal abnormalities, and developmental delay. We demonstrate that heterogeneous de novo missense mutations in three genes within the mitogen-activated protein kinase (MAPK) pathway cause CFC syndrome. The majority of cases (18 out of 23) are caused by mutations in BRAF, a gene frequently mutated in cancer. Of the 11 mutations identified, two result in amino acid substitutions that occur in tumors, but most are unique and suggest previously unknown mechanisms of B-Raf activation. Furthermore, three of five individuals without BRAF mutations had missense mutations in either MEK1 or MEK2, downstream effectors of B-Raf. Our findings highlight the involvement of the MAPK pathway in human development and will provide a molecular diagnosis of CFC syndrome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rodriguez-Viciana, Pablo -- Tetsu, Osamu -- Tidyman, William E -- Estep, Anne L -- Conger, Brenda A -- Cruz, Molly Santa -- McCormick, Frank -- Rauen, Katherine A -- HD048502/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2006 Mar 3;311(5765):1287-90. Epub 2006 Jan 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Comprehensive Cancer Center and Cancer Research Institute, University of California, San Francisco, CA 94115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16439621" target="_blank"〉PubMed〈/a〉
    Keywords: Abnormalities, Multiple/*genetics ; Adolescent ; Adult ; Amino Acid Substitution ; Child ; Child, Preschool ; Craniofacial Abnormalities/genetics ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Female ; *Germ-Line Mutation ; Growth Disorders/genetics ; Heart Defects, Congenital/genetics ; Humans ; Infant ; MAP Kinase Kinase 1/genetics ; MAP Kinase Kinase 2/genetics ; MAP Kinase Kinase Kinases/metabolism ; MAP Kinase Signaling System ; Male ; Mitogen-Activated Protein Kinases/genetics/*metabolism ; Mutation, Missense ; Phosphorylation ; Proto-Oncogene Proteins B-raf/genetics ; Skin Abnormalities/genetics ; Syndrome ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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    Nuclear gene indicates coat-color polymorphism in mammoths (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-07-11
    Description: By amplifying the melanocortin type 1 receptor from the woolly mammoth, we can report the complete nucleotide sequence of a nuclear-encoded gene from an extinct species. We found two alleles and show that one allele produces a functional protein whereas the other one encodes a protein with strongly reduced activity. This finding suggests that mammoths may have been polymorphic in coat color, with both dark- and light-haired individuals co-occurring.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rompler, Holger -- Rohland, Nadin -- Lalueza-Fox, Carles -- Willerslev, Eske -- Kuznetsova, Tatyana -- Rabeder, Gernot -- Bertranpetit, Jaume -- Schoneberg, Torsten -- Hofreiter, Michael -- New York, N.Y. -- Science. 2006 Jul 7;313(5783):62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Biochemistry, Institute of Biochemistry, Medical Faculty, University of Leipzig, 04103 Leipzig, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16825562" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Amino Acid Substitution ; Animals ; Cell Nucleus/genetics ; Elephants/*genetics ; Genotype ; *Hair ; Hair Color/*genetics ; Molecular Sequence Data ; Mutation ; Phenotype ; Pigmentation/*genetics ; Polymerase Chain Reaction ; *Polymorphism, Genetic ; Polymorphism, Single Nucleotide ; Receptor, Melanocortin, Type 1/chemistry/*genetics ; Transfection ; alpha-MSH/analogs & derivatives/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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    Impaired control of IRES-mediated translation in X-linked dyskeratosis congenita (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-05-13
    Description: The DKC1 gene encodes a pseudouridine synthase that modifies ribosomal RNA (rRNA). DKC1 is mutated in people with X-linked dyskeratosis congenita (X-DC), a disease characterized by bone marrow failure, skin abnormalities, and increased susceptibility to cancer. How alterations in ribosome modification might lead to cancer and other features of the disease remains unknown. Using an unbiased proteomics strategy, we discovered a specific defect in IRES (internal ribosome entry site)-dependent translation in Dkc1(m) mice and in cells from X-DC patients. This defect results in impaired translation of messenger RNAs containing IRES elements, including those encoding the tumor suppressor p27(Kip1) and the antiapoptotic factors Bcl-xL and XIAP (X-linked Inhibitor of Apoptosis Protein). Moreover, Dkc1(m) ribosomes were unable to direct translation from IRES elements present in viral messenger RNAs. These findings reveal a potential mechanism by which defective ribosome activity leads to disease and cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yoon, Andrew -- Peng, Guang -- Brandenburger, Yves -- Zollo, Ornella -- Xu, Wei -- Rego, Eduardo -- Ruggero, Davide -- New York, N.Y. -- Science. 2006 May 12;312(5775):902-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Human Genetics Program, Fox Chase Cancer Center, Philadelphia, PA 19111, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16690864" target="_blank"〉PubMed〈/a〉
    Keywords: *5' Untranslated Regions ; Animals ; Cell Cycle Proteins/chemistry/*genetics/physiology ; Cell Line ; Cells, Cultured ; Cyclin-Dependent Kinase Inhibitor p27/biosynthesis/genetics ; Dyskeratosis Congenita/*genetics ; Humans ; Insect Viruses/genetics ; Lymphocytes/metabolism ; Male ; Mice ; Nuclear Proteins/chemistry/*genetics/physiology ; Oligonucleotide Array Sequence Analysis ; Point Mutation ; Polyribosomes/metabolism ; *Protein Biosynthesis ; Proteomics ; Pseudouridine/metabolism ; RNA Viruses/genetics ; RNA, Messenger/*genetics/metabolism ; RNA, Ribosomal/metabolism ; Transfection ; X-Linked Inhibitor of Apoptosis Protein/biosynthesis/genetics ; bcl-X Protein/biosynthesis/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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