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  • Cell Line  (944)
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  • American Association for the Advancement of Science (AAAS)  (2,308)
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  • 1
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    Local DNA topography correlates with functional noncoding regions of the human genome (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-03-17
    Description: The three-dimensional molecular structure of DNA, specifically the shape of the backbone and grooves of genomic DNA, can be dramatically affected by nucleotide changes, which can cause differences in protein-binding affinity and phenotype. We developed an algorithm to measure constraint on the basis of similarity of DNA topography among multiple species, using hydroxyl radical cleavage patterns to interrogate the solvent-accessible surface area of DNA. This algorithm found that 12% of bases in the human genome are evolutionarily constrained-double the number detected by nucleotide sequence-based algorithms. Topography-informed constrained regions correlated with functional noncoding elements, including enhancers, better than did regions identified solely on the basis of nucleotide sequence. These results support the idea that the molecular shape of DNA is under selection and can identify evolutionary history.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2749491/" 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/PMC2749491/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Parker, Stephen C J -- Hansen, Loren -- Abaan, Hatice Ozel -- Tullius, Thomas D -- Margulies, Elliott H -- R01 HG003541/HG/NHGRI NIH HHS/ -- R01 HG003541-03/HG/NHGRI NIH HHS/ -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2009 Apr 17;324(5925):389-92. doi: 10.1126/science.1169050. Epub 2009 Mar 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Bioinformatics Program, Boston University, Boston, MA 02215, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19286520" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Amino Acid Motifs ; Base Sequence ; Binding Sites ; Conserved Sequence ; DNA/*chemistry/genetics ; Deoxyribonuclease I/metabolism ; Early Growth Response Protein 1/genetics/metabolism ; Evolution, Molecular ; *Genome, Human ; Humans ; Mutant Proteins/metabolism ; Nucleic Acid Conformation ; Phenotype ; Polymorphism, Single Nucleotide ; Selection, Genetic
    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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    A crystal structure of the bifunctional antibiotic simocyclinone D8, bound to DNA gyrase (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-12-08
    Description: Simocyclinones are bifunctional antibiotics that inhibit bacterial DNA gyrase by preventing DNA binding to the enzyme. We report the crystal structure of the complex formed between the N-terminal domain of the Escherichia coli gyrase A subunit and simocyclinone D8, revealing two binding pockets that separately accommodate the aminocoumarin and polyketide moieties of the antibiotic. These are close to, but distinct from, the quinolone-binding site, consistent with our observations that several mutations in this region confer resistance to both agents. Biochemical studies show that the individual moieties of simocyclinone D8 are comparatively weak inhibitors of gyrase relative to the parent compound, but their combination generates a more potent inhibitor. Our results should facilitate the design of drug molecules that target these unexploited binding pockets.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Edwards, Marcus J -- Flatman, Ruth H -- Mitchenall, Lesley A -- Stevenson, Clare E M -- Le, Tung B K -- Clarke, Thomas A -- McKay, Adam R -- Fiedler, Hans-Peter -- Buttner, Mark J -- Lawson, David M -- Maxwell, Anthony -- Biotechnology and Biological Sciences Research Council/United Kingdom -- New York, N.Y. -- Science. 2009 Dec 4;326(5958):1415-8. doi: 10.1126/science.1179123.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Chemistry, John Innes Centre, Colney, Norwich NR4 7UH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965760" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Anti-Bacterial Agents/chemistry/metabolism/pharmacology ; Binding Sites ; Coumarins/chemistry/metabolism/pharmacology ; Crystallography, X-Ray ; DNA Gyrase/*chemistry/genetics/*metabolism ; DNA, Bacterial/metabolism ; Drug Resistance, Bacterial ; Escherichia coli/drug effects/*enzymology/genetics ; Glycosides/chemistry/metabolism/pharmacology ; Ligands ; Models, Molecular ; Molecular Sequence Data ; Molecular Weight ; Mutagenesis, Site-Directed ; Mutation ; Protein Multimerization ; Protein Structure, Tertiary ; Topoisomerase II Inhibitors
    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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    Hemagglutinin receptor binding avidity drives influenza A virus antigenic drift (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-11-11
    Description: Rapid antigenic evolution in the influenza A virus hemagglutinin precludes effective vaccination with existing vaccines. To understand this phenomenon, we passaged virus in mice immunized with influenza vaccine. Neutralizing antibodies selected mutants with single-amino acid hemagglutinin substitutions that increased virus binding to cell surface glycan receptors. Passaging these high-avidity binding mutants in naive mice, but not immune mice, selected for additional hemagglutinin substitutions that decreased cellular receptor binding avidity. Analyzing a panel of monoclonal antibody hemagglutinin escape mutants revealed a positive correlation between receptor binding avidity and escape from polyclonal antibodies. We propose that in response to variation in neutralizing antibody pressure between individuals, influenza A virus evolves by adjusting receptor binding avidity via amino acid substitutions throughout the hemagglutinin globular domain, many of which simultaneously alter antigenicity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2784927/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2784927/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hensley, Scott E -- Das, Suman R -- Bailey, Adam L -- Schmidt, Loren M -- Hickman, Heather D -- Jayaraman, Akila -- Viswanathan, Karthik -- Raman, Rahul -- Sasisekharan, Ram -- Bennink, Jack R -- Yewdell, Jonathan W -- GM 57073/GM/NIGMS NIH HHS/ -- U54 GM62116/GM/NIGMS NIH HHS/ -- Z01 AI001014-01/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2009 Oct 30;326(5953):734-6. doi: 10.1126/science.1178258.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19900932" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Neutralizing/immunology ; Antibodies, Viral/immunology ; Antigenic Variation/genetics/*immunology ; Cell Line ; Hemagglutinin Glycoproteins, Influenza Virus/genetics/immunology/*metabolism ; Influenza A Virus, H1N1 Subtype/genetics/*immunology ; Influenza Vaccines/immunology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Models, Immunological ; Mutation ; Receptors, Virus/*metabolism ; Serial Passage
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Biomedical research. Researchers generally happy with final stem cell rules (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-07-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holden, Constance -- New York, N.Y. -- Science. 2009 Jul 10;325(5937):131. doi: 10.1126/science.325_131.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19589969" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; *Embryo Research/economics ; *Embryonic Stem Cells ; Financing, Government ; *Guidelines as Topic ; Humans ; National Institutes of Health (U.S.) ; Registries ; *Research Support as Topic ; United States
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Structure of rotavirus outer-layer protein VP7 bound with a neutralizing Fab (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-06-13
    Description: Rotavirus outer-layer protein VP7 is a principal target of protective antibodies. Removal of free calcium ions (Ca2+) dissociates VP7 trimers into monomers, releasing VP7 from the virion, and initiates penetration-inducing conformational changes in the other outer-layer protein, VP4. We report the crystal structure at 3.4 angstrom resolution of VP7 bound with the Fab fragment of a neutralizing monoclonal antibody. The Fab binds across the outer surface of the intersubunit contact, which contains two Ca2+ sites. Mutations that escape neutralization by other antibodies suggest that the same region bears the epitopes of most neutralizing antibodies. The monovalent Fab is sufficient to neutralize infectivity. We propose that neutralizing antibodies against VP7 act by stabilizing the trimer, thereby inhibiting the uncoating trigger for VP4 rearrangement. A disulfide-linked trimer is a potential subunit immunogen.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2995306/" 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/PMC2995306/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Aoki, Scott T -- Settembre, Ethan C -- Trask, Shane D -- Greenberg, Harry B -- Harrison, Stephen C -- Dormitzer, Philip R -- AI-21362/AI/NIAID NIH HHS/ -- CA-13202/CA/NCI NIH HHS/ -- DK-56339/DK/NIDDK NIH HHS/ -- R37 CA013202/CA/NCI NIH HHS/ -- R37 CA013202-38/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Jun 12;324(5933):1444-7. doi: 10.1126/science.1170481.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Medicine, Children's Hospital, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19520960" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Antibodies, Monoclonal/chemistry/immunology/metabolism ; Antibodies, Viral/chemistry/*immunology/metabolism ; Antigens, Viral/*chemistry/genetics/*immunology/metabolism ; Binding Sites ; Binding Sites, Antibody ; Calcium/metabolism ; Capsid Proteins/*chemistry/genetics/*immunology/metabolism ; Crystallography, X-Ray ; Epitopes/immunology ; Immunoglobulin Fab Fragments/chemistry/*immunology/metabolism ; Models, Molecular ; Molecular Sequence Data ; Mutation ; Neutralization Tests ; Protein Folding ; Protein Multimerization ; Protein Structure, Tertiary ; Protein Subunits ; Recombinant Proteins/chemistry ; Rotavirus/*chemistry/immunology ; Serotyping
    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 P-glycoprotein reveals a molecular basis for poly-specific drug binding (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-03-28
    Description: P-glycoprotein (P-gp) detoxifies cells by exporting hundreds of chemically unrelated toxins but has been implicated in multidrug resistance (MDR) in the treatment of cancers. Substrate promiscuity is a hallmark of P-gp activity, thus a structural description of poly-specific drug-binding is important for the rational design of anticancer drugs and MDR inhibitors. The x-ray structure of apo P-gp at 3.8 angstroms reveals an internal cavity of approximately 6000 angstroms cubed with a 30 angstrom separation of the two nucleotide-binding domains. Two additional P-gp structures with cyclic peptide inhibitors demonstrate distinct drug-binding sites in the internal cavity capable of stereoselectivity that is based on hydrophobic and aromatic interactions. Apo and drug-bound P-gp structures have portals open to the cytoplasm and the inner leaflet of the lipid bilayer for drug entry. The inward-facing conformation represents an initial stage of the transport cycle that is competent for drug binding.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2720052/" 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/PMC2720052/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Aller, Stephen G -- Yu, Jodie -- Ward, Andrew -- Weng, Yue -- Chittaboina, Srinivas -- Zhuo, Rupeng -- Harrell, Patina M -- Trinh, Yenphuong T -- Zhang, Qinghai -- Urbatsch, Ina L -- Chang, Geoffrey -- F32 GM078914/GM/NIGMS NIH HHS/ -- F32 GM078914-03/GM/NIGMS NIH HHS/ -- GM073197/GM/NIGMS NIH HHS/ -- GM078914/GM/NIGMS NIH HHS/ -- GM61905/GM/NIGMS NIH HHS/ -- P50 GM073197/GM/NIGMS NIH HHS/ -- P50 GM073197-050002/GM/NIGMS NIH HHS/ -- R01 GM061905/GM/NIGMS NIH HHS/ -- R01 GM061905-09/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2009 Mar 27;323(5922):1718-22. doi: 10.1126/science.1168750.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Scripps Research Institute, 10550 North Torrey Pines Road, CB105, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19325113" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Amino Acid Sequence ; Animals ; Apoproteins/chemistry/metabolism ; Binding Sites ; Cell Membrane/chemistry ; Crystallography, X-Ray ; Hydrophobic and Hydrophilic Interactions ; Lipid Bilayers/chemistry ; Mice ; Models, Molecular ; Molecular Sequence Data ; P-Glycoprotein/antagonists & inhibitors/*chemistry/*metabolism ; Peptides, Cyclic/*chemistry/*metabolism ; Protein Binding ; Protein Conformation ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Stereoisomerism ; Verapamil/metabolism/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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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
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  • 8
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    DNA binding site sequence directs glucocorticoid receptor structure and activity (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-04-18
    Description: Genes are not simply turned on or off, but instead their expression is fine-tuned to meet the needs of a cell. How genes are modulated so precisely is not well understood. The glucocorticoid receptor (GR) regulates target genes by associating with specific DNA binding sites, the sequences of which differ between genes. Traditionally, these binding sites have been viewed only as docking sites. Using structural, biochemical, and cell-based assays, we show that GR binding sequences, differing by as little as a single base pair, differentially affect GR conformation and regulatory activity. We therefore propose that DNA is a sequence-specific allosteric ligand of GR that tailors the activity of the receptor toward specific target genes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2777810/" 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/PMC2777810/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Meijsing, Sebastiaan H -- Pufall, Miles A -- So, Alex Y -- Bates, Darren L -- Chen, Lin -- Yamamoto, Keith R -- GM08537/GM/NIGMS NIH HHS/ -- R01 CA020535/CA/NCI NIH HHS/ -- R01 CA020535-31/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2009 Apr 17;324(5925):407-10. doi: 10.1126/science.1164265.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular and Molecular Pharmacology, University of California, San Francisco, CA 94158, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19372434" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Binding Sites ; Cell Line, Tumor ; Crystallography, X-Ray ; DNA/*chemistry/*metabolism ; Humans ; Ligands ; Models, Molecular ; Mutation ; Protein Conformation ; Protein Isoforms/chemistry/metabolism ; Protein Multimerization ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Rats ; Receptors, Glucocorticoid/chemistry/genetics/*metabolism ; Transcriptional Activation
    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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  • 9
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    Biomedical research. A first step in relaxing restrictions on stem cell research (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-03-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holden, Constance -- New York, N.Y. -- Science. 2009 Mar 13;323(5920):1412-3. doi: 10.1126/science.323.5920.1412.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19286523" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Embryo Research/economics/*legislation & jurisprudence ; *Embryonic Stem Cells ; Financing, Government/legislation & jurisprudence ; Guidelines as Topic ; Humans ; National Institutes of Health (U.S.) ; Pluripotent Stem Cells ; Research Support as Topic/*legislation & jurisprudence ; United States
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    Biochemistry. Through a mirror, differently (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-03-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sheps, Jonathan A -- New York, N.Y. -- Science. 2009 Mar 27;323(5922):1679-80. doi: 10.1126/science.1172428.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Genetics and Developmental Biology, BC Cancer Research Centre, British Columbia Cancer Agency, Vancouver, BC V5Z 1L3 Canada. jsheps@bccrc.ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19325102" target="_blank"〉PubMed〈/a〉
    Keywords: Binding Sites ; Biological Transport ; Crystallography, X-Ray ; Drug Design ; Lipid Bilayers/chemistry ; Models, Biological ; Oligopeptides/chemistry/metabolism ; P-Glycoprotein/*chemistry/*metabolism ; Peptides, Cyclic/*chemistry/*metabolism ; Protein Binding ; Protein Conformation ; Stereoisomerism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 11
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    Reversal of RNA dominance by displacement of protein sequestered on triplet repeat RNA (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-07-18
    Description: Genomic expansions of simple tandem repeats can give rise to toxic RNAs that contain expanded repeats. In myotonic dystrophy, the expression of expanded CUG repeats (CUGexp) causes abnormal regulation of alternative splicing and neuromuscular dysfunction. We used a transgenic mouse model to show that derangements of myotonic dystrophy are reversed by a morpholino antisense oligonucleotide, CAG25, that binds to CUGexp RNA and blocks its interaction with muscleblind-like 1 (MBNL1), a CUGexp-binding protein. CAG25 disperses nuclear foci of CUGexp RNA and reduces the overall burden of this toxic RNA. As MBNL1 is released from sequestration, the defect of alternative splicing regulation is corrected, thereby restoring ion channel function. These findings suggest an alternative use of antisense methods, to inhibit deleterious interactions of proteins with pathogenic RNAs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4109973/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4109973/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wheeler, Thurman M -- Sobczak, Krzysztof -- Lueck, John D -- Osborne, Robert J -- Lin, Xiaoyan -- Dirksen, Robert T -- Thornton, Charles A -- AR/NS48143/AR/NIAMS NIH HHS/ -- AR046806/AR/NIAMS NIH HHS/ -- K08 NS064293/NS/NINDS NIH HHS/ -- K24 AR048143/AR/NIAMS NIH HHS/ -- NIDCR-T32DE07202/DE/NIDCR NIH HHS/ -- R01 AR046806/AR/NIAMS NIH HHS/ -- R01 AR049077/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 2009 Jul 17;325(5938):336-9. doi: 10.1126/science.1173110.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Neurology, Pharmacology and Physiology, University of Rochester, Rochester, NY 14642, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19608921" target="_blank"〉PubMed〈/a〉
    Keywords: 3' Untranslated Regions/genetics/*metabolism ; Actins/genetics ; Alternative Splicing ; Animals ; Cell Line ; Cell Nucleus/metabolism ; Chloride Channels/metabolism ; DNA-Binding Proteins/*metabolism ; Humans ; Mice ; Mice, Knockout ; Mice, Transgenic ; Myotonic Dystrophy/*drug therapy/*genetics/metabolism ; Myotonin-Protein Kinase ; Oligodeoxyribonucleotides, Antisense/*pharmacology/therapeutic use ; Protein-Serine-Threonine Kinases/genetics ; RNA, Messenger/genetics ; RNA-Binding Proteins/*metabolism ; Transcription, Genetic ; *Trinucleotide Repeat Expansion
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Biomedical policy. Draft stem cell guidelines please many, disappoint some (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-04-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holden, Constance -- Kaiser, Jocelyn -- New York, N.Y. -- Science. 2009 Apr 24;324(5926):446. doi: 10.1126/science.324_446.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19390007" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Embryo Research/economics/*legislation & jurisprudence ; Embryonic Stem Cells ; Financing, Government/*legislation & jurisprudence ; Guidelines as Topic ; Humans ; National Institutes of Health (U.S.) ; Public Policy ; Research Support as Topic/*legislation & jurisprudence ; *Stem Cells ; United States
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 13
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    Diversity and complexity in DNA recognition by transcription factors (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-05-16
    Description: Sequence preferences of DNA binding proteins are a primary mechanism by which cells interpret the genome. Despite the central importance of these proteins in physiology, development, and evolution, comprehensive DNA binding specificities have been determined experimentally for only a few proteins. Here, we used microarrays containing all 10-base pair sequences to examine the binding specificities of 104 distinct mouse DNA binding proteins representing 22 structural classes. Our results reveal a complex landscape of binding, with virtually every protein analyzed possessing unique preferences. Roughly half of the proteins each recognized multiple distinctly different sequence motifs, challenging our molecular understanding of how proteins interact with their DNA binding sites. This complexity in DNA recognition may be important in gene regulation and in the evolution of transcriptional regulatory networks.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2905877/" 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/PMC2905877/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Badis, Gwenael -- Berger, Michael F -- Philippakis, Anthony A -- Talukder, Shaheynoor -- Gehrke, Andrew R -- Jaeger, Savina A -- Chan, Esther T -- Metzler, Genita -- Vedenko, Anastasia -- Chen, Xiaoyu -- Kuznetsov, Hanna -- Wang, Chi-Fong -- Coburn, David -- Newburger, Daniel E -- Morris, Quaid -- Hughes, Timothy R -- Bulyk, Martha L -- R01 HG003985/HG/NHGRI NIH HHS/ -- R01 HG003985-01/HG/NHGRI NIH HHS/ -- R01 HG003985-02/HG/NHGRI NIH HHS/ -- R01 HG003985-03/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2009 Jun 26;324(5935):1720-3. doi: 10.1126/science.1162327. Epub 2009 May 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Banting and Best Department of Medical Research, University of Toronto, Toronto, ON M5S 3E1, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19443739" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Amino Acid Sequence ; Animals ; Base Sequence ; Binding Sites ; DNA/chemistry/*metabolism ; Electrophoretic Mobility Shift Assay ; Gene Expression Regulation ; Gene Regulatory Networks ; Humans ; Mice ; Protein Array Analysis ; Protein Binding ; Protein Structure, Tertiary ; Recombinant Fusion Proteins/chemistry/metabolism ; Transcription Factors/*chemistry/*metabolism
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  • 14
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    S-nitrosylation of Drp1 mediates beta-amyloid-related mitochondrial fission and neuronal injury (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-04-04
    Description: Mitochondria continuously undergo two opposing processes, fission and fusion. The disruption of this dynamic equilibrium may herald cell injury or death and may contribute to developmental and neurodegenerative disorders. Nitric oxide functions as a signaling molecule, but in excess it mediates neuronal injury, in part via mitochondrial fission or fragmentation. However, the underlying mechanism for nitric oxide-induced pathological fission remains unclear. We found that nitric oxide produced in response to beta-amyloid protein, thought to be a key mediator of Alzheimer's disease, triggered mitochondrial fission, synaptic loss, and neuronal damage, in part via S-nitrosylation of dynamin-related protein 1 (forming SNO-Drp1). Preventing nitrosylation of Drp1 by cysteine mutation abrogated these neurotoxic events. SNO-Drp1 is increased in brains of human Alzheimer's disease patients and may thus contribute to the pathogenesis of neurodegeneration.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2823371/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2823371/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cho, Dong-Hyung -- Nakamura, Tomohiro -- Fang, Jianguo -- Cieplak, Piotr -- Godzik, Adam -- Gu, Zezong -- Lipton, Stuart A -- P01 ES016738/ES/NIEHS NIH HHS/ -- P01 ES016738-01/ES/NIEHS NIH HHS/ -- P01 ES016738-010003/ES/NIEHS NIH HHS/ -- P01 ES016738-02/ES/NIEHS NIH HHS/ -- P01 ES016738-020003/ES/NIEHS NIH HHS/ -- P01 HD029587/HD/NICHD NIH HHS/ -- P01 HD029587-16/HD/NICHD NIH HHS/ -- P01 HD29587/HD/NICHD NIH HHS/ -- P30 NS057096/NS/NINDS NIH HHS/ -- P30 NS057096-04/NS/NINDS NIH HHS/ -- R01 EY005477/EY/NEI NIH HHS/ -- R01 EY005477-25/EY/NEI NIH HHS/ -- R01 EY05477/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 2009 Apr 3;324(5923):102-5. doi: 10.1126/science.1171091.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Neuroscience, Aging, and Stem Cell Research, Burnham Institute for Medical Research, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19342591" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/metabolism/pathology ; Amino Acid Motifs ; Amyloid beta-Peptides/*metabolism/pharmacology ; Animals ; Cell Line ; Cell Line, Tumor ; Cerebral Cortex/cytology ; Cysteine/analogs & derivatives/genetics/metabolism/pharmacology ; Female ; GTP Phosphohydrolases/chemistry/*metabolism ; Humans ; Male ; Mice ; Mice, Transgenic ; Microtubule-Associated Proteins/chemistry/*metabolism ; Mitochondria/drug effects/physiology/*ultrastructure ; Mitochondrial Proteins/chemistry/*metabolism ; Models, Molecular ; Mutation ; Neurons/drug effects/*ultrastructure ; Nitric Oxide/*metabolism ; Peptide Fragments/metabolism/pharmacology ; Protein Multimerization ; Protein Structure, Tertiary ; S-Nitrosothiols/pharmacology
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  • 15
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    Regulation of neuronal survival factor MEF2D by chaperone-mediated autophagy (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-01-03
    Description: Chaperone-mediated autophagy controls the degradation of selective cytosolic proteins and may protect neurons against degeneration. In a neuronal cell line, we found that chaperone-mediated autophagy regulated the activity of myocyte enhancer factor 2D (MEF2D), a transcription factor required for neuronal survival. MEF2D was observed to continuously shuttle to the cytoplasm, interact with the chaperone Hsc70, and undergo degradation. Inhibition of chaperone-mediated autophagy caused accumulation of inactive MEF2D in the cytoplasm. MEF2D levels were increased in the brains of alpha-synuclein transgenic mice and patients with Parkinson's disease. Wild-type alpha-synuclein and a Parkinson's disease-associated mutant disrupted the MEF2D-Hsc70 binding and led to neuronal death. Thus, chaperone-mediated autophagy modulates the neuronal survival machinery, and dysregulation of this pathway is associated with Parkinson's disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2666000/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2666000/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yang, Qian -- She, Hua -- Gearing, Marla -- Colla, Emanuela -- Lee, Michael -- Shacka, John J -- Mao, Zixu -- AG023695/AG/NIA NIH HHS/ -- NS038065/NS/NINDS NIH HHS/ -- NS048254/NS/NINDS NIH HHS/ -- NS055077/NS/NINDS NIH HHS/ -- NS47466/NS/NINDS NIH HHS/ -- NS57098/NS/NINDS NIH HHS/ -- P30 NS055077/NS/NINDS NIH HHS/ -- P30 NS055077-01A2/NS/NINDS NIH HHS/ -- P50 AG025688/AG/NIA NIH HHS/ -- P50 AG025688-03/AG/NIA NIH HHS/ -- R01 AG023695/AG/NIA NIH HHS/ -- R01 AG023695-02/AG/NIA NIH HHS/ -- R01 AG023695-03/AG/NIA NIH HHS/ -- R01 AG023695-04/AG/NIA NIH HHS/ -- R01 AG023695-05/AG/NIA NIH HHS/ -- R01 NS048254/NS/NINDS NIH HHS/ -- R01 NS048254-02/NS/NINDS NIH HHS/ -- R01 NS048254-03/NS/NINDS NIH HHS/ -- R01 NS048254-04/NS/NINDS NIH HHS/ -- R01 NS048254-05/NS/NINDS NIH HHS/ -- R01 NS048254-06/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2009 Jan 2;323(5910):124-7. doi: 10.1126/science.1166088.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Emory University School of Medicine, Atlanta, GA 30322, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19119233" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Ammonium Chloride/pharmacology ; Animals ; *Autophagy ; Brain/metabolism ; Cell Line ; Cell Nucleus/metabolism ; Cell Survival ; Cytoplasm/metabolism ; DNA/metabolism ; HSC70 Heat-Shock Proteins/metabolism ; Lysosomal-Associated Membrane Protein 2/metabolism ; Lysosomes/metabolism ; MADS Domain Proteins/*metabolism ; MEF2 Transcription Factors ; Mice ; Mice, Transgenic ; Molecular Chaperones/*metabolism ; Myogenic Regulatory Factors/chemistry/*metabolism ; Neurons/cytology/*metabolism ; Parkinson Disease/metabolism ; Protein Binding ; Protein Transport ; Rats ; Rats, Long-Evans ; alpha-Synuclein/genetics/metabolism
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    Genome-wide RNAi screen identifies Letm1 as a mitochondrial Ca2+/H+ antiporter (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-10-03
    Description: Mitochondria are integral components of cellular calcium (Ca2+) signaling. Calcium stimulates mitochondrial adenosine 5'-triphosphate production, but can also initiate apoptosis. In turn, cytoplasmic Ca2+ concentrations are regulated by mitochondria. Although several transporter and ion-channel mechanisms have been measured in mitochondria, the molecules that govern Ca2+ movement across the inner mitochondrial membrane are unknown. We searched for genes that regulate mitochondrial Ca2+ and H+ concentrations using a genome-wide Drosophila RNA interference (RNAi) screen. The mammalian homolog of one Drosophila gene identified in the screen, Letm1, was found to specifically mediate coupled Ca2+/H+ exchange. RNAi knockdown, overexpression, and liposome reconstitution of the purified Letm1 protein demonstrate that Letm1 is a mitochondrial Ca2+/H+ antiporter.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4067766/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4067766/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jiang, Dawei -- Zhao, Linlin -- Clapham, David E -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Oct 2;326(5949):144-7. doi: 10.1126/science.1175145.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cardiology, Howard Hughes Medical Institute, Children's Hospital Boston, Manton Center for Orphan Disease, and Department of Neurobiology, Harvard Medical School, Enders Building 1309, 320 Longwood Avenue, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19797662" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antiporters/*genetics/metabolism ; Calcium/*metabolism ; Calcium-Binding Proteins/*genetics/*metabolism ; Cation Transport Proteins/genetics/metabolism ; Cell Line ; Drosophila Proteins/*genetics/metabolism ; Drosophila melanogaster/*genetics/metabolism ; Genome, Human ; Genome, Insect ; HeLa Cells ; Humans ; Hydrogen/metabolism ; Hydrogen-Ion Concentration ; Ion Transport ; Membrane Potential, Mitochondrial ; Membrane Proteins/*genetics/*metabolism ; Mitochondria/*metabolism ; Mitochondrial Membranes/metabolism ; Mitochondrial Proteins/genetics/*metabolism ; Proteolipids/metabolism ; *RNA Interference
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    Cell biology. Overcoming opposition, Brazil banks on stem cells (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-04-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Leite, Marcelo -- New York, N.Y. -- Science. 2009 Apr 3;324(5923):26. doi: 10.1126/science.324.5923.26.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19342562" target="_blank"〉PubMed〈/a〉
    Keywords: Biomedical Research/economics ; Bioreactors ; Brazil ; Cell Culture Techniques ; Cell Line ; *Embryo Research/economics ; *Embryonic Stem Cells/cytology ; Financing, Government ; Humans ; *Pluripotent Stem Cells/cytology ; Research Support as Topic
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  • 18
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    The hallucinogen N,N-dimethyltryptamine (DMT) is an endogenous sigma-1 receptor regulator (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-02-14
    Description: The sigma-1 receptor is widely distributed in the central nervous system and periphery. Originally mischaracterized as an opioid receptor, the sigma-1 receptor binds a vast number of synthetic compounds but does not bind opioid peptides; it is currently considered an orphan receptor. The sigma-1 receptor pharmacophore includes an alkylamine core, also found in the endogenous compound N,N-dimethyltryptamine (DMT). DMT acts as a hallucinogen, but its receptor target has been unclear. DMT bound to sigma-1 receptors and inhibited voltage-gated sodium ion (Na+) channels in both native cardiac myocytes and heterologous cells that express sigma-1 receptors. DMT induced hypermobility in wild-type mice but not in sigma-1 receptor knockout mice. These biochemical, physiological, and behavioral experiments indicate that DMT is an endogenous agonist for the sigma-1 receptor.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2947205/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2947205/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fontanilla, Dominique -- Johannessen, Molly -- Hajipour, Abdol R -- Cozzi, Nicholas V -- Jackson, Meyer B -- Ruoho, Arnold E -- F31 DA022932/DA/NIDA NIH HHS/ -- NS30016/NS/NINDS NIH HHS/ -- R01 MH065503/MH/NIMH NIH HHS/ -- R01 MH065503-01A1/MH/NIMH NIH HHS/ -- R01 NS030016/NS/NINDS NIH HHS/ -- R01 NS030016-08/NS/NINDS NIH HHS/ -- R01 NS030016-09/NS/NINDS NIH HHS/ -- T32 GM08688/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2009 Feb 13;323(5916):934-7. doi: 10.1126/science.1166127.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of Wisconsin School of Medicine and Public Health, Madison, WI 53706, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19213917" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; COS Cells ; Cell Line ; Cells, Cultured ; Cercopithecus aethiops ; Guinea Pigs ; Hallucinogens/*metabolism ; Ligands ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Myocardium/metabolism ; N,N-Dimethyltryptamine/*metabolism ; Rats ; Receptors, sigma/agonists/antagonists & inhibitors/*metabolism ; Tryptamines/metabolism
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  • 19
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    Structure of the LKB1-STRAD-MO25 complex reveals an allosteric mechanism of kinase activation (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-11-07
    Description: The LKB1 tumor suppressor is a protein kinase that controls the activity of adenosine monophosphate-activated protein kinase (AMPK). LKB1 activity is regulated by the pseudokinase STRADalpha and the scaffolding protein MO25alpha through an unknown, phosphorylation-independent, mechanism. We describe the structure of the core heterotrimeric LKB1-STRADalpha-MO25alpha complex, revealing an unusual allosteric mechanism of LKB1 activation. STRADalpha adopts a closed conformation typical of active protein kinases and binds LKB1 as a pseudosubstrate. STRADalpha and MO25alpha promote the active conformation of LKB1, which is stabilized by MO25alpha interacting with the LKB1 activation loop. This previously undescribed mechanism of kinase activation may be relevant to understanding the evolution of other pseudokinases. The structure also reveals how mutations found in Peutz-Jeghers syndrome and in various sporadic cancers impair LKB1 function.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3518268/" 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/PMC3518268/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zeqiraj, Elton -- Filippi, Beatrice Maria -- Deak, Maria -- Alessi, Dario R -- van Aalten, Daan M F -- 087590/Wellcome Trust/United Kingdom -- C33794/A10969/Cancer Research UK/United Kingdom -- G0900138/Medical Research Council/United Kingdom -- MC_U127070193/Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2009 Dec 18;326(5960):1707-11. doi: 10.1126/science.1178377. Epub 2009 Nov 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular Microbiology, College of Life Sciences, University of Dundee, Dundee DD1 5EH, Scotland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19892943" target="_blank"〉PubMed〈/a〉
    Keywords: AMP-Activated Protein Kinases/metabolism ; Adaptor Proteins, Vesicular Transport/*chemistry/metabolism ; Allosteric Regulation ; Amino Acid Sequence ; Binding Sites ; Calcium-Binding Proteins/*chemistry/metabolism ; Crystallography, X-Ray ; Enzyme Activation ; Humans ; Models, Molecular ; Molecular Sequence Data ; Multiprotein Complexes/chemistry/metabolism ; Mutant Proteins/chemistry/metabolism ; Mutation ; Phosphorylation ; Protein Binding ; Protein Conformation ; Protein Interaction Domains and Motifs ; Protein Structure, Tertiary ; Protein-Serine-Threonine Kinases/*chemistry/metabolism
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  • 20
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    The aryl hydrocarbon nuclear translocator alters CD30-mediated NF-kappaB-dependent transcription (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-01-10
    Description: Expression and signaling of CD30, a tumor necrosis factor receptor family member, is up-regulated in numerous lymphoid-derived neoplasias, most notably anaplastic large-cell lymphoma (ALCL) and Hodgkin's lymphoma. To gain insight into the mechanism of CD30 signaling, we used an affinity purification strategy that led to the identification of the aryl hydrocarbon receptor nuclear translocator (ARNT) as a CD30-interacting protein that modulated the activity of the RelB subunit of the transcription factor nuclear factor kappaB (NF-kappaB). ALCL cells that were deficient in ARNT exhibited defects in RelB recruitment to NF-kappaB-responsive promoters, whereas RelA recruitment to the same sites was potentiated, resulting in the augmented expression of these NF-kappaB-responsive genes. These findings indicate that ARNT functions in concert with RelB in a CD30-induced negative feedback mechanism.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2682336/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2682336/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wright, Casey W -- Duckett, Colin S -- R01 GM067827/GM/NIGMS NIH HHS/ -- R01 GM067827-04/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2009 Jan 9;323(5911):251-5. doi: 10.1126/science.1162818.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19131627" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Antigens, CD30/*metabolism ; Aryl Hydrocarbon Receptor Nuclear Translocator/chemistry/genetics/*metabolism ; Cell Line ; Cell Line, Tumor ; DNA/metabolism ; Feedback, Physiological ; Gene Expression Regulation ; Humans ; Lymphoma, Large-Cell, Anaplastic/genetics/metabolism ; Molecular Sequence Data ; NF-kappa B/genetics/metabolism ; Promoter Regions, Genetic ; Protein Structure, Tertiary ; Receptors, Tumor Necrosis Factor, Type II/metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Transcription Factor RelB/genetics/*metabolism ; *Transcription, Genetic ; Transcriptional Activation
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    The cAMP sensor Epac2 is a direct target of antidiabetic sulfonylurea drugs (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-08-01
    Description: Epac2, a guanine nucleotide exchange factor for the small guanosine triphosphatase Rap1, is activated by adenosine 3',5'-monophosphate. Fluorescence resonance energy transfer and binding experiments revealed that sulfonylureas, widely used antidiabetic drugs, interact directly with Epac2. Sulfonylureas activated Rap1 specifically through Epac2. Sulfonylurea-stimulated insulin secretion was reduced both in vitro and in vivo in mice lacking Epac2, and the glucose-lowering effect of the sulfonylurea tolbutamide was decreased in these mice. Epac2 thus contributes to the effect of sulfonylureas to promote insulin secretion. Because Epac2 is also required for the action of incretins, gut hormones crucial for potentiating insulin secretion, it may be a promising target for antidiabetic drug development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Chang-Liang -- Katoh, Megumi -- Shibasaki, Tadao -- Minami, Kohtaro -- Sunaga, Yasuhiro -- Takahashi, Harumi -- Yokoi, Norihide -- Iwasaki, Masahiro -- Miki, Takashi -- Seino, Susumu -- New York, N.Y. -- Science. 2009 Jul 31;325(5940):607-10. doi: 10.1126/science.1172256.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Cellular and Molecular Medicine, Department of Physiology and Cell Biology, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19644119" target="_blank"〉PubMed〈/a〉
    Keywords: 8-Bromo Cyclic Adenosine Monophosphate/pharmacology ; Animals ; Blood Glucose/analysis ; COS Cells ; Carrier Proteins/genetics/*metabolism ; Cell Line ; Cercopithecus aethiops ; Cyclic AMP/*metabolism ; Fluorescence Resonance Energy Transfer ; Glucose/administration & dosage ; Glyburide/metabolism/pharmacology ; Guanine Nucleotide Exchange Factors/genetics/*metabolism ; Hypoglycemic Agents/chemistry/*metabolism/pharmacology ; Insulin/blood/secretion ; Islets of Langerhans/secretion ; Mice ; Mice, Inbred C57BL ; Sulfonylurea Compounds/chemistry/*metabolism/pharmacology ; Tolbutamide/metabolism/pharmacology ; rap1 GTP-Binding Proteins/metabolism
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    Extinction-reconsolidation boundaries: key to persistent attenuation of fear memories (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-04-04
    Description: Dysregulation of the fear system is at the core of many psychiatric disorders. Much progress has been made in uncovering the neural basis of fear learning through studies in which associative emotional memories are formed by pairing an initially neutral stimulus (conditioned stimulus, CS; e.g., a tone) to an unconditioned stimulus (US; e.g., a shock). Despite recent advances, the question of how to persistently weaken aversive CS-US associations, or dampen traumatic memories in pathological cases, remains a major dilemma. Two paradigms (blockade of reconsolidation and extinction) have been used in the laboratory to reduce acquired fear. Unfortunately, their clinical efficacy is limited: Reconsolidation blockade typically requires potentially toxic drugs, and extinction is not permanent. Here, we describe a behavioral design in which a fear memory in rats is destabilized and reinterpreted as safe by presenting an isolated retrieval trial before an extinction session. This procedure permanently attenuates the fear memory without the use of drugs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3625935/" 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/PMC3625935/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Monfils, Marie-H -- Cowansage, Kiriana K -- Klann, Eric -- LeDoux, Joseph E -- F31 MH083472/MH/NIMH NIH HHS/ -- F31 MH083472-01A1/MH/NIMH NIH HHS/ -- F31MH083472/MH/NIMH NIH HHS/ -- K05 MH067048/MH/NIMH NIH HHS/ -- NS034007/NS/NINDS NIH HHS/ -- NS047384/NS/NINDS NIH HHS/ -- P50 MH058911/MH/NIMH NIH HHS/ -- R01 MH046516/MH/NIMH NIH HHS/ -- R37 MH038774/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2009 May 15;324(5929):951-5. doi: 10.1126/science.1167975. Epub 2009 Apr 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Neural Science, New York University, New York, NY 10003, USA. monfils@mail.utexas.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19342552" target="_blank"〉PubMed〈/a〉
    Keywords: Amygdala/physiology ; Animals ; Conditioning, Classical ; Extinction, Psychological/*physiology ; *Fear ; Male ; Memory/*physiology ; Mental Recall/*physiology ; Phosphorylation ; Rats ; Receptors, AMPA/metabolism
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    RIP3, an energy metabolism regulator that switches TNF-induced cell death from apoptosis to necrosis (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-06-06
    Description: Necrosis can be induced by stimulating death receptors with tumor necrosis factor (TNF) or other agonists; however, the underlying mechanism differentiating necrosis from apoptosis is largely unknown. We identified the protein kinase receptor-interacting protein 3 (RIP3) as a molecular switch between TNF-induced apoptosis and necrosis in NIH 3T3 cells and found that RIP3 was required for necrosis in other cells. RIP3 did not affect RIP1-mediated apoptosis but was required for RIP1-mediated necrosis and the enhancement of necrosis by the caspase inhibitor zVAD. By activating key enzymes of metabolic pathways, RIP3 regulates TNF-induced reactive oxygen species production, which partially accounts for RIP3's ability to promote necrosis. Our data suggest that modulation of energy metabolism in response to death stimuli has an important role in the choice between apoptosis and necrosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Duan-Wu -- Shao, Jing -- Lin, Juan -- Zhang, Na -- Lu, Bao-Ju -- Lin, Sheng-Cai -- Dong, Meng-Qiu -- Han, Jiahuai -- New York, N.Y. -- Science. 2009 Jul 17;325(5938):332-6. doi: 10.1126/science.1172308. Epub 2009 Jun 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Key Laboratory of the Ministry of Education for Cell Biology and Tumor Cell Engineering, School of Life Sciences, Xiamen University, Xiamen, Fujian 361005, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19498109" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Chloromethyl Ketones/pharmacology ; Animals ; *Apoptosis ; Cell Line ; Energy Metabolism ; Glutamate Dehydrogenase/metabolism ; Glutamate-Ammonia Ligase/metabolism ; Glycogen Phosphorylase/metabolism ; Mice ; NIH 3T3 Cells ; *Necrosis ; RNA Interference ; Reactive Oxygen Species/metabolism ; Receptor-Interacting Protein Serine-Threonine Kinases/genetics/*metabolism ; Tumor Necrosis Factor-alpha/*pharmacology
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    Biochemistry. Force signaling in biology (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-06-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gebhardt, J Christof M -- Rief, Matthias -- New York, N.Y. -- Science. 2009 Jun 5;324(5932):1278-80. doi: 10.1126/science.1175874.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Physik Department E22, Technische Universitat Munchen, James-Franck-Strasse, 85748 Munchen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19498156" target="_blank"〉PubMed〈/a〉
    Keywords: ADAM Proteins/*metabolism ; Binding Sites ; Blood Coagulation/physiology ; Hemostasis/*physiology ; Humans ; *Mechanical Phenomena ; Optical Tweezers ; Protein Conformation ; Protein Folding ; Protein Multimerization ; Protein Structure, Tertiary ; Stress, Mechanical ; von Willebrand Factor/*chemistry/*metabolism
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  • 25
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    Rab35 controls actin bundling by recruiting fascin as an effector protein (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-09-05
    Description: Actin filaments are key components of the eukaryotic cytoskeleton that provide mechanical structure and generate forces during cell shape changes, growth, and migration. Actin filaments are dynamically assembled into higher-order structures at specified locations to regulate diverse functions. The Rab family of small guanosine triphosphatases is evolutionarily conserved and mediates intracellular vesicle trafficking. We found that Rab35 regulates the assembly of actin filaments during bristle development in Drosophila and filopodia formation in cultured cells. These effects were mediated by the actin-bundling protein fascin, which directly associated with active Rab35. Targeting Rab35 to the outer mitochondrial membrane triggered actin recruitment, demonstrating a role for an intracellular trafficking protein in localized actin assembly.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Jun -- Fonovic, Marko -- Suyama, Kaye -- Bogyo, Matthew -- Scott, Matthew P -- U54 RR020843/RR/NCRR NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Sep 4;325(5945):1250-4. doi: 10.1126/science.1174921.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Biology, Stanford University School of Medicine, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19729655" target="_blank"〉PubMed〈/a〉
    Keywords: Actin Cytoskeleton/*metabolism/ultrastructure ; Actins/*metabolism ; Animals ; Carrier Proteins/*metabolism ; Cell Line ; Cell Membrane/metabolism ; Drosophila/anatomy & histology/growth & development/metabolism ; Drosophila Proteins/genetics/*metabolism ; HeLa Cells ; Humans ; Mice ; Microfilament Proteins/*metabolism ; Mitochondrial Membranes/metabolism ; NIH 3T3 Cells ; Pseudopodia/metabolism/ultrastructure ; RNA Interference ; Recombinant Fusion Proteins/metabolism ; rab GTP-Binding Proteins/genetics/*metabolism
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  • 26
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    The insect neuropeptide PTTH activates receptor tyrosine kinase torso to initiate metamorphosis (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-12-08
    Description: Holometabolous insects undergo complete metamorphosis to become sexually mature adults. Metamorphosis is initiated by brain-derived prothoracicotropic hormone (PTTH), which stimulates the production of the molting hormone ecdysone via an incompletely defined signaling pathway. Here we demonstrate that Torso, a receptor tyrosine kinase that regulates embryonic terminal cell fate in Drosophila, is the PTTH receptor. Trunk, the embryonic Torso ligand, is related to PTTH, and ectopic expression of PTTH in the embryo partially rescues trunk mutants. In larvae, torso is expressed specifically in the prothoracic gland (PG), and its loss phenocopies the removal of PTTH. The activation of Torso by PTTH stimulates extracellular signal-regulated kinase (ERK) phosphorylation, and the loss of ERK in the PG phenocopies the loss of PTTH and Torso. We conclude that PTTH initiates metamorphosis by activation of the Torso/ERK pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rewitz, Kim F -- Yamanaka, Naoki -- Gilbert, Lawrence I -- O'Connor, Michael B -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Dec 4;326(5958):1403-5. doi: 10.1126/science.1176450.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Cell Biology, and Development, University of Minnesota, Minneapolis, MN 55455, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965758" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Bombyx/*genetics/metabolism ; Cell Line ; Drosophila Proteins/chemistry/genetics/*metabolism ; Drosophila melanogaster/embryology/genetics/*growth & development/metabolism ; Embryo, Nonmammalian/metabolism ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Insect Hormones/chemistry/*metabolism ; Larva/growth & development ; Ligands ; *Metamorphosis, Biological ; Molecular Sequence Data ; Neurons/metabolism ; Phosphorylation ; Pupa/growth & development ; RNA Interference ; Receptor Protein-Tyrosine Kinases/genetics/*metabolism ; Signal Transduction
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  • 27
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    Synthetic heterochromatin bypasses RNAi and centromeric repeats to establish functional centromeres (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-06-27
    Description: In the central domain of fission yeast centromeres, the kinetochore is assembled on CENP-A(Cnp1) nucleosomes. Normally, small interfering RNAs generated from flanking outer repeat transcripts direct histone H3 lysine 9 methyltransferase Clr4 to homologous loci to form heterochromatin. Outer repeats, RNA interference (RNAi), and centromeric heterochromatin are required to establish CENP-A(Cnp1) chromatin. We demonstrated that tethering Clr4 via DNA-binding sites at euchromatic loci induces heterochromatin assembly, with or without active RNAi. This synthetic heterochromatin completely substitutes for outer repeats on plasmid-based minichromosomes, promoting de novo CENP-A(Cnp1) and kinetochore assembly, to allow their mitotic segregation, even with RNAi inactive. Thus, the role of outer repeats in centromere establishment is simply the provision of RNAi substrates to direct heterochromatin formation; H3K9 methylation-dependent heterochromatin is alone sufficient to form functional centromeres.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2949999/" 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/PMC2949999/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kagansky, Alexander -- Folco, Hernan Diego -- Almeida, Ricardo -- Pidoux, Alison L -- Boukaba, Abdelhalim -- Simmer, Femke -- Urano, Takeshi -- Hamilton, Georgina L -- Allshire, Robin C -- 065061/Wellcome Trust/United Kingdom -- 065061/Z/Wellcome Trust/United Kingdom -- G0301153/Medical Research Council/United Kingdom -- G0301153(69173)/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2009 Jun 26;324(5935):1716-9. doi: 10.1126/science.1172026.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust Centre for Cell Biology, School of Biological Sciences, The University of Edinburgh, 6.34 Swann Building, Edinburgh EH9 3JR, Scotland, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19556509" target="_blank"〉PubMed〈/a〉
    Keywords: Binding Sites ; Cell Cycle Proteins/metabolism ; Centromere/chemistry/*metabolism/ultrastructure ; *Chromatin Assembly and Disassembly ; Chromosomal Proteins, Non-Histone/metabolism ; Chromosome Segregation ; DNA-Binding Proteins/genetics/metabolism ; Heterochromatin/*metabolism ; Histones/metabolism ; Kinetochores/metabolism ; Methyltransferases/metabolism ; Mitosis ; *RNA Interference ; Recombinant Fusion Proteins/metabolism ; Saccharomyces cerevisiae Proteins/genetics/metabolism ; Schizosaccharomyces/genetics/*metabolism ; Schizosaccharomyces pombe Proteins/metabolism ; Transcription Factors/genetics/metabolism ; Transcription, Genetic
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  • 28
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    KLF family members regulate intrinsic axon regeneration ability (2009)
    American Association for the Advancement of Science (AAAS)
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    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
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    Burst spiking of a single cortical neuron modifies global brain state (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-05-02
    Description: Different global patterns of brain activity are associated with distinct arousal and behavioral states of an animal, but how the brain rapidly switches between different states remains unclear. We here report that repetitive high-frequency burst spiking of a single rat cortical neuron could trigger a switch between the cortical states resembling slow-wave and rapid-eye-movement sleep. This is reflected in the switching of the membrane potential of the stimulated neuron from slow UP/DOWN oscillations to a persistent-UP state or vice versa, with concurrent changes in the temporal pattern of cortical local field potential (LFP) recorded several millimeters away. These results point to the power of single cortical neurons in modulating the behavioral state of an animal.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2913066/" 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/PMC2913066/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Cheng-Yu T -- Poo, Mu-Ming -- Dan, Yang -- R01 EY018861/EY/NEI NIH HHS/ -- R01 EY018861-01/EY/NEI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 May 1;324(5927):643-6. doi: 10.1126/science.1169957.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neurobiology, Department of Molecular and Cell Biology, Helen Wills Institute of Neuroscience, University of California, Berkeley, CA 94720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19407203" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Behavior, Animal ; Electroencephalography ; Membrane Potentials ; Neurons/*physiology ; Patch-Clamp Techniques ; Rats ; Rats, Long-Evans ; Sleep Stages ; Sleep, REM ; Somatosensory Cortex/cytology/*physiology ; Visual Cortex/cytology/*physiology
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    Glioma-derived mutations in IDH1 dominantly inhibit IDH1 catalytic activity and induce HIF-1alpha (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-04-11
    Description: Heterozygous mutations in the gene encoding isocitrate dehydrogenase-1 (IDH1) occur in certain human brain tumors, but their mechanistic role in tumor development is unknown. We have shown that tumor-derived IDH1 mutations impair the enzyme's affinity for its substrate and dominantly inhibit wild-type IDH1 activity through the formation of catalytically inactive heterodimers. Forced expression of mutant IDH1 in cultured cells reduces formation of the enzyme product, alpha-ketoglutarate (alpha-KG), and increases the levels of hypoxia-inducible factor subunit HIF-1alpha, a transcription factor that facilitates tumor growth when oxygen is low and whose stability is regulated by alpha-KG. The rise in HIF-1alpha levels was reversible by an alpha-KG derivative. HIF-1alpha levels were higher in human gliomas harboring an IDH1 mutation than in tumors without a mutation. Thus, IDH1 appears to function as a tumor suppressor that, when mutationally inactivated, contributes to tumorigenesis in part through induction of the HIF-1 pathway.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3251015/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3251015/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhao, Shimin -- Lin, Yan -- Xu, Wei -- Jiang, Wenqing -- Zha, Zhengyu -- Wang, Pu -- Yu, Wei -- Li, Zhiqiang -- Gong, Lingling -- Peng, Yingjie -- Ding, Jianping -- Lei, Qunying -- Guan, Kun-Liang -- Xiong, Yue -- R01 CA068377/CA/NCI NIH HHS/ -- R01 CA068377-14/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2009 Apr 10;324(5924):261-5. doi: 10.1126/science.1170944.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular and Cell Biology Laboratory, Institute of Biomedical Sciences, Fudan University, 130 Dong-An Road, Shanghai 200032, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19359588" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Aged ; Astrocytoma/genetics/metabolism ; Biocatalysis ; Brain Neoplasms/*genetics/metabolism ; Cell Line ; Child ; Female ; Gene Expression Regulation, Neoplastic ; Genes, Tumor Suppressor ; Glioblastoma/genetics/metabolism ; Glioma/*genetics/metabolism ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit/antagonists & ; inhibitors/genetics/*metabolism ; Isocitrate Dehydrogenase/chemistry/*genetics/*metabolism ; Ketoglutaric Acids/metabolism ; Male ; Middle Aged ; Mutant Proteins/chemistry/metabolism ; Oligodendroglioma/genetics/metabolism ; Oxalates/pharmacology ; Protein Multimerization
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    Knockout rats via embryo microinjection of zinc-finger nucleases (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-07-25
    Description: The toolbox of rat genetics currently lacks the ability to introduce site-directed, heritable mutations into the genome to create knockout animals. By using engineered zinc-finger nucleases (ZFNs) designed to target an integrated reporter and two endogenous rat genes, Immunoglobulin M (IgM) and Rab38, we demonstrate that a single injection of DNA or messenger RNA encoding ZFNs into the one-cell rat embryo leads to a high frequency of animals carrying 25 to 100% disruption at the target locus. These mutations are faithfully and efficiently transmitted through the germline. Our data demonstrate the feasibility of targeted gene disruption in multiple rat strains within 4 months time, paving the way to a humanized monoclonal antibody platform and additional human disease models.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2831805/" 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/PMC2831805/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Geurts, Aron M -- Cost, Gregory J -- Freyvert, Yevgeniy -- Zeitler, Bryan -- Miller, Jeffrey C -- Choi, Vivian M -- Jenkins, Shirin S -- Wood, Adam -- Cui, Xiaoxia -- Meng, Xiangdong -- Vincent, Anna -- Lam, Stephen -- Michalkiewicz, Mieczyslaw -- Schilling, Rebecca -- Foeckler, Jamie -- Kalloway, Shawn -- Weiler, Hartmut -- Menoret, Severine -- Anegon, Ignacio -- Davis, Gregory D -- Zhang, Lei -- Rebar, Edward J -- Gregory, Philip D -- Urnov, Fyodor D -- Jacob, Howard J -- Buelow, Roland -- 5P01HL082798-03/HL/NHLBI NIH HHS/ -- 5U01HL066579-08/HL/NHLBI NIH HHS/ -- P01 HL082798/HL/NHLBI NIH HHS/ -- P01 HL082798-03/HL/NHLBI NIH HHS/ -- U01 HL066579/HL/NHLBI NIH HHS/ -- U01 HL066579-08/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2009 Jul 24;325(5939):433. doi: 10.1126/science.1172447.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Human and Molecular Genetics Center, Medical College of Wisconsin, Milwaukee, WI 52336, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19628861" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Dna ; Embryo, Mammalian ; Endodeoxyribonucleases/genetics/*metabolism ; Feasibility Studies ; Female ; *Gene Knockout Techniques ; Green Fluorescent Proteins ; Immunoglobulin M/*genetics ; Male ; *Microinjections ; Molecular Sequence Data ; Mutagenesis, Site-Directed ; RNA, Messenger ; Rats ; *Zinc Fingers/genetics ; rab GTP-Binding Proteins/*genetics
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    Identification of splenic reservoir monocytes and their deployment to inflammatory sites (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-08-01
    Description: A current paradigm states that monocytes circulate freely and patrol blood vessels but differentiate irreversibly into dendritic cells (DCs) or macrophages upon tissue entry. Here we show that bona fide undifferentiated monocytes reside in the spleen and outnumber their equivalents in circulation. The reservoir monocytes assemble in clusters in the cords of the subcapsular red pulp and are distinct from macrophages and DCs. In response to ischemic myocardial injury, splenic monocytes increase their motility, exit the spleen en masse, accumulate in injured tissue, and participate in wound healing. These observations uncover a role for the spleen as a site for storage and rapid deployment of monocytes and identify splenic monocytes as a resource that the body exploits to regulate inflammation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2803111/" 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/PMC2803111/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Swirski, Filip K -- Nahrendorf, Matthias -- Etzrodt, Martin -- Wildgruber, Moritz -- Cortez-Retamozo, Virna -- Panizzi, Peter -- Figueiredo, Jose-Luiz -- Kohler, Rainer H -- Chudnovskiy, Aleksey -- Waterman, Peter -- Aikawa, Elena -- Mempel, Thorsten R -- Libby, Peter -- Weissleder, Ralph -- Pittet, Mikael J -- 1R01HL095612/HL/NHLBI NIH HHS/ -- P01 A154904/PHS HHS/ -- P01 AI054904/AI/NIAID NIH HHS/ -- P01 AI054904-010001/AI/NIAID NIH HHS/ -- P50 CA086355/CA/NCI NIH HHS/ -- P50 CA086355-07/CA/NCI NIH HHS/ -- P50 CA86355/CA/NCI NIH HHS/ -- R00 HL094533/HL/NHLBI NIH HHS/ -- R01 HL095629/HL/NHLBI NIH HHS/ -- R01 HL096576/HL/NHLBI NIH HHS/ -- R24 CA69246/CA/NCI NIH HHS/ -- U01 HL080731/HL/NHLBI NIH HHS/ -- U01 HL080731-05/HL/NHLBI NIH HHS/ -- U54 CA126515/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2009 Jul 31;325(5940):612-6. doi: 10.1126/science.1175202.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA. fswirski@mgh.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19644120" target="_blank"〉PubMed〈/a〉
    Keywords: Angiotensin II/blood/pharmacology ; Animals ; Antigens, Ly/metabolism ; Bone Marrow Cells/physiology ; Cell Differentiation ; Cell Movement ; Cell Size ; Female ; Inflammation/*pathology ; Mice ; Mice, Inbred C57BL ; Monocytes/cytology/*physiology ; Myocardial Infarction/immunology/*pathology/*physiopathology ; Myocardium/*immunology/*pathology ; Rats ; Rats, Wistar ; Receptors, Angiotensin/metabolism ; Spleen/cytology/*immunology ; Splenectomy
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    Stem cells. CIRM awards seek to move cell therapies to the clinic (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-11-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaiser, Jocelyn -- New York, N.Y. -- Science. 2009 Nov 6;326(5954):780-1. doi: 10.1126/science.326_780a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19892950" target="_blank"〉PubMed〈/a〉
    Keywords: *Academies and Institutes ; Adult Stem Cells ; *Biological Therapy ; California ; Cell Line ; Embryonic Stem Cells ; Genetic Therapy ; Humans ; Induced Pluripotent Stem Cells ; National Institutes of Health (U.S.) ; *Research Support as Topic ; *Stem Cell Transplantation ; *Stem Cells ; United States
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  • 34
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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
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    Biochemistry. Nascent proteins caught in the act (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-12-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kampmann, Martin -- Blobel, Gunter -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Dec 4;326(5958):1352-3. doi: 10.1126/science.1183690.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and The Rockefeller University, New York, NY 10065, USA. martin.kampmann@rockefeller.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965743" target="_blank"〉PubMed〈/a〉
    Keywords: Binding Sites ; Cryoelectron Microscopy ; Endoplasmic Reticulum/metabolism/ultrastructure ; Escherichia coli Proteins/chemistry/genetics/*metabolism/ultrastructure ; Gene Expression Regulation, Bacterial ; Membrane Proteins/chemistry/*metabolism/ultrastructure ; Operon ; Protein Biosynthesis ; Protein Multimerization ; Protein Sorting Signals ; Protein Transport ; Proteins/chemistry/*metabolism/ultrastructure ; RNA, Transfer/metabolism ; Ribosomes/*metabolism/ultrastructure ; Signal Recognition Particle/chemistry/metabolism/ultrastructure ; Transcription, Genetic ; Tryptophanase/chemistry/*genetics/metabolism
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    The structure of rat liver vault at 3.5 angstrom resolution (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-01-20
    Description: Vaults are among the largest cytoplasmic ribonucleoprotein particles and are found in numerous eukaryotic species. Roles in multidrug resistance and innate immunity have been suggested, but the cellular function remains unclear. We have determined the x-ray structure of rat liver vault at 3.5 angstrom resolution and show that the cage structure consists of a dimer of half-vaults, with each half-vault comprising 39 identical major vault protein (MVP) chains. Each MVP monomer folds into 12 domains: nine structural repeat domains, a shoulder domain, a cap-helix domain, and a cap-ring domain. Interactions between the 42-turn-long cap-helix domains are key to stabilizing the particle. The shoulder domain is structurally similar to a core domain of stomatin, a lipid-raft component in erythrocytes and epithelial cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tanaka, Hideaki -- Kato, Koji -- Yamashita, Eiki -- Sumizawa, Tomoyuki -- Zhou, Yong -- Yao, Min -- Iwasaki, Kenji -- Yoshimura, Masato -- Tsukihara, Tomitake -- New York, N.Y. -- Science. 2009 Jan 16;323(5912):384-8. doi: 10.1126/science.1164975.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Protein Research, Osaka University, 3-2 Yamadaoka, Suita, Osaka 565-0871, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19150846" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Crystallization ; Crystallography, X-Ray ; Dimerization ; Liver/*chemistry ; Models, Molecular ; Protein Conformation ; Protein Folding ; Protein Structure, Quaternary ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Rats ; Vault Ribonucleoprotein Particles/*chemistry
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    Analysis of Drosophila segmentation network identifies a JNK pathway factor overexpressed in kidney cancer (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-01-24
    Description: We constructed a large-scale functional network model in Drosophila melanogaster built around two key transcription factors involved in the process of embryonic segmentation. Analysis of the model allowed the identification of a new role for the ubiquitin E3 ligase complex factor SPOP. In Drosophila, the gene encoding SPOP is a target of segmentation transcription factors. Drosophila SPOP mediates degradation of the Jun kinase phosphatase Puckered, thereby inducing tumor necrosis factor (TNF)/Eiger-dependent apoptosis. In humans, we found that SPOP plays a conserved role in TNF-mediated JNK signaling and was highly expressed in 99% of clear cell renal cell carcinomas (RCCs), the most prevalent form of kidney cancer. SPOP expression distinguished histological subtypes of RCC and facilitated identification of clear cell RCC as the primary tumor for metastatic lesions.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2756524/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2756524/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, Jiang -- Ghanim, Murad -- Xue, Lei -- Brown, Christopher D -- Iossifov, Ivan -- Angeletti, Cesar -- Hua, Sujun -- Negre, Nicolas -- Ludwig, Michael -- Stricker, Thomas -- Al-Ahmadie, Hikmat A -- Tretiakova, Maria -- Camp, Robert L -- Perera-Alberto, Montse -- Rimm, David L -- Xu, Tian -- Rzhetsky, Andrey -- White, Kevin P -- P50 GM081892/GM/NIGMS NIH HHS/ -- P50 GM081892-01A1/GM/NIGMS NIH HHS/ -- R01 HG003012/HG/NHGRI NIH HHS/ -- R01 HG003012-04/HG/NHGRI NIH HHS/ -- UL1 RR024999/RR/NCRR NIH HHS/ -- UL1 RR024999-02/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2009 Feb 27;323(5918):1218-22. doi: 10.1126/science.1157669. Epub 2009 Jan 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Genomics and Systems Biology, University of Chicago and Argonne National Laboratory, Chicago, IL 60637, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19164706" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Apoptosis ; Carcinoma, Renal Cell/*genetics/metabolism ; Cell Line ; Compound Eye, Arthropod/embryology/metabolism ; Drosophila Proteins/genetics/metabolism ; Drosophila melanogaster/embryology/*genetics/metabolism ; Embryo, Nonmammalian/metabolism ; Fushi Tarazu Transcription Factors/genetics/metabolism ; Gene Expression Profiling ; Gene Regulatory Networks ; Homeodomain Proteins/genetics/metabolism ; Humans ; Janus Kinases/*metabolism ; Kidney/metabolism ; Kidney Neoplasms/*genetics/metabolism ; Molecular Sequence Data ; Nervous System/embryology ; Nuclear Proteins/*genetics/metabolism ; Phosphoprotein Phosphatases/metabolism ; Phosphorylation ; Repressor Proteins/*genetics/metabolism ; *Signal Transduction ; Transcription Factors/genetics/metabolism ; Transcription, Genetic
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    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
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    Calcineurin/NFAT signaling is required for neuregulin-regulated Schwann cell differentiation (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-01-31
    Description: Schwann cells develop from multipotent neural crest cells and form myelin sheaths around axons that allow rapid transmission of action potentials. Neuregulin signaling through the ErbB receptor regulates Schwann cell development; however, the downstream pathways are not fully defined. We find that mice lacking calcineurin B1 in the neural crest have defects in Schwann cell differentiation and myelination. Neuregulin addition to Schwann cell precursors initiates an increase in cytoplasmic Ca2+, which activates calcineurin and the downstream transcription factors NFATc3 and c4. Purification of NFAT protein complexes shows that Sox10 is an NFAT nuclear partner and synergizes with NFATc4 to activate Krox20, which regulates genes necessary for myelination. Our studies demonstrate that calcineurin and NFAT are essential for neuregulin and ErbB signaling, neural crest diversification, and differentiation of Schwann cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2790385/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2790385/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kao, Shih-Chu -- Wu, Hai -- Xie, Jianming -- Chang, Ching-Pin -- Ranish, Jeffrey A -- Graef, Isabella A -- Crabtree, Gerald R -- AI60037/AI/NIAID NIH HHS/ -- HD55391/HD/NICHD NIH HHS/ -- NS046789/NS/NINDS NIH HHS/ -- R01 AI060037/AI/NIAID NIH HHS/ -- R01 AI060037-01/AI/NIAID NIH HHS/ -- R01 AI060037-02/AI/NIAID NIH HHS/ -- R01 AI060037-03/AI/NIAID NIH HHS/ -- R01 AI060037-04/AI/NIAID NIH HHS/ -- R01 AI060037-05/AI/NIAID NIH HHS/ -- R01 HD055391/HD/NICHD NIH HHS/ -- R01 NS046789/NS/NINDS NIH HHS/ -- R01 NS046789-01/NS/NINDS NIH HHS/ -- R01 NS046789-02/NS/NINDS NIH HHS/ -- R01 NS046789-03/NS/NINDS NIH HHS/ -- R01 NS046789-04/NS/NINDS NIH HHS/ -- R01 NS046789-05/NS/NINDS NIH HHS/ -- R21 NS061702/NS/NINDS NIH HHS/ -- R21 NS061702-01/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Jan 30;323(5914):651-4. doi: 10.1126/science.1166562.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Stanford University, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19179536" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcineurin/*metabolism ; Calcium/metabolism ; Cell Differentiation ; Cell Line ; Coculture Techniques ; Early Growth Response Protein 2/metabolism ; Ganglia, Spinal/cytology ; Mice ; Myelin Sheath/physiology ; NFATC Transcription Factors/*metabolism ; Neural Crest/cytology/metabolism ; Neuregulins/*metabolism ; Phosphorylation ; Receptor, ErbB-2/metabolism ; Receptor, ErbB-3 ; SOXE Transcription Factors/metabolism ; Schwann Cells/*cytology/*metabolism ; *Signal Transduction
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    Cell biology. Evolving cell signals (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-09-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Collins, Mark O -- New York, N.Y. -- Science. 2009 Sep 25;325(5948):1635-6. doi: 10.1126/science.1180331.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Proteomic Mass Spectrometry Group, Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, UK. moc@sanger.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19779182" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; *Biological Evolution ; CDC2 Protein Kinase/antagonists & inhibitors/metabolism ; *Evolution, Molecular ; Fungi/metabolism ; Phosphorylation ; Protein Binding ; Protein Folding ; Protein Structure, Tertiary ; Protein-Serine-Threonine Kinases/metabolism ; Protein-Tyrosine Kinases/metabolism ; Proteins/*chemistry/*metabolism ; Serine/metabolism ; *Signal Transduction ; Threonine/metabolism ; Tyrosine/metabolism
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    Circadian control of the NAD+ salvage pathway by CLOCK-SIRT1 (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-03-17
    Description: Many metabolic and physiological processes display circadian oscillations. We have shown that the core circadian regulator, CLOCK, is a histone acetyltransferase whose activity is counterbalanced by the nicotinamide adenine dinucleotide (NAD+)-dependent histone deacetylase SIRT1. Here we show that intracellular NAD+ levels cycle with a 24-hour rhythm, an oscillation driven by the circadian clock. CLOCK:BMAL1 regulates the circadian expression of NAMPT (nicotinamide phosphoribosyltransferase), an enzyme that provides a rate-limiting step in the NAD+ salvage pathway. SIRT1 is recruited to the Nampt promoter and contributes to the circadian synthesis of its own coenzyme. Using the specific inhibitor FK866, we demonstrated that NAMPT is required to modulate circadian gene expression. Our findings in mouse embryo fibroblasts reveal an interlocked transcriptional-enzymatic feedback loop that governs the molecular interplay between cellular metabolism and circadian rhythms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nakahata, Yasukazu -- Sahar, Saurabh -- Astarita, Giuseppe -- Kaluzova, Milota -- Sassone-Corsi, Paolo -- R01-GM081634/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2009 May 1;324(5927):654-7. doi: 10.1126/science.1170803. Epub 2009 Mar 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, School of Medicine, University of California, Irvine, Irvine, CA 92697, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19286518" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors ; Acrylamides/pharmacology ; Animals ; Basic Helix-Loop-Helix Transcription Factors/metabolism ; Biological Clocks ; CLOCK Proteins ; Cell Line ; Chromatin Assembly and Disassembly ; *Circadian Rhythm ; Cytokines/antagonists & inhibitors/genetics/*metabolism ; Enzyme Inhibitors/pharmacology ; *Feedback, Physiological ; *Gene Expression Regulation ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Knockout ; NAD/*metabolism ; Niacinamide/metabolism ; Nicotinamide Phosphoribosyltransferase/antagonists & ; inhibitors/genetics/*metabolism ; Piperidines/pharmacology ; Promoter Regions, Genetic ; Sirtuin 1 ; Sirtuins/*metabolism ; Trans-Activators/genetics/*metabolism ; Transcription, Genetic
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    Dopamine controls persistence of long-term memory storage (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-08-22
    Description: The paradigmatic feature of long-term memory (LTM) is its persistence. However, little is known about the mechanisms that make some LTMs last longer than others. In rats, a long-lasting fear LTM vanished rapidly when the D1 dopamine receptor antagonist SCH23390 was injected into the dorsal hippocampus 12 hours, but not immediately or 9 hours, after the fearful experience. Conversely, intrahippocampal application of the D1 agonist SK38393 at the same critical post-training time converted a rapidly decaying fear LTM into a persistent one. This effect was mediated by brain-derived neurotrophic factor and regulated by the ventral tegmental area (VTA). Thus, the persistence of LTM depends on activation of VTA/hippocampus dopaminergic connections and can be specifically modulated by manipulating this system at definite post-learning time points.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rossato, Janine I -- Bevilaqua, Lia R M -- Izquierdo, Ivan -- Medina, Jorge H -- Cammarota, Martin -- New York, N.Y. -- Science. 2009 Aug 21;325(5943):1017-20. doi: 10.1126/science.1172545.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centro de Memoria, Instituto do Cerebro, Pontificia Universidade Catolica do Rio Grande do Sul, Porto Alegre, Brazil.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19696353" target="_blank"〉PubMed〈/a〉
    Keywords: 2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine/pharmacology ; 8-Bromo Cyclic Adenosine Monophosphate/pharmacology ; Animals ; Benzazepines/pharmacology ; Brain-Derived Neurotrophic Factor/metabolism ; Dopamine/*physiology ; Dopamine Agonists/pharmacology ; Dopamine Antagonists/pharmacology ; Fear ; Hippocampus/drug effects/*physiology ; Male ; Memory/drug effects/*physiology ; Phosphorylation ; Rats ; Rats, Wistar ; Receptors, Dopamine D1/agonists/antagonists & inhibitors/metabolism ; Receptors, N-Methyl-D-Aspartate/metabolism ; Time Factors ; Tyrosine 3-Monooxygenase ; Ventral Tegmental Area/*physiology
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    Stretching single talin rod molecules activates vinculin binding (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-01-31
    Description: The molecular mechanism by which a mechanical stimulus is translated into a chemical response in biological systems is still unclear. We show that mechanical stretching of single cytoplasmic proteins can activate binding of other molecules. We used magnetic tweezers, total internal reflection fluorescence, and atomic force microscopy to investigate the effect of force on the interaction between talin, a protein that links liganded membrane integrins to the cytoskeleton, and vinculin, a focal adhesion protein that is activated by talin binding, leading to reorganization of the cytoskeleton. Application of physiologically relevant forces caused stretching of single talin rods that exposed cryptic binding sites for vinculin. Thus in the talin-vinculin system, molecular mechanotransduction can occur by protein binding after exposure of buried binding sites in the talin-vinculin system. Such protein stretching may be a more general mechanism for force transduction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉del Rio, Armando -- Perez-Jimenez, Raul -- Liu, Ruchuan -- Roca-Cusachs, Pere -- Fernandez, Julio M -- Sheetz, Michael P -- New York, N.Y. -- Science. 2009 Jan 30;323(5914):638-41. doi: 10.1126/science.1162912.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, Columbia University, New York, NY 10027, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19179532" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Biophysical Phenomena ; Chickens ; Mechanotransduction, Cellular ; Microscopy, Fluorescence ; Models, Molecular ; Photobleaching ; Protein Binding ; Protein Conformation ; Protein Folding ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Recombinant Proteins/chemistry/metabolism ; Talin/*chemistry/*metabolism ; Vinculin/*chemistry/*metabolism
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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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    Cell biology. The force is with us (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-01-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schwartz, Martin A -- New York, N.Y. -- Science. 2009 Jan 30;323(5914):588-9. doi: 10.1126/science.1169414.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, Cardiovascular Research Center and Mellon Urological Cancer Research Institute, University of Virginia, Charlottesville, VA 22908, USA. maschwartz@virginia.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19179515" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Binding Sites ; Cell Adhesion ; Fibronectins/chemistry/*metabolism ; Focal Adhesion Protein-Tyrosine Kinases/metabolism ; Humans ; Integrin alpha5beta1/chemistry/*metabolism ; *Mechanotransduction, Cellular ; Protein Binding ; Protein Folding ; Protein Structure, Tertiary ; Talin/chemistry/*metabolism ; Vinculin/*metabolism
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    Regulators of PP2C phosphatase activity function as abscisic acid sensors (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-05-02
    Description: The plant hormone abscisic acid (ABA) acts as a developmental signal and as an integrator of environmental cues such as drought and cold. Key players in ABA signal transduction include the type 2C protein phosphatases (PP2Cs) ABI1 and ABI2, which act by negatively regulating ABA responses. In this study, we identify interactors of ABI1 and ABI2 which we have named regulatory components of ABA receptor (RCARs). In Arabidopsis, RCARs belong to a family with 14 members that share structural similarity with class 10 pathogen-related proteins. RCAR1 was shown to bind ABA, to mediate ABA-dependent inactivation of ABI1 or ABI2 in vitro, and to antagonize PP2C action in planta. Other RCARs also mediated ABA-dependent regulation of ABI1 and ABI2, consistent with a combinatorial assembly of receptor complexes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ma, Yue -- Szostkiewicz, Izabela -- Korte, Arthur -- Moes, Daniele -- Yang, Yi -- Christmann, Alexander -- Grill, Erwin -- New York, N.Y. -- Science. 2009 May 22;324(5930):1064-8. doi: 10.1126/science.1172408. Epub 2009 Apr 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lehrstuhl fur Botanik, Technische Universitat Munchen, Am Hochanger 4, D-85354 Freising, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19407143" target="_blank"〉PubMed〈/a〉
    Keywords: Abscisic Acid/*metabolism/pharmacology ; Amino Acid Sequence ; Arabidopsis/genetics/*metabolism/physiology ; Arabidopsis Proteins/antagonists & inhibitors/chemistry/genetics/*metabolism ; Binding Sites ; Carrier Proteins/chemistry/genetics/*metabolism ; Gene Expression Regulation, Plant ; Germination ; Molecular Sequence Data ; Phosphoprotein Phosphatases/antagonists & ; inhibitors/chemistry/genetics/*metabolism ; Plant Roots/growth & development ; Plant Stomata/physiology ; Plants, Genetically Modified ; Point Mutation ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Stereoisomerism ; Up-Regulation
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    Fast synaptic subcortical control of hippocampal circuits (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-10-17
    Description: Cortical information processing is under state-dependent control of subcortical neuromodulatory systems. Although this modulatory effect is thought to be mediated mainly by slow nonsynaptic metabotropic receptors, other mechanisms, such as direct synaptic transmission, are possible. Yet, it is currently unknown if any such form of subcortical control exists. Here, we present direct evidence of a strong, spatiotemporally precise excitatory input from an ascending neuromodulatory center. Selective stimulation of serotonergic median raphe neurons produced a rapid activation of hippocampal interneurons. At the network level, this subcortical drive was manifested as a pattern of effective disynaptic GABAergic inhibition that spread throughout the circuit. This form of subcortical network regulation should be incorporated into current concepts of normal and pathological cortical function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Varga, Viktor -- Losonczy, Attila -- Zemelman, Boris V -- Borhegyi, Zsolt -- Nyiri, Gabor -- Domonkos, Andor -- Hangya, Balazs -- Holderith, Noemi -- Magee, Jeffrey C -- Freund, Tamas F -- HHMI55005608/Howard Hughes Medical Institute/ -- MH-54671/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2009 Oct 16;326(5951):449-53. doi: 10.1126/science.1178307.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Experimental Medicine, Budapest 1083, Hungary. vargav@koki.hu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19833972" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Electric Stimulation ; Excitatory Postsynaptic Potentials ; Glutamic Acid/physiology ; Hippocampus/cytology/*physiology ; Inhibitory Postsynaptic Potentials ; Interneurons/*physiology ; Mice ; Neural Inhibition/physiology ; Neural Pathways/physiology ; Neurons, Afferent/*physiology ; Patch-Clamp Techniques ; Photic Stimulation ; Raphe Nuclei/cytology/*physiology ; Rats ; Rats, Sprague-Dawley ; Serotonin/*physiology ; Synapses/*physiology ; Synaptic Potentials/*physiology
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    Ventral tegmental area BDNF induces an opiate-dependent-like reward state in naive rats (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-05-30
    Description: The neural mechanisms underlying the transition from a drug-nondependent to a drug-dependent state remain elusive. Chronic exposure to drugs has been shown to increase brain-derived neurotrophic factor (BDNF) levels in ventral tegmental area (VTA) neurons. BDNF infusions into the VTA potentiate several behavioral effects of drugs, including psychomotor sensitization and cue-induced drug seeking. We found that a single infusion of BDNF into the VTA promotes a shift from a dopamine-independent to a dopamine-dependent opiate reward system, identical to that seen when an opiate-naive rat becomes dependent and withdrawn. This shift involves a switch in the gamma-aminobutyric acid type A (GABAA) receptors of VTA GABAergic neurons, from inhibitory to excitatory signaling.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2913611/" 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/PMC2913611/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vargas-Perez, Hector -- Ting-A Kee, Ryan -- Walton, Christine H -- Hansen, D Micah -- Razavi, Rozita -- Clarke, Laura -- Bufalino, Mary Rose -- Allison, David W -- Steffensen, Scott C -- van der Kooy, Derek -- AA13666/AA/NIAAA NIH HHS/ -- R01 AA013666/AA/NIAAA NIH HHS/ -- R01 AA013666-09/AA/NIAAA NIH HHS/ -- R01 AA020919/AA/NIAAA NIH HHS/ -- New York, N.Y. -- Science. 2009 Jun 26;324(5935):1732-4. doi: 10.1126/science.1168501. Epub 2009 May 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics, University of Toronto, 160 College Street, Toronto, Ontario M5S 3E1, Canada. vargashector@yahoo.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19478142" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bicuculline/pharmacology ; Brain-Derived Neurotrophic Factor/administration & ; dosage/genetics/*metabolism/*pharmacology ; Conditioning (Psychology) ; Dopamine/physiology ; Dopamine Antagonists/administration & dosage/pharmacology ; Flupenthixol/administration & dosage/pharmacology ; GABA Agonists/pharmacology ; GABA Antagonists/pharmacology ; Heroin Dependence/metabolism ; Male ; Morphine/administration & dosage ; Muscimol/pharmacology ; Opioid-Related Disorders/*metabolism ; RNA, Messenger/genetics/metabolism ; Rats ; Rats, Wistar ; Receptors, GABA-A/metabolism ; *Reward ; Signal Transduction ; Substance Withdrawal Syndrome/metabolism ; Ventral Tegmental Area/drug effects/*metabolism
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    Chronic stress causes frontostriatal reorganization and affects decision-making (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-08-01
    Description: The ability to shift between different behavioral strategies is necessary for appropriate decision-making. Here, we show that chronic stress biases decision-making strategies, affecting the ability of stressed animals to perform actions on the basis of their consequences. Using two different operant tasks, we revealed that, in making choices, rats subjected to chronic stress became insensitive to changes in outcome value and resistant to changes in action-outcome contingency. Furthermore, chronic stress caused opposing structural changes in the associative and sensorimotor corticostriatal circuits underlying these different behavioral strategies, with atrophy of medial prefrontal cortex and the associative striatum and hypertrophy of the sensorimotor striatum. These data suggest that the relative advantage of circuits coursing through sensorimotor striatum observed after chronic stress leads to a bias in behavioral strategies toward habit.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dias-Ferreira, Eduardo -- Sousa, Joao C -- Melo, Irene -- Morgado, Pedro -- Mesquita, Ana R -- Cerqueira, Joao J -- Costa, Rui M -- Sousa, Nuno -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2009 Jul 31;325(5940):621-5. doi: 10.1126/science.1171203.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Life and Health Sciences Research Institute (ICVS), School of Health Sciences, University of Minho, 4710-057 Braga, Portugal.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19644122" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Atrophy ; Cell Count ; Choice Behavior ; Chronic Disease ; Corpus Striatum/*pathology ; *Decision Making ; Dendrites/pathology ; Frontal Lobe/*pathology ; Habits ; Hypertrophy ; Neural Pathways/pathology ; Neurons/pathology ; Prefrontal Cortex/pathology ; Rats ; Rats, Long-Evans ; Rats, Wistar ; Reinforcement (Psychology) ; Stress, Psychological/*pathology/*psychology
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    A role for the CHC22 clathrin heavy-chain isoform in human glucose metabolism (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-05-30
    Description: Intracellular trafficking of the glucose transporter GLUT4 from storage compartments to the plasma membrane is triggered in muscle and fat during the body's response to insulin. Clathrin is involved in intracellular trafficking, and in humans, the clathrin heavy-chain isoform CHC22 is highly expressed in skeletal muscle. We found a role for CHC22 in the formation of insulin-responsive GLUT4 compartments in human muscle and adipocytes. CHC22 also associated with expanded GLUT4 compartments in muscle from type 2 diabetic patients. Tissue-specific introduction of CHC22 in mice, which have only a pseudogene for this protein, caused aberrant localization of GLUT4 transport pathway components in their muscle, as well as features of diabetes. Thus, CHC22-dependent membrane trafficking constitutes a species-restricted pathway in human muscle and fat with potential implications for type 2 diabetes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2975026/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2975026/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vassilopoulos, Stephane -- Esk, Christopher -- Hoshino, Sachiko -- Funke, Birgit H -- Chen, Chih-Ying -- Plocik, Alex M -- Wright, Woodring E -- Kucherlapati, Raju -- Brodsky, Frances M -- GM038093/GM/NIGMS NIH HHS/ -- HD47863/HD/NICHD NIH HHS/ -- R01 GM038093/GM/NIGMS NIH HHS/ -- R01 GM038093-19/GM/NIGMS NIH HHS/ -- R01 GM038093-19S1/GM/NIGMS NIH HHS/ -- R01 GM038093-20A1/GM/NIGMS NIH HHS/ -- R01 HD047863/HD/NICHD NIH HHS/ -- R01 HD047863-01/HD/NICHD NIH HHS/ -- R01 HD047863-02/HD/NICHD NIH HHS/ -- R01 HD047863-03/HD/NICHD NIH HHS/ -- R01 HD047863-04/HD/NICHD NIH HHS/ -- R01 HD047863-05/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2009 May 29;324(5931):1192-6. doi: 10.1126/science.1171529.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bioengineering and Therapeutic Sciences, University of California, School of Pharmacy, San Francisco (UCSF), San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19478182" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes/cytology/*metabolism/ultrastructure ; Animals ; Blood Glucose/metabolism ; Cell Differentiation ; Cell Line ; Cell Membrane/metabolism ; Clathrin/chemistry/*metabolism ; Clathrin Heavy Chains ; Clathrin-Coated Vesicles/*metabolism ; Diabetes Mellitus, Type 2/*metabolism ; Glucose/*metabolism ; Glucose Transporter Type 4/*metabolism ; Humans ; Insulin/blood/pharmacology ; Mice ; Mice, Transgenic ; Muscle Fibers, Skeletal/metabolism ; Muscle, Skeletal/*metabolism/ultrastructure ; Myoblasts/cytology/metabolism/ultrastructure ; Protein Isoforms/chemistry/metabolism ; Protein Transport ; Signal Transduction
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    Structural insight into nascent polypeptide chain-mediated translational stalling (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-11-26
    Description: Expression of the Escherichia coli tryptophanase operon depends on ribosome stalling during translation of the upstream TnaC leader peptide, a process for which interactions between the TnaC nascent chain and the ribosomal exit tunnel are critical. We determined a 5.8 angstrom-resolution cryo-electron microscopy and single-particle reconstruction of a ribosome stalled during translation of the tnaC leader gene. The nascent chain was extended within the exit tunnel, making contacts with ribosomal components at distinct sites. Upon stalling, two conserved residues within the peptidyltransferase center adopted conformations that preclude binding of release factors. We propose a model whereby interactions within the tunnel are relayed to the peptidyltransferase center to inhibit translation. Moreover, we show that nascent chains adopt distinct conformations within the ribosomal exit tunnel.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2920484/" 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/PMC2920484/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Seidelt, Birgit -- Innis, C Axel -- Wilson, Daniel N -- Gartmann, Marco -- Armache, Jean-Paul -- Villa, Elizabeth -- Trabuco, Leonardo G -- Becker, Thomas -- Mielke, Thorsten -- Schulten, Klaus -- Steitz, Thomas A -- Beckmann, Roland -- GM022778/GM/NIGMS NIH HHS/ -- P41 RR005969/RR/NCRR NIH HHS/ -- P41 RR005969-19/RR/NCRR NIH HHS/ -- P41-RR05969/RR/NCRR NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Dec 4;326(5958):1412-5. doi: 10.1126/science.1177662. Epub 2009 Oct 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gene Center and Center for Integrated Protein Science Munich (CIPSM), Department for Chemistry and Biochemistry, University of Munich, Feodor-Lynen-Strasse 25, 81377 Munich, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19933110" target="_blank"〉PubMed〈/a〉
    Keywords: Binding Sites ; Cryoelectron Microscopy ; Escherichia coli/*genetics/metabolism ; Escherichia coli Proteins/*chemistry/genetics/*metabolism/ultrastructure ; Gene Expression Regulation, Bacterial ; Image Processing, Computer-Assisted ; Models, Biological ; Models, Molecular ; Operon ; Peptidyl Transferases/metabolism ; *Protein Biosynthesis ; Protein Conformation ; RNA-Binding Proteins/chemistry/metabolism/ultrastructure ; Ribosomal Proteins/chemistry/metabolism/ultrastructure ; Ribosomes/*metabolism/ultrastructure ; Tryptophanase/biosynthesis/*genetics
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    Two chemoreceptors mediate developmental effects of dauer pheromone in C. elegans (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-10-03
    Description: Intraspecific chemical communication is mediated by signals called pheromones. Caenorhabditis elegans secretes a mixture of small molecules (collectively termed dauer pheromone) that regulates entry into the alternate dauer larval stage and also modulates adult behavior via as yet unknown receptors. Here, we identify two heterotrimeric GTP-binding protein (G protein)-coupled receptors (GPCRs) that mediate dauer formation in response to a subset of dauer pheromone components. The SRBC-64 and SRBC-66 GPCRs are members of the large Caenorhabditis-specific SRBC subfamily and are expressed in the ASK chemosensory neurons, which are required for pheromone-induced dauer formation. Expression of both, but not each receptor alone, confers pheromone-mediated effects on heterologous cells. Identification of dauer pheromone receptors will allow a better understanding of the signaling cascades that transduce the context-dependent effects of ecologically important chemical signals.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4448937/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4448937/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Kyuhyung -- Sato, Koji -- Shibuya, Mayumi -- Zeiger, Danna M -- Butcher, Rebecca A -- Ragains, Justin R -- Clardy, Jon -- Touhara, Kazushige -- Sengupta, Piali -- F32 GM077943/GM/NIGMS NIH HHS/ -- P30 NS045713/NS/NINDS NIH HHS/ -- P30 NS45713/NS/NINDS NIH HHS/ -- R01 CA024487/CA/NCI NIH HHS/ -- R01 CA24487/CA/NCI NIH HHS/ -- R01 GM056223/GM/NIGMS NIH HHS/ -- R01 GM56223/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2009 Nov 13;326(5955):994-8. doi: 10.1126/science.1176331. Epub 2009 Oct 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology and National Center for Behavioral Genomics, Brandeis University, Waltham, MA 02454, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19797623" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis elegans/genetics/*growth & development/*physiology ; Caenorhabditis elegans Proteins/genetics/physiology ; Calcium/metabolism ; Cell Line ; Chemoreceptor Cells/metabolism ; Cyclic AMP/metabolism ; Cyclic GMP/metabolism ; GTP-Binding Protein alpha Subunits, Gi-Go/physiology ; Gene Expression Regulation, Developmental ; Genes, Helminth ; Guanylate Cyclase/antagonists & inhibitors/metabolism ; Hexoses/chemistry/physiology ; Humans ; Mutation ; Pheromones/*physiology ; Receptors, G-Protein-Coupled ; Reproduction ; Signal Transduction ; Transfection
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    Global analysis of short RNAs reveals widespread promoter-proximal stalling and arrest of Pol II in Drosophila (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-12-17
    Description: Emerging evidence indicates that gene expression in higher organisms is regulated by RNA polymerase II stalling during early transcription elongation. To probe the mechanisms responsible for this regulation, we developed methods to isolate and characterize short RNAs derived from stalled RNA polymerase II in Drosophila cells. Significant levels of these short RNAs were generated from more than one-third of all genes, indicating that promoter-proximal stalling is a general feature of early polymerase elongation. Nucleotide composition of the initially transcribed sequence played an important role in promoting transcriptional stalling by rendering polymerase elongation complexes highly susceptible to backtracking and arrest. These results indicate that the intrinsic efficiency of early elongation can greatly affect gene expression.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3435875/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3435875/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nechaev, Sergei -- Fargo, David C -- dos Santos, Gilberto -- Liu, Liwen -- Gao, Yuan -- Adelman, Karen -- ZIA ES101987-05/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2010 Jan 15;327(5963):335-8. doi: 10.1126/science.1181421. Epub 2009 Dec 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20007866" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Composition ; Cell Line ; Drosophila melanogaster ; *Gene Expression Regulation ; *Genes, Insect ; Genome, Insect ; Oligonucleotide Array Sequence Analysis ; *Promoter Regions, Genetic ; RNA/genetics/*metabolism ; RNA Caps/genetics/metabolism ; RNA Polymerase II/*metabolism ; RNA, Messenger/genetics/metabolism ; Transcription Initiation Site ; *Transcription, Genetic
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    Medicine. A reinnervating microRNA (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-12-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brown, Robert H -- New York, N.Y. -- Science. 2009 Dec 11;326(5959):1494-5. doi: 10.1126/science.1183842.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neurology, Biochemistry and Molecular Pharmacology and Program in Neuroscience, University of Massachusetts Medical School, 55 Lake Avenue North, Worcester, MA 01655, USA. robert.brown@umassmed.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20007892" target="_blank"〉PubMed〈/a〉
    Keywords: Amyotrophic Lateral Sclerosis/pathology/*physiopathology ; Animals ; Binding Sites ; Carrier Proteins/metabolism ; Disease Models, Animal ; Histone Deacetylases/metabolism ; Mice ; Mice, Transgenic ; MicroRNAs/genetics/*metabolism ; Muscle Cells/enzymology ; Muscle Denervation ; Muscle, Skeletal/innervation/metabolism ; Myostatin/genetics ; Neuromuscular Junction/*pathology/*physiology ; RNA Interference ; Sequence Analysis, RNA ; Signal Transduction
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    Common regulatory variation impacts gene expression in a cell type-dependent manner (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-08-01
    Description: Studies correlating genetic variation to gene expression facilitate the interpretation of common human phenotypes and disease. As functional variants may be operating in a tissue-dependent manner, we performed gene expression profiling and association with genetic variants (single-nucleotide polymorphisms) on three cell types of 75 individuals. We detected cell type-specific genetic effects, with 69 to 80% of regulatory variants operating in a cell type-specific manner, and identified multiple expressive quantitative trait loci (eQTLs) per gene, unique or shared among cell types and positively correlated with the number of transcripts per gene. Cell type-specific eQTLs were found at larger distances from genes and at lower effect size, similar to known enhancers. These data suggest that the complete regulatory variant repertoire can only be uncovered in the context of cell-type specificity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2867218/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2867218/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dimas, Antigone S -- Deutsch, Samuel -- Stranger, Barbara E -- Montgomery, Stephen B -- Borel, Christelle -- Attar-Cohen, Homa -- Ingle, Catherine -- Beazley, Claude -- Gutierrez Arcelus, Maria -- Sekowska, Magdalena -- Gagnebin, Marilyne -- Nisbett, James -- Deloukas, Panos -- Dermitzakis, Emmanouil T -- Antonarakis, Stylianos E -- 077011/Wellcome Trust/United Kingdom -- 077046/Wellcome Trust/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2009 Sep 4;325(5945):1246-50. doi: 10.1126/science.1174148. Epub 2009 Jul 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, CB10 1HH, Cambridge, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19644074" target="_blank"〉PubMed〈/a〉
    Keywords: Allelic Imbalance ; B-Lymphocytes ; Cell Line ; Enhancer Elements, Genetic ; Fibroblasts ; Gene Expression Profiling ; *Gene Expression Regulation ; Gene Frequency ; Genotype ; Humans ; *Polymorphism, Single Nucleotide ; *Quantitative Trait Loci ; RNA, Messenger/genetics/metabolism ; *Regulatory Elements, Transcriptional ; Statistics, Nonparametric ; T-Lymphocytes
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    Regulation of hypoxia-inducible factor 2alpha signaling by the stress-responsive deacetylase sirtuin 1 (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-06-06
    Description: To survive in hostile environments, organisms activate stress-responsive transcriptional regulators that coordinately increase production of protective factors. Hypoxia changes cellular metabolism and thus activates redox-sensitive as well as oxygen-dependent signal transducers. We demonstrate that Sirtuin 1 (Sirt1), a redox-sensing deacetylase, selectively stimulates activity of the transcription factor hypoxia-inducible factor 2 alpha (HIF-2alpha) during hypoxia. The effect of Sirt1 on HIF-2alpha required direct interaction of the proteins and intact deacetylase activity of Sirt1. Select lysine residues in HIF-2alpha that are acetylated during hypoxia confer repression of Sirt1 augmentation by small-molecule inhibitors. In cultured cells and mice, decreasing or increasing Sirt1 activity or levels affected expression of the HIF-2alpha target gene erythropoietin accordingly. Thus, Sirt1 promotes HIF-2 signaling during hypoxia and likely other environmental stresses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dioum, Elhadji M -- Chen, Rui -- Alexander, Matthew S -- Zhang, Quiyang -- Hogg, Richard T -- Gerard, Robert D -- Garcia, Joseph A -- I01 BX000446/BX/BLRD VA/ -- New York, N.Y. -- Science. 2009 Jun 5;324(5932):1289-93. doi: 10.1126/science.1169956.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Veterans Affairs North Texas Health Care System, Department of Medicine, 4500 South Lancaster Road, Dallas, TX 75216, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19498162" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Amino Acid Substitution ; Animals ; Basic Helix-Loop-Helix Transcription Factors/chemistry/genetics/*metabolism ; *Cell Hypoxia ; Cell Line ; Cell Line, Tumor ; Erythropoietin/genetics ; Gene Expression Regulation ; Humans ; Kidney/metabolism ; Liver/embryology/metabolism ; Mice ; Mice, Knockout ; Mutant Proteins/chemistry/metabolism ; Oxidation-Reduction ; *Signal Transduction ; Sirtuin 1 ; Sirtuins/genetics/*metabolism
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    Overexpression of alpha2A-adrenergic receptors contributes to type 2 diabetes (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-12-08
    Description: Several common genetic variations have been associated with type 2 diabetes, but the exact disease mechanisms are still poorly elucidated. Using congenic strains from the diabetic Goto-Kakizaki rat, we identified a 1.4-megabase genomic locus that was linked to impaired insulin granule docking at the plasma membrane and reduced beta cell exocytosis. In this locus, Adra2a, encoding the alpha2A-adrenergic receptor [alpha(2A)AR], was significantly overexpressed. Alpha(2A)AR mediates adrenergic suppression of insulin secretion. Pharmacological receptor antagonism, silencing of receptor expression, or blockade of downstream effectors rescued insulin secretion in congenic islets. Furthermore, we identified a single-nucleotide polymorphism in the human ADRA2A gene for which risk allele carriers exhibited overexpression of alpha(2A)AR, reduced insulin secretion, and increased type 2 diabetes risk. Human pancreatic islets from risk allele carriers exhibited reduced granule docking and secreted less insulin in response to glucose; both effects were counteracted by pharmacological alpha(2A)AR antagonists.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rosengren, Anders H -- Jokubka, Ramunas -- Tojjar, Damon -- Granhall, Charlotte -- Hansson, Ola -- Li, Dai-Qing -- Nagaraj, Vini -- Reinbothe, Thomas M -- Tuncel, Jonatan -- Eliasson, Lena -- Groop, Leif -- Rorsman, Patrik -- Salehi, Albert -- Lyssenko, Valeriya -- Luthman, Holger -- Renstrom, Erik -- New York, N.Y. -- Science. 2010 Jan 8;327(5962):217-20. doi: 10.1126/science.1176827. Epub 2009 Nov 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lund University Diabetes Centre, Malmo, SE-20502 Malmo, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965390" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adrenergic alpha-2 Receptor Agonists ; Adrenergic alpha-2 Receptor Antagonists ; Adrenergic alpha-Agonists/pharmacology ; Adrenergic alpha-Antagonists/pharmacology ; Adult ; Aged ; Animals ; Animals, Congenic ; Blood Glucose/metabolism ; Cell Membrane/metabolism ; Cyclic AMP/metabolism ; Diabetes Mellitus, Type 2/*genetics/metabolism ; Exocytosis ; Genetic Association Studies ; Genetic Predisposition to Disease ; Humans ; Insulin/blood/*secretion ; Insulin-Secreting Cells/*secretion ; Middle Aged ; Polymorphism, Single Nucleotide ; RNA Interference ; Rats ; Rats, Inbred Strains ; Receptors, Adrenergic, alpha-2/*genetics/*metabolism ; Risk Factors ; Secretory Vesicles/metabolism ; Up-Regulation ; Young Adult
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    Induction of synaptic long-term potentiation after opioid withdrawal (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-07-11
    Description: mu-Opioid receptor (MOR) agonists represent the gold standard for the treatment of severe pain but may paradoxically also enhance pain sensitivity, that is, lead to opioid-induced hyperalgesia (OIH). We show that abrupt withdrawal from MOR agonists induces long-term potentiation (LTP) at the first synapse in pain pathways. Induction of opioid withdrawal LTP requires postsynaptic activation of heterotrimeric guanine nucleotide-binding proteins and N-methyl-d-aspartate receptors and a rise of postsynaptic calcium concentrations. In contrast, the acute depression by opioids is induced presynaptically at these synapses. Withdrawal LTP can be prevented by tapered withdrawal and shares pharmacology and signal transduction pathways with OIH. These findings provide a previously unrecognized target to selectively combat pro-nociceptive effects of opioids without compromising opioid analgesia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Drdla, Ruth -- Gassner, Matthias -- Gingl, Ewald -- Sandkuhler, Jurgen -- P 18129/Austrian Science Fund FWF/Austria -- New York, N.Y. -- Science. 2009 Jul 10;325(5937):207-10. doi: 10.1126/science.1171759.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurophysiology, Center for Brain Research, Medical University of Vienna, Spitalgasse 4, 1090 Vienna, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19590003" target="_blank"〉PubMed〈/a〉
    Keywords: Analgesics, Opioid/administration & dosage/*adverse effects/pharmacology ; Animals ; Calcium/metabolism ; Enkephalin, Ala(2)-MePhe(4)-Gly(5)-/administration & dosage/adverse ; effects/pharmacology ; Evoked Potentials ; GTP-Binding Proteins/metabolism ; Hyperalgesia/chemically induced ; *Long-Term Potentiation/drug effects ; Male ; Nerve Fibers, Unmyelinated/physiology ; Patch-Clamp Techniques ; Piperidines/administration & dosage/adverse effects/pharmacology ; Posterior Horn Cells/drug effects/physiology ; Rats ; Rats, Sprague-Dawley ; Receptors, N-Methyl-D-Aspartate/metabolism ; Receptors, Opioid, mu/*agonists ; Signal Transduction ; Substance Withdrawal Syndrome/*physiopathology ; Synapses/drug effects/*physiology
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    Poly(ADP-ribose)-dependent regulation of DNA repair by the chromatin remodeling enzyme ALC1 (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-08-08
    Description: Posttranslational modifications play key roles in regulating chromatin plasticity. Although various chromatin-remodeling enzymes have been described that respond to specific histone modifications, little is known about the role of poly[adenosine 5'-diphosphate (ADP)-ribose] in chromatin remodeling. Here, we identify a chromatin-remodeling enzyme, ALC1 (Amplified in Liver Cancer 1, also known as CHD1L), that interacts with poly(ADP-ribose) and catalyzes PARP1-stimulated nucleosome sliding. Our results define ALC1 as a DNA damage-response protein whose role in this process is sustained by its association with known DNA repair factors and its rapid poly(ADP-ribose)-dependent recruitment to DNA damage sites. Furthermore, we show that depletion or overexpression of ALC1 results in sensitivity to DNA-damaging agents. Collectively, these results provide new insights into the mechanisms by which poly(ADP-ribose) regulates DNA repair.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3443743/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3443743/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ahel, Dragana -- Horejsi, Zuzana -- Wiechens, Nicola -- Polo, Sophie E -- Garcia-Wilson, Elisa -- Ahel, Ivan -- Flynn, Helen -- Skehel, Mark -- West, Stephen C -- Jackson, Stephen P -- Owen-Hughes, Tom -- Boulton, Simon J -- 064414/Wellcome Trust/United Kingdom -- 11224/Cancer Research UK/United Kingdom -- A3549/Cancer Research UK/United Kingdom -- A5290/Cancer Research UK/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Cancer Research UK/United Kingdom -- Department of Health/United Kingdom -- New York, N.Y. -- Science. 2009 Sep 4;325(5945):1240-3. doi: 10.1126/science.1177321. Epub 2009 Aug 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉DNA Damage Response Laboratory, Clare Hall, London Research Institute, South Mimms EN6 3LD, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19661379" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphatases/metabolism ; Adenosine Triphosphate/metabolism ; Cell Line ; Chromatin/*metabolism ; *Chromatin Assembly and Disassembly ; DNA Damage ; DNA Helicases/chemistry/genetics/*metabolism ; *DNA Repair ; DNA-Binding Proteins/chemistry/genetics/*metabolism ; Humans ; Hydrogen Peroxide/pharmacology ; Immunoprecipitation ; Kinetics ; Mutant Proteins/chemistry/metabolism ; Nucleosomes/metabolism ; Phleomycins/pharmacology ; Poly Adenosine Diphosphate Ribose/*metabolism ; Poly(ADP-ribose) Polymerase Inhibitors ; Poly(ADP-ribose) Polymerases/metabolism ; Protein Structure, Tertiary ; Radiation, Ionizing ; Recombinant Proteins/chemistry/metabolism
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    Ankyrin-G promotes cyclic nucleotide-gated channel transport to rod photoreceptor sensory cilia (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-03-21
    Description: Cyclic nucleotide-gated (CNG) channels localize exclusively to the plasma membrane of photosensitive outer segments of rod photoreceptors where they generate the electrical response to light. Here, we report the finding that targeting of CNG channels to the rod outer segment required their interaction with ankyrin-G. Ankyrin-G localized exclusively to rod outer segments, coimmunoprecipitated with the CNG channel, and bound to the C-terminal domain of the channel beta1 subunit. Ankyrin-G depletion in neonatal mouse retinas markedly reduced CNG channel expression. Transgenic expression of CNG channel beta-subunit mutants in Xenopus rods showed that ankyrin-G binding was necessary and sufficient for targeting of the beta1 subunit to outer segments. Thus, ankyrin-G is required for transport of CNG channels to the plasma membrane of rod outer segments.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2792576/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2792576/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kizhatil, Krishnakumar -- Baker, Sheila A -- Arshavsky, Vadim Y -- Bennett, Vann -- EY12859/EY/NEI NIH HHS/ -- P30 EY005722/EY/NEI NIH HHS/ -- P30 EY005722-23/EY/NEI NIH HHS/ -- R01 EY012859/EY/NEI NIH HHS/ -- R01 EY012859-10/EY/NEI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Mar 20;323(5921):1614-7. doi: 10.1126/science.1169789.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Duke University Medical Center, Durham, NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19299621" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Animals, Genetically Modified ; Ankyrins/*metabolism ; Cattle ; Cell Line ; Cell Membrane/metabolism ; Cilia/*metabolism ; Cyclic Nucleotide-Gated Cation Channels/*metabolism ; Humans ; Mice ; Molecular Sequence Data ; Nerve Tissue Proteins/metabolism ; Recombinant Fusion Proteins/metabolism ; Rod Cell Outer Segment/*metabolism ; Xenopus laevis
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    Generation of functional ventricular heart muscle from mouse ventricular progenitor cells (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-10-17
    Description: The mammalian heart is formed from distinct sets of first and second heart field (FHF and SHF, respectively) progenitors. Although multipotent progenitors have previously been shown to give rise to cardiomyocytes, smooth muscle, and endothelial cells, the mechanism governing the generation of large numbers of differentiated progeny remains poorly understood. We have employed a two-colored fluorescent reporter system to isolate FHF and SHF progenitors from developing mouse embryos and embryonic stem cells. Genome-wide profiling of coding and noncoding transcripts revealed distinct molecular signatures of these progenitor populations. We further identify a committed ventricular progenitor cell in the Islet 1 lineage that is capable of limited in vitro expansion, differentiation, and assembly into functional ventricular muscle tissue, representing a combination of tissue engineering and stem cell biology.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2895998/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2895998/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Domian, Ibrahim J -- Chiravuri, Murali -- van der Meer, Peter -- Feinberg, Adam W -- Shi, Xi -- Shao, Ying -- Wu, Sean M -- Parker, Kevin Kit -- Chien, Kenneth R -- K08 HL081086/HL/NHLBI NIH HHS/ -- K08 HL081086-01/HL/NHLBI NIH HHS/ -- K08 HL091209/HL/NHLBI NIH HHS/ -- R01 HL079126/HL/NHLBI NIH HHS/ -- R01 HL079126-01A1/HL/NHLBI NIH HHS/ -- T32 HL002807/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2009 Oct 16;326(5951):426-9. doi: 10.1126/science.1177350.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cardiovascular Research Center, Massachusetts General Hospital, Charles River Plaza, CPZN 3200, 185 Cambridge Street, Boston, MA 02114-2790, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19833966" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Cell Cycle ; Cell Differentiation ; Cell Line ; Cell Lineage ; Cells, Cultured ; Embryonic Stem Cells/*cytology/physiology ; Gene Expression ; Heart/embryology ; Heart Ventricles/*cytology/embryology ; Mice ; Mice, Transgenic ; Muscle Development ; Myocardial Contraction ; Myocytes, Cardiac/*cytology/physiology ; Oligonucleotide Array Sequence Analysis ; *Tissue Engineering ; *Ventricular Function
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    RSY-1 is a local inhibitor of presynaptic assembly in C. elegans (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-03-17
    Description: As fundamental units of neuronal communication, chemical synapses are composed of presynaptic and postsynaptic specializations that form at specific locations with defined shape and size. Synaptic assembly must be tightly regulated to prevent overgrowth of the synapse size and number, but the molecular mechanisms that inhibit synapse assembly are poorly understood. We identified regulator of synaptogenesis-1 (RSY-1) as an evolutionarily conserved molecule that locally antagonized presynaptic assembly. The loss of RSY-1 in Caenorhabditis elegans led to formation of extra synapses and recruitment of excessive synaptic material to presynaptic sites. RSY-1 directly interacted with and negatively regulated SYD-2/liprin-alpha, a master assembly molecule that recruits numerous synaptic components to presynaptic sites. RSY-1 also bound and regulated SYD-1, a synaptic protein required for proper functioning of SYD-2. Thus, local inhibitory mechanisms govern synapse formation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3087376/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3087376/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Patel, Maulik R -- Shen, Kang -- 1R01NS048392/NS/NINDS NIH HHS/ -- R01 NS048392/NS/NINDS NIH HHS/ -- R01 NS048392-05/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Mar 13;323(5920):1500-3. doi: 10.1126/science.1169025.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neurosciences Program, Stanford University, 385 Serra Mall, Herrin Labs, Room 144, Stanford University, Stanford,CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19286562" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Genetically Modified ; Caenorhabditis elegans/genetics/*physiology ; Caenorhabditis elegans Proteins/chemistry/genetics/*metabolism ; Carrier Proteins/metabolism ; Cell Line ; Cell Nucleus/metabolism ; Humans ; Mutation ; Nerve Tissue Proteins/metabolism ; Nuclear Proteins/chemistry/genetics/*metabolism ; Phosphoproteins/genetics/metabolism ; Protein Binding ; Protein Interaction Mapping ; Protein Isoforms/chemistry/genetics/metabolism ; Protein Structure, Tertiary ; Recombinant Fusion Proteins/metabolism ; Synapses/metabolism/*physiology
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    Mammalian expression of infrared fluorescent proteins engineered from a bacterial phytochrome (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-05-09
    Description: Visibly fluorescent proteins (FPs) from jellyfish and corals have revolutionized many areas of molecular and cell biology, but the use of FPs in intact animals, such as mice, has been handicapped by poor penetration of excitation light. We now show that a bacteriophytochrome from Deinococcus radiodurans, incorporating biliverdin as the chromophore, can be engineered into monomeric, infrared-fluorescent proteins (IFPs), with excitation and emission maxima of 684 and 708 nm, respectively; extinction coefficient 〉90,000 M(-1) cm(-1); and quantum yield of 0.07. IFPs express well in mammalian cells and mice and spontaneously incorporate biliverdin, which is ubiquitous as the initial intermediate in heme catabolism but has negligible fluorescence by itself. Because their wavelengths penetrate tissue well, IFPs are suitable for whole-body imaging. The IFPs developed here provide a scaffold for further engineering.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2763207/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2763207/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shu, Xiaokun -- Royant, Antoine -- Lin, Michael Z -- Aguilera, Todd A -- Lev-Ram, Varda -- Steinbach, Paul A -- Tsien, Roger Y -- R01 CA158448/CA/NCI NIH HHS/ -- R01 GM086197/GM/NIGMS NIH HHS/ -- R01 GM086197-01/GM/NIGMS NIH HHS/ -- R01 NS027177/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 May 8;324(5928):804-7. doi: 10.1126/science.1168683.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of California at San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0647, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19423828" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviridae/genetics ; Amino Acid Sequence ; Animals ; *Biliverdine/chemistry/metabolism ; Cell Line ; Deinococcus/*chemistry ; Diagnostic Imaging ; Fluorescence ; Humans ; Liver/anatomy & histology ; *Luminescent Proteins/chemistry/metabolism ; Mice ; Molecular Sequence Data ; *Phytochrome/chemistry/genetics/metabolism ; *Protein Engineering ; Recombinant Fusion Proteins/chemistry/metabolism ; Spectrophotometry, Infrared ; Whole Body Imaging
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    Apicomplexan parasites co-opt host calpains to facilitate their escape from infected cells (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-04-04
    Description: Apicomplexan parasites, including Plasmodium falciparum and Toxoplasma gondii (the causative agents of malaria and toxoplasmosis, respectively), are responsible for considerable morbidity and mortality worldwide. These pathogenic protozoa replicate within an intracellular vacuole inside of infected host cells, from which they must escape to initiate a new lytic cycle. By integrating cell biological, pharmacological, and genetic approaches, we provide evidence that both Plasmodium and Toxoplasma hijack host cell calpain proteases to facilitate parasite egress. Immunodepletion or inhibition of calpain-1 in hypotonically lysed and resealed erythrocytes prevented the escape of P. falciparum parasites, which was restored by adding purified calpain-1. Similarly, efficient egress of T. gondii from mammalian fibroblasts was blocked by either small interfering RNA-mediated suppression or genetic deletion of calpain activity and could be restored by genetic complementation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3391539/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3391539/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chandramohanadas, Rajesh -- Davis, Paul H -- Beiting, Daniel P -- Harbut, Michael B -- Darling, Claire -- Velmourougane, Geetha -- Lee, Ming Yeh -- Greer, Peter A -- Roos, David S -- Greenbaum, Doron C -- F32 AI075846/AI/NIAID NIH HHS/ -- F32 AI075846-02/AI/NIAID NIH HHS/ -- F32 AI077268/AI/NIAID NIH HHS/ -- F32 AI077268-02/AI/NIAID NIH HHS/ -- R37 AI028724/AI/NIAID NIH HHS/ -- R37 AI028724-17/AI/NIAID NIH HHS/ -- T32 GM008076/GM/NIGMS NIH HHS/ -- T32 GM008076-24/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2009 May 8;324(5928):794-7. doi: 10.1126/science.1171085. Epub 2009 Apr 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of Pennsylvania, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19342550" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calpain/blood/genetics/*metabolism ; Cell Line ; Cell Line, Tumor ; Erythrocytes/*parasitology ; Fibroblasts/parasitology ; Humans ; Leucine/analogs & derivatives/pharmacology ; Life Cycle Stages ; Merozoites/physiology ; Mice ; Mice, Knockout ; Plasmodium falciparum/growth & development/metabolism/*pathogenicity/physiology ; RNA, Small Interfering ; Schizonts/physiology ; Toxoplasma/growth & development/metabolism/*pathogenicity/physiology
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    Jmjd6 catalyses lysyl-hydroxylation of U2AF65, a protein associated with RNA splicing (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-07-04
    Description: The finding that the metazoan hypoxic response is regulated by oxygen-dependent posttranslational hydroxylations, which regulate the activity and lifetime of hypoxia-inducible factor (HIF), has raised the question of whether other hydroxylases are involved in the regulation of gene expression. We reveal that the splicing factor U2 small nuclear ribonucleoprotein auxiliary factor 65-kilodalton subunit (U2AF65) undergoes posttranslational lysyl-5-hydroxylation catalyzed by the Fe(II) and 2-oxoglutarate-dependent dioxygenase Jumonji domain-6 protein (Jmjd6). Jmjd6 is a nuclear protein that has an important role in vertebrate development and is a human homolog of the HIF asparaginyl-hydroxylase. Jmjd6 is shown to change alternative RNA splicing of some, but not all, of the endogenous and reporter genes, supporting a specific role for Jmjd6 in the regulation of RNA splicing.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Webby, Celia J -- Wolf, Alexander -- Gromak, Natalia -- Dreger, Mathias -- Kramer, Holger -- Kessler, Benedikt -- Nielsen, Michael L -- Schmitz, Corinna -- Butler, Danica S -- Yates, John R 3rd -- Delahunty, Claire M -- Hahn, Phillip -- Lengeling, Andreas -- Mann, Matthias -- Proudfoot, Nicholas J -- Schofield, Christopher J -- Bottger, Angelika -- 084655/Wellcome Trust/United Kingdom -- G9826944/Medical Research Council/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2009 Jul 3;325(5936):90-3. doi: 10.1126/science.1175865.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Chemistry Research Laboratory and Oxford Centre for Integrative Systems Biology, University of Oxford, 12 Mansfield Road, Oxford, Oxon OX1 3TA, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19574390" target="_blank"〉PubMed〈/a〉
    Keywords: *Alternative Splicing ; Amino Acid Sequence ; Biocatalysis ; Cell Line ; Chromatography, Liquid ; HeLa Cells ; Humans ; Hydroxylation ; Jumonji Domain-Containing Histone Demethylases ; Lysine/metabolism ; Molecular Sequence Data ; Nuclear Proteins/chemistry/*metabolism ; Protein Processing, Post-Translational ; RNA, Small Interfering ; Receptors, Cell Surface/genetics/*metabolism ; Recombinant Proteins/metabolism ; Ribonucleoproteins/chemistry/*metabolism ; Tandem Mass Spectrometry ; Tropomyosin/genetics
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    The nuclear DNA base 5-hydroxymethylcytosine is present in Purkinje neurons and the brain (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-04-18
    Description: Despite the importance of epigenetic regulation in neurological disorders, little is known about neuronal chromatin. Cerebellar Purkinje neurons have large and euchromatic nuclei, whereas granule cell nuclei are small and have a more typical heterochromatin distribution. While comparing the abundance of 5-methylcytosine in Purkinje and granule cell nuclei, we detected the presence of an unusual DNA nucleotide. Using thin-layer chromatography, high-pressure liquid chromatography, and mass spectrometry, we identified the nucleotide as 5-hydroxymethyl-2'-deoxycytidine (hmdC). hmdC constitutes 0.6% of total nucleotides in Purkinje cells, 0.2% in granule cells, and is not present in cancer cell lines. hmdC is a constituent of nuclear DNA that is highly abundant in the brain, suggesting a role in epigenetic control of neuronal function.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3263819/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3263819/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kriaucionis, Skirmantas -- Heintz, Nathaniel -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 May 15;324(5929):929-30. doi: 10.1126/science.1169786. Epub 2009 Apr 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Biology, Howard Hughes Medical Institute, Rockefeller University, New York, NY 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19372393" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Brain Chemistry ; Cell Line ; Cerebellum/*chemistry/cytology ; Chromatography, High Pressure Liquid ; Chromatography, Thin Layer ; Cytosine/*analogs & derivatives/analysis ; DNA/*chemistry ; DNA Damage ; Deoxycytidine/*analogs & derivatives/analysis ; Humans ; Mass Spectrometry ; Mice ; Purkinje Cells/*chemistry
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    Energy-efficient action potentials in hippocampal mossy fibers (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-09-12
    Description: Action potentials in nonmyelinated axons are considered to contribute substantially to activity-dependent brain metabolism. Here we show that fast Na+ current decay and delayed K+ current onset during action potentials in nonmyelinated mossy fibers of the rat hippocampus minimize the overlap of their respective ion fluxes. This results in total Na+ influx and associated energy demand per action potential of only 1.3 times the theoretical minimum, in contrast to the factor of 4 used in previous energy budget calculations for neural activity. Analysis of ionic conductance parameters revealed that the properties of Na+ and K+ channels are matched to make axonal action potentials energy-efficient, minimizing their contribution to activity-dependent metabolism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Alle, Henrik -- Roth, Arnd -- Geiger, Jorg R P -- New York, N.Y. -- Science. 2009 Sep 11;325(5946):1405-8. doi: 10.1126/science.1174331.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Independent Hertie Research Group, Max-Planck-Institute for Brain Research, 60528 Frankfurt, Germany. henrik.alle@charite.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19745156" target="_blank"〉PubMed〈/a〉
    Keywords: *Action Potentials ; Animals ; Axons/physiology ; *Energy Metabolism ; Mossy Fibers, Hippocampal/*physiology ; Patch-Clamp Techniques ; Potassium/metabolism ; Potassium Channels/metabolism ; Presynaptic Terminals/physiology ; Rats ; Rats, Wistar ; Sodium/metabolism ; Sodium Channels/metabolism ; Sodium-Potassium-Exchanging ATPase/metabolism ; Synaptic Transmission
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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
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    State stem cell initiatives. CIRM close-hauled, seeks bonds to sustain headway (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-03-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holden, Constance -- New York, N.Y. -- Science. 2009 Mar 27;323(5922):1660-1. doi: 10.1126/science.323.5922.1660a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19325091" target="_blank"〉PubMed〈/a〉
    Keywords: *Academies and Institutes/economics/organization & administration ; *Biomedical Research/economics ; California ; Cell Line ; Clinical Trials as Topic ; Embryo Research/economics/legislation & jurisprudence ; *Embryonic Stem Cells ; Financing, Government ; Humans ; National Institutes of Health (U.S.) ; Research Support as Topic ; State Government ; *Stem Cells ; United States
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    ATP-citrate lyase links cellular metabolism to histone acetylation (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-05-23
    Description: Histone acetylation in single-cell eukaryotes relies on acetyl coenzyme A (acetyl-CoA) synthetase enzymes that use acetate to produce acetyl-CoA. Metazoans, however, use glucose as their main carbon source and have exposure only to low concentrations of extracellular acetate. We have shown that histone acetylation in mammalian cells is dependent on adenosine triphosphate (ATP)-citrate lyase (ACL), the enzyme that converts glucose-derived citrate into acetyl-CoA. We found that ACL is required for increases in histone acetylation in response to growth factor stimulation and during differentiation, and that glucose availability can affect histone acetylation in an ACL-dependent manner. Together, these findings suggest that ACL activity is required to link growth factor-induced increases in nutrient metabolism to the regulation of histone acetylation and gene expression.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2746744/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2746744/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wellen, Kathryn E -- Hatzivassiliou, Georgia -- Sachdeva, Uma M -- Bui, Thi V -- Cross, Justin R -- Thompson, Craig B -- R01 CA092660/CA/NCI NIH HHS/ -- R01 CA092660-09/CA/NCI NIH HHS/ -- R01 CA105463/CA/NCI NIH HHS/ -- T32-HL07439-27/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2009 May 22;324(5930):1076-80. doi: 10.1126/science.1164097.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cancer Biology, Abramson Family Cancer Research Institute, University of Pennsylvania, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19461003" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; ATP Citrate (pro-S)-Lyase/genetics/*metabolism ; Acetate-CoA Ligase/genetics/metabolism ; Acetyl Coenzyme A/metabolism ; Acetylation ; Adipocytes/cytology/metabolism ; Animals ; Cell Differentiation ; Cell Line ; Cell Line, Tumor ; Cell Nucleus/enzymology ; Cell Proliferation ; Citric Acid/metabolism ; Cytoplasm/enzymology ; Gene Expression Regulation ; Glucose/*metabolism ; Glycolysis ; Histone Deacetylase Inhibitors ; Histone Deacetylases/metabolism ; Histones/*metabolism ; Humans ; Intercellular Signaling Peptides and Proteins/metabolism ; Interleukin-3/metabolism ; Mice ; RNA Interference ; Transcription, Genetic
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    Obama executive order. For Congress and NIH, headaches ahead on stem cells (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-03-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holden, Constance -- New York, N.Y. -- Science. 2009 Mar 20;323(5921):1552-3. doi: 10.1126/science.323.5921.1552a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19299595" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Cloning, Organism/legislation & jurisprudence ; Embryo Research/ethics/*legislation & jurisprudence ; *Embryonic Stem Cells ; Financing, Government/legislation & jurisprudence ; Government Regulation ; Guidelines as Topic ; Humans ; National Institutes of Health (U.S.) ; Politics ; Research Support as Topic/*legislation & jurisprudence ; United States
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    PTPsigma is a receptor for chondroitin sulfate proteoglycan, an inhibitor of neural regeneration (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-10-17
    Description: Chondroitin sulfate proteoglycans (CSPGs) present a barrier to axon regeneration. However, no specific receptor for the inhibitory effect of CSPGs has been identified. We showed that a transmembrane protein tyrosine phosphatase, PTPsigma, binds with high affinity to neural CSPGs. Binding involves the chondroitin sulfate chains and a specific site on the first immunoglobulin-like domain of PTPsigma. In culture, PTPsigma(-/-) neurons show reduced inhibition by CSPG. A PTPsigma fusion protein probe can detect cognate ligands that are up-regulated specifically at neural lesion sites. After spinal cord injury, PTPsigma gene disruption enhanced the ability of axons to penetrate regions containing CSPG. These results indicate that PTPsigma can act as a receptor for CSPGs and may provide new therapeutic approaches to neural regeneration.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2811318/" 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/PMC2811318/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shen, Yingjie -- Tenney, Alan P -- Busch, Sarah A -- Horn, Kevin P -- Cuascut, Fernando X -- Liu, Kai -- He, Zhigang -- Silver, Jerry -- Flanagan, John G -- R01 EY011559/EY/NEI NIH HHS/ -- R01 NS025713/NS/NINDS NIH HHS/ -- R37 HD029417/HD/NICHD NIH HHS/ -- R37 NS025713/NS/NINDS NIH HHS/ -- R37 NS025713-22/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2009 Oct 23;326(5952):592-6. doi: 10.1126/science.1178310. Epub 2009 Oct 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology and Program in Neuroscience, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19833921" target="_blank"〉PubMed〈/a〉
    Keywords: Aggrecans/metabolism ; Animals ; Astrocytes/metabolism ; Axons/physiology ; Binding Sites ; Cells, Cultured ; Chondroitin Sulfate Proteoglycans/chemistry/*metabolism ; Chondroitin Sulfates/metabolism ; Female ; Ganglia, Spinal/cytology/metabolism ; Ligands ; Mice ; *Nerve Regeneration ; Nerve Tissue Proteins/chemistry/*metabolism ; Neurites/physiology ; Neurons/*physiology ; Protein Binding ; Protein Interaction Domains and Motifs ; Proteoglycans/chemistry/*metabolism ; Receptor-Like Protein Tyrosine Phosphatases, Class ; 2/chemistry/genetics/*metabolism ; Recombinant Fusion Proteins/chemistry/metabolism ; Spinal Cord/metabolism/pathology ; Spinal Cord Injuries/*metabolism/pathology/physiopathology
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    Spinal endocannabinoids and CB1 receptors mediate C-fiber-induced heterosynaptic pain sensitization (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-08-08
    Description: Diminished synaptic inhibition in the spinal dorsal horn is a major contributor to chronic pain. Pathways that reduce synaptic inhibition in inflammatory and neuropathic pain states have been identified, but central hyperalgesia and diminished dorsal horn synaptic inhibition also occur in the absence of inflammation or neuropathy, solely triggered by intense nociceptive (C-fiber) input to the spinal dorsal horn. We found that endocannabinoids, produced upon strong nociceptive stimulation, activated type 1 cannabinoid (CB1) receptors on inhibitory dorsal horn neurons to reduce the synaptic release of gamma-aminobutyric acid and glycine and thus rendered nociceptive neurons excitable by nonpainful stimuli. Our results suggest that spinal endocannabinoids and CB1 receptors on inhibitory dorsal horn interneurons act as mediators of heterosynaptic pain sensitization and play an unexpected role in dorsal horn pain-controlling circuits.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2835775/" 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/PMC2835775/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pernia-Andrade, Alejandro J -- Kato, Ako -- Witschi, Robert -- Nyilas, Rita -- Katona, Istvan -- Freund, Tamas F -- Watanabe, Masahiko -- Filitz, Jorg -- Koppert, Wolfgang -- Schuttler, Jurgen -- Ji, Guangchen -- Neugebauer, Volker -- Marsicano, Giovanni -- Lutz, Beat -- Vanegas, Horacio -- Zeilhofer, Hanns Ulrich -- NS11255/NS/NINDS NIH HHS/ -- NS38261/NS/NINDS NIH HHS/ -- P01 NS011255/NS/NINDS NIH HHS/ -- P01 NS011255-32A20042/NS/NINDS NIH HHS/ -- P01 NS011255-330042/NS/NINDS NIH HHS/ -- R01 NS038261/NS/NINDS NIH HHS/ -- R01 NS038261-08/NS/NINDS NIH HHS/ -- R01 NS038261-09/NS/NINDS NIH HHS/ -- R01 NS038261-10/NS/NINDS NIH HHS/ -- R01 NS038261-10S1/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2009 Aug 7;325(5941):760-4. doi: 10.1126/science.1171870.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Pharmacology and Toxicology, University of Zurich, Winterthurerstrasse 190, CH-8057 Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19661434" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Cannabinoid Receptor Modulators/*physiology ; Electric Stimulation ; *Endocannabinoids ; Excitatory Postsynaptic Potentials ; Female ; Humans ; Hyperalgesia/*physiopathology ; Inhibitory Postsynaptic Potentials ; Interneurons/physiology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Nerve Fibers, Unmyelinated/*physiology ; Neural Inhibition ; Pain/*physiopathology ; Piperidines/administration & dosage/pharmacology ; Posterior Horn Cells/*physiology ; Pyrazoles/administration & dosage/pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptor, Cannabinoid, CB1/antagonists & inhibitors/*metabolism ; Spinal Cord/cytology/physiology ; *Synaptic Transmission ; Young Adult
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    Comment on "Detection, stimulation, and inhibition of neuronal signals with high-density nanowire transistor arrays" (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-03-17
    Description: Patolsky et al. (Reports, 25 August 2006, p. 1100) used silicon nanowires to record action potentials in rat neuronal axons and found increases in conductance of about 85 nanosiemens. We point out that the data correspond to voltage changes of about -85 millivolts on the nanowire and that conceivable mechanisms of axon-nanowire interaction lead to signals that are opposite in sign or smaller by orders of magnitude.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fromherz, Peter -- Voelker, Moritz -- New York, N.Y. -- Science. 2009 Mar 13;323(5920):1429; author reply 1429. doi: 10.1126/science.1155416.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Membrane and Neurophysics, Max Planck Institute for Biochemistry, D82152 Martinsried/Munich, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19286538" target="_blank"〉PubMed〈/a〉
    Keywords: *Action Potentials ; Animals ; Axons/*physiology ; Electric Conductivity ; Electric Stimulation ; Ion Channel Gating ; *Nanowires ; Neural Inhibition ; Neurons/*physiology ; Rats ; Semiconductors ; Silicon ; Sodium/metabolism ; Static Electricity ; Transistors, Electronic
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    Sending signals dynamically (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-04-11
    Description: Proteins mediate transmission of signals along intercellular and intracellular pathways and between the exterior and the interior of a cell. The dynamic properties of signaling proteins are crucial to their functions. We discuss emerging paradigms for the role of protein dynamics in signaling. A central tenet is that proteins fluctuate among many states on evolutionarily selected energy landscapes. Upstream signals remodel this landscape, causing signaling proteins to transmit information to downstream partners. New methods provide insight into the dynamic properties of signaling proteins at the atomic scale. The next stages in the signaling hierarchy-how multiple signals are integrated and how cellular signaling pathways are organized in space and time-present exciting challenges for the future, requiring bold multidisciplinary approaches.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2921701/" 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/PMC2921701/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smock, Robert G -- Gierasch, Lila M -- DP1 OD000945/OD/NIH HHS/ -- DP1 OD000945-03/OD/NIH HHS/ -- GM027616/GM/NIGMS NIH HHS/ -- OD000945/OD/NIH HHS/ -- R01 GM027616/GM/NIGMS NIH HHS/ -- R01 GM027616-30/GM/NIGMS NIH HHS/ -- T32 GM008515/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2009 Apr 10;324(5924):198-203. doi: 10.1126/science.1169377.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biology, University of Massachusetts, Amherst, MA 01003, USA. rsmock@student.umass.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19359576" target="_blank"〉PubMed〈/a〉
    Keywords: Binding Sites ; Intercellular Signaling Peptides and Proteins/*chemistry/*metabolism ; Intracellular Signaling Peptides and Proteins/antagonists & ; inhibitors/*chemistry/*metabolism ; Models, Molecular ; Motion ; PDZ Domains ; Protein Binding ; Protein Interaction Domains and Motifs ; Protein Multimerization ; Protein Structure, Tertiary ; *Signal Transduction ; Thermodynamics
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    The E3 ligase TRAF6 regulates Akt ubiquitination and activation (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-08-29
    Description: Akt signaling plays a central role in many biological functions, such as cell proliferation and apoptosis. Because Akt (also known as protein kinase B) resides primarily in the cytosol, it is not known how these signaling molecules are recruited to the plasma membrane and subsequently activated by growth factor stimuli. We found that the protein kinase Akt undergoes lysine-63 chain ubiquitination, which is important for Akt membrane localization and phosphorylation. TRAF6 was found to be a direct E3 ligase for Akt and was essential for Akt ubiquitination, membrane recruitment, and phosphorylation upon growth-factor stimulation. The human cancer-associated Akt mutant displayed an increase in Akt ubiquitination, in turn contributing to the enhancement of Akt membrane localization and phosphorylation. Thus, Akt ubiquitination is an important step for oncogenic Akt activation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3008763/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3008763/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yang, Wei-Lei -- Wang, Jing -- Chan, Chia-Hsin -- Lee, Szu-Wei -- Campos, Alejandro D -- Lamothe, Betty -- Hur, Lana -- Grabiner, Brian C -- Lin, Xin -- Darnay, Bryant G -- Lin, Hui-Kuan -- R01 CA149321/CA/NCI NIH HHS/ -- R01 CA149321-02/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2009 Aug 28;325(5944):1134-8. doi: 10.1126/science.1175065.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Oncology, The University of Texas M. D. Anderson Cancer Center, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19713527" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Animals ; Apoptosis ; Cell Line ; Cell Line, Tumor ; Cell Membrane/*metabolism ; Humans ; Insulin-Like Growth Factor I/pharmacology ; Interleukin-1beta/pharmacology ; Lipopolysaccharides/pharmacology ; Mice ; Neoplasm Transplantation ; Neoplasms, Experimental/metabolism ; Phosphatidylinositol Phosphates/metabolism ; Phosphorylation ; Proto-Oncogene Proteins c-akt/chemistry/*metabolism ; *Signal Transduction ; TNF Receptor-Associated Factor 6/genetics/*metabolism ; Transplantation, Heterologous ; Ubiquitin-Protein Ligases/*metabolism ; Ubiquitination
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    A Cdc20-APC ubiquitin signaling pathway regulates presynaptic differentiation (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-11-11
    Description: Presynaptic axonal differentiation is essential for synapse formation and the establishment of neuronal circuits. However, the mechanisms that coordinate presynaptic development in the brain are largely unknown. We found that the major mitotic E3 ubiquitin ligase Cdc20-anaphase promoting complex (Cdc20-APC) regulates presynaptic differentiation in primary postmitotic mammalian neurons and in the rat cerebellar cortex. Cdc20-APC triggered the degradation of the transcription factor NeuroD2 and thereby promoted presynaptic differentiation. The NeuroD2 target gene encoding Complexin II, which acts locally at presynaptic sites, mediated the ability of NeuroD2 to suppress presynaptic differentiation. Thus, our findings define a Cdc20-APC ubiquitin signaling pathway that governs presynaptic development, which holds important implications for neuronal connectivity and plasticity in the brain.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2846784/" 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/PMC2846784/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yang, Yue -- Kim, Albert H -- Yamada, Tomoko -- Wu, Bei -- Bilimoria, Parizad M -- Ikeuchi, Yoshiho -- de la Iglesia, Nuria -- Shen, Jie -- Bonni, Azad -- F32 CA124028/CA/NCI NIH HHS/ -- NS041021/NS/NINDS NIH HHS/ -- NS051255/NS/NINDS NIH HHS/ -- R01 NS041021/NS/NINDS NIH HHS/ -- R01 NS041021-06/NS/NINDS NIH HHS/ -- R01 NS041021-07/NS/NINDS NIH HHS/ -- R01 NS041021-08/NS/NINDS NIH HHS/ -- R01 NS051255/NS/NINDS NIH HHS/ -- R01 NS051255-02/NS/NINDS NIH HHS/ -- R01 NS051255-03/NS/NINDS NIH HHS/ -- R01 NS051255-04/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2009 Oct 23;326(5952):575-8. doi: 10.1126/science.1177087.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19900895" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Vesicular Transport/genetics/metabolism ; Anaphase-Promoting Complex-Cyclosome ; Animals ; Axons/metabolism/*physiology/ultrastructure ; Basic Helix-Loop-Helix Transcription Factors/genetics/metabolism ; Cdc20 Proteins ; Cell Cycle Proteins/genetics/*metabolism ; Cerebellar Cortex/cytology/metabolism/ultrastructure ; Gene Knockdown Techniques ; Mutant Proteins/metabolism ; Nerve Tissue Proteins/genetics/metabolism ; Neuropeptides/genetics/metabolism ; Presynaptic Terminals/*metabolism ; Rats ; *Signal Transduction ; Synapses/*metabolism ; Synapsins/metabolism ; Synaptic Vesicles/genetics/metabolism ; Ubiquitin/*metabolism ; Ubiquitin-Protein Ligase Complexes/genetics/*metabolism ; Ubiquitin-Protein Ligases/*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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    Spinal cord stimulation restores locomotion in animal models of Parkinson's disease (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-03-21
    Description: Dopamine replacement therapy is useful for treating motor symptoms in the early phase of Parkinson's disease, but it is less effective in the long term. Electrical deep-brain stimulation is a valuable complement to pharmacological treatment but involves a highly invasive surgical procedure. We found that epidural electrical stimulation of the dorsal columns in the spinal cord restores locomotion in both acute pharmacologically induced dopamine-depleted mice and in chronic 6-hydroxydopamine-lesioned rats. The functional recovery was paralleled by a disruption of aberrant low-frequency synchronous corticostriatal oscillations, leading to the emergence of neuronal activity patterns that resemble the state normally preceding spontaneous initiation of locomotion. We propose that dorsal column stimulation might become an efficient and less invasive alternative for treatment of Parkinson's disease in the future.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2669752/" 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/PMC2669752/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fuentes, Romulo -- Petersson, Per -- Siesser, William B -- Caron, Marc G -- Nicolelis, Miguel A L -- R21 NS049534/NS/NINDS NIH HHS/ -- R21 NS049534-01A2/NS/NINDS NIH HHS/ -- R21 NS049534-02/NS/NINDS NIH HHS/ -- R33 NS049534/NS/NINDS NIH HHS/ -- R33 NS049534-03/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2009 Mar 20;323(5921):1578-82. doi: 10.1126/science.1164901.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Duke University Medical Center, Durham, NC 27710, USA. fuentes@neuro.duke.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19299613" target="_blank"〉PubMed〈/a〉
    Keywords: Afferent Pathways/physiology ; Animals ; Combined Modality Therapy ; Corpus Striatum/physiopathology ; Dopamine/metabolism ; *Electric Stimulation Therapy ; Electrodes, Implanted ; Electrophysiological Phenomena ; Humans ; Levodopa/administration & dosage/therapeutic use ; *Locomotion ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Motor Cortex/physiopathology ; Neurons/physiology ; Oxidopamine/pharmacology ; Parkinson Disease/physiopathology/*therapy ; Parkinsonian Disorders/physiopathology/*therapy ; Rats ; Spinal Cord/*physiology ; alpha-Methyltyrosine/pharmacology
    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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    Circadian clock feedback cycle through NAMPT-mediated NAD+ biosynthesis (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-03-21
    Description: The circadian clock is encoded by a transcription-translation feedback loop that synchronizes behavior and metabolism with the light-dark cycle. Here we report that both the rate-limiting enzyme in mammalian nicotinamide adenine dinucleotide (NAD+) biosynthesis, nicotinamide phosphoribosyltransferase (NAMPT), and levels of NAD+ display circadian oscillations that are regulated by the core clock machinery in mice. Inhibition of NAMPT promotes oscillation of the clock gene Per2 by releasing CLOCK:BMAL1 from suppression by SIRT1. In turn, the circadian transcription factor CLOCK binds to and up-regulates Nampt, thus completing a feedback loop involving NAMPT/NAD+ and SIRT1/CLOCK:BMAL1.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2738420/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2738420/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ramsey, Kathryn Moynihan -- Yoshino, Jun -- Brace, Cynthia S -- Abrassart, Dana -- Kobayashi, Yumiko -- Marcheva, Biliana -- Hong, Hee-Kyung -- Chong, Jason L -- Buhr, Ethan D -- Lee, Choogon -- Takahashi, Joseph S -- Imai, Shin-Ichiro -- Bass, Joseph -- AG02150/AG/NIA NIH HHS/ -- P01 AG011412/AG/NIA NIH HHS/ -- P50 MH074924/MH/NIMH NIH HHS/ -- R01 AG024150/AG/NIA NIH HHS/ -- R01 AG024150-05/AG/NIA NIH HHS/ -- T32 DK007169/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 May 1;324(5927):651-4. doi: 10.1126/science.1171641. Epub 2009 Mar 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Northwestern University Feinberg School of Medicine, 2200 Campus Drive, Evanston, IL 60208-3500, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19299583" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors ; Acrylamides/pharmacology ; Adipose Tissue, White/metabolism ; Animals ; Basic Helix-Loop-Helix Transcription Factors/genetics/metabolism ; *Biological Clocks ; CLOCK Proteins ; Cell Cycle Proteins/genetics ; Cell Line ; Cell Line, Tumor ; *Circadian Rhythm ; Cytokines/antagonists & inhibitors/genetics/*metabolism ; Enzyme Inhibitors/pharmacology ; *Feedback, Physiological ; Gene Expression Regulation ; Hepatocytes/metabolism ; Humans ; Liver/metabolism ; Mice ; NAD/*biosynthesis ; Nicotinamide Phosphoribosyltransferase/antagonists & ; inhibitors/genetics/*metabolism ; Nuclear Proteins/genetics ; Period Circadian Proteins ; Piperidines/pharmacology ; Protein Binding ; Sirtuin 1 ; Sirtuins/metabolism ; Trans-Activators/genetics/metabolism ; Transcription Factors/genetics ; Transcription, Genetic
    Print ISSN: 0036-8075
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    Structure of monomeric yeast and mammalian Sec61 complexes interacting with the translating ribosome (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-11-26
    Description: The trimeric Sec61/SecY complex is a protein-conducting channel (PCC) for secretory and membrane proteins. Although Sec complexes can form oligomers, it has been suggested that a single copy may serve as an active PCC. We determined subnanometer-resolution cryo-electron microscopy structures of eukaryotic ribosome-Sec61 complexes. In combination with biochemical data, we found that in both idle and active states, the Sec complex is not oligomeric and interacts mainly via two cytoplasmic loops with the universal ribosomal adaptor site. In the active state, the ribosomal tunnel and a central pore of the monomeric PCC were occupied by the nascent chain, contacting loop 6 of the Sec complex. This provides a structural basis for the activity of a solitary Sec complex in cotranslational protein translocation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2920595/" 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/PMC2920595/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Becker, Thomas -- Bhushan, Shashi -- Jarasch, Alexander -- Armache, Jean-Paul -- Funes, Soledad -- Jossinet, Fabrice -- Gumbart, James -- Mielke, Thorsten -- Berninghausen, Otto -- Schulten, Klaus -- Westhof, Eric -- Gilmore, Reid -- Mandon, Elisabet C -- Beckmann, Roland -- GM35687/GM/NIGMS NIH HHS/ -- P41 RR005969/RR/NCRR NIH HHS/ -- P41 RR005969-19/RR/NCRR NIH HHS/ -- P41-RR05969/RR/NCRR NIH HHS/ -- R01-GM067887/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2009 Dec 4;326(5958):1369-73. doi: 10.1126/science.1178535. Epub 2009 Oct 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gene Center Munich and Center for Integrated Protein Science, Department of Chemistry and Biochemistry, Ludwig-Maximilians-Universitat Munchen, Feodor-Lynen-Strasse 25, 81377 Munich, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19933108" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Cryoelectron Microscopy ; Dogs ; Image Processing, Computer-Assisted ; Membrane Proteins/*chemistry/*metabolism/ultrastructure ; Models, Molecular ; *Protein Biosynthesis ; Protein Conformation ; Protein Multimerization ; Protein Structure, Secondary ; *Protein Transport ; Proteins/chemistry/*metabolism/ultrastructure ; Ribosomes/*metabolism/ultrastructure ; Saccharomyces cerevisiae Proteins/*chemistry/*metabolism/ultrastructure
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    Structural basis of immune evasion at the site of CD4 attachment on HIV-1 gp120 (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-12-08
    Description: The site on HIV-1 gp120 that binds to the CD4 receptor is vulnerable to antibodies. However, most antibodies that interact with this site cannot neutralize HIV-1. To understand the basis of this resistance, we determined co-crystal structures for two poorly neutralizing, CD4-binding site (CD4BS) antibodies, F105 and b13, in complexes with gp120. Both antibodies exhibited approach angles to gp120 similar to those of CD4 and a rare, broadly neutralizing CD4BS antibody, b12. Slight differences in recognition, however, resulted in substantial differences in F105- and b13-bound conformations relative to b12-bound gp120. Modeling and binding experiments revealed these conformations to be poorly compatible with the viral spike. This incompatibility, the consequence of slight differences in CD4BS recognition, renders HIV-1 resistant to all but the most accurately targeted antibodies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2862588/" 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/PMC2862588/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Lei -- Kwon, Young Do -- Zhou, Tongqing -- Wu, Xueling -- O'Dell, Sijy -- Cavacini, Lisa -- Hessell, Ann J -- Pancera, Marie -- Tang, Min -- Xu, Ling -- Yang, Zhi-Yong -- Zhang, Mei-Yun -- Arthos, James -- Burton, Dennis R -- Dimitrov, Dimiter S -- Nabel, Gary J -- Posner, Marshall R -- Sodroski, Joseph -- Wyatt, Richard -- Mascola, John R -- Kwong, Peter D -- Z99 AI999999/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2009 Nov 20;326(5956):1123-7. doi: 10.1126/science.1175868.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Vaccine Research Center, National Institute of Allergy and Infectious Diseases, 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/19965434" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Antibodies, Neutralizing/chemistry/*immunology/metabolism ; Antigens, CD4/chemistry/*metabolism ; Binding Sites ; Binding Sites, Antibody ; Crystallography, X-Ray ; Epitopes ; HIV Antibodies/*chemistry/*immunology/metabolism ; HIV Envelope Protein gp120/*chemistry/*immunology/metabolism ; Hiv-1 ; Humans ; Hydrophobic and Hydrophilic Interactions ; *Immune Evasion ; Models, Molecular ; Molecular Sequence Data ; Peptide Fragments/chemistry/immunology/metabolism ; Protein Conformation
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    Activation of the PI3K pathway in cancer through inhibition of PTEN by exchange factor P-REX2a (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-09-05
    Description: PTEN (phosphatase and tensin homolog on chromosome 10) is a tumor suppressor whose cellular regulation remains incompletely understood. We identified phosphatidylinositol 3,4,5-trisphosphate RAC exchanger 2a (P-REX2a) as a PTEN-interacting protein. P-REX2a mRNA was more abundant in human cancer cells and significantly increased in tumors with wild-type PTEN that expressed an activated mutant of PIK3CA encoding the p110 subunit of phosphoinositide 3-kinase subunit alpha (PI3Kalpha). P-REX2a inhibited PTEN lipid phosphatase activity and stimulated the PI3K pathway only in the presence of PTEN. P-REX2a stimulated cell growth and cooperated with a PIK3CA mutant to promote growth factor-independent proliferation and transformation. Depletion of P-REX2a reduced amounts of phosphorylated AKT and growth in human cell lines with intact PTEN. Thus, P-REX2a is a component of the PI3K pathway that can antagonize PTEN in cancer cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2936784/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2936784/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fine, Barry -- Hodakoski, Cindy -- Koujak, Susan -- Su, Tao -- Saal, Lao H -- Maurer, Matthew -- Hopkins, Benjamin -- Keniry, Megan -- Sulis, Maria Luisa -- Mense, Sarah -- Hibshoosh, Hanina -- Parsons, Ramon -- CA097403/CA/NCI NIH HHS/ -- P01 CA097403/CA/NCI NIH HHS/ -- P01 CA097403-01A10003/CA/NCI NIH HHS/ -- P01 CA097403-06A1/CA/NCI NIH HHS/ -- R01 CA082783/CA/NCI NIH HHS/ -- R01 CA082783-06/CA/NCI NIH HHS/ -- R01 CA082783-07/CA/NCI NIH HHS/ -- R01 CA082783-08/CA/NCI NIH HHS/ -- R01 CA082783-09/CA/NCI NIH HHS/ -- R01 CA082783-10/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2009 Sep 4;325(5945):1261-5. doi: 10.1126/science.1173569.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Cancer Genetics and Herbert Irving Comprehensive Cancer Center, Columbia University, 1130 St. Nicholas Avenue, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19729658" target="_blank"〉PubMed〈/a〉
    Keywords: Breast Neoplasms/genetics/metabolism/pathology ; Cell Line ; Cell Line, Tumor ; Cell Proliferation ; Female ; GTPase-Activating Proteins/genetics/*metabolism ; Guanine Nucleotide Exchange Factors ; Humans ; Male ; Mutation ; Neoplasms/genetics/*metabolism/pathology ; PTEN Phosphohydrolase/*antagonists & inhibitors/chemistry/genetics/*metabolism ; Phosphatidylinositol 3-Kinases/*metabolism ; Phosphorylation ; Protein Binding ; Protein Structure, Tertiary ; Proto-Oncogene Proteins c-akt/metabolism ; Signal Transduction
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    Generation of medaka fish haploid embryonic stem cells (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-10-17
    Description: Haploid embryonic stem (ES) cells combine haploidy and pluripotency, enabling direct genetic analyses of recessive phenotypes in vertebrate cells. Haploid cells have been elusive for culture, due to their inferior growth and genomic instability. Here, we generated gynogenetic medaka embryos and obtained three haploid ES cell lines that retained pluripotency and competitive growth. Upon nuclear transfer into unfertilized oocytes, the haploid ES cells, even after genetic engineering, generated viable offspring capable of germline transmission. Hence, haploid medaka ES cells stably maintain normal growth, pluripotency, and genomic integrity. Mosaic oocytes created by combining a mitotic nucleus and a meiotic nucleus can generate fertile fish offspring. Haploid ES cells may offer a yeast-like system for analyzing recessive phenotypes in numerous cell lineages of vertebrates in vitro.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yi, Meisheng -- Hong, Ni -- Hong, Yunhan -- New York, N.Y. -- Science. 2009 Oct 16;326(5951):430-3. doi: 10.1126/science.1175151.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, National University of Singapore, 10 Kent Ridge Crescent, Singapore 119260.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19833967" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Line ; Cell Proliferation ; Cell Shape ; Chromosomal Instability ; Cloning, Organism ; Crosses, Genetic ; Diploidy ; Embryo, Nonmammalian/cytology ; Embryonic Stem Cells/cytology/*physiology ; Female ; *Haploidy ; Male ; Nuclear Transfer Techniques ; Oocytes ; *Oryzias/embryology/genetics/physiology ; Phenotype ; Pluripotent Stem Cells/cytology/*physiology ; Transplantation Chimera
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    Developmental biology. Pluripotent chromatin state (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-01-10
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4126799/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4126799/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chi, Andrew S -- Bernstein, Bradley E -- U54 HG004570/HG/NHGRI NIH HHS/ -- U54 HG004570-01/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2009 Jan 9;323(5911):220-1. doi: 10.1126/science.1166261.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Pathology Unit and Center for Cancer Research, Massachusetts General Hospital, Charlestown, MA 02129, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19131621" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Line ; Cell Lineage ; Chromatin/*physiology ; Chromatin Assembly and Disassembly ; Embryonic Stem Cells/*physiology ; Gene Expression Regulation, Developmental ; Nucleosomes/physiology ; Pluripotent Stem Cells/*physiology ; Polycomb-Group Proteins ; Repressor Proteins/metabolism ; Transcription Factors/metabolism ; *Transcription, Genetic
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    Neuroscience. Erasing fear memories (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-09-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pizzorusso, Tommaso -- New York, N.Y. -- Science. 2009 Sep 4;325(5945):1214-5. doi: 10.1126/science.1179697.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Istituto Neuroscienze CNR, via Moruzzi, 1 56100 Pisa, Italy. tommaso.pizzorusso@in.cnr.it〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19729646" target="_blank"〉PubMed〈/a〉
    Keywords: Amygdala/cytology/growth & development/*physiology ; Animals ; Chondroitin ABC Lyase/metabolism ; Chondroitin Sulfate Proteoglycans/metabolism/*physiology ; Conditioning, Classical ; *Extinction, Psychological ; Extracellular Matrix/physiology ; *Fear ; Memory/*physiology ; Mice ; Neuronal Plasticity ; Rats ; Visual Cortex/growth & development/physiology
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    AMPK regulates the circadian clock by cryptochrome phosphorylation and degradation (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-10-17
    Description: Circadian clocks coordinate behavioral and physiological processes with daily light-dark cycles by driving rhythmic transcription of thousands of genes. Whereas the master clock in the brain is set by light, pacemakers in peripheral organs, such as the liver, are reset by food availability, although the setting, or "entrainment," mechanisms remain mysterious. Studying mouse fibroblasts, we demonstrated that the nutrient-responsive adenosine monophosphate-activated protein kinase (AMPK) phosphorylates and destabilizes the clock component cryptochrome 1 (CRY1). In mouse livers, AMPK activity and nuclear localization were rhythmic and inversely correlated with CRY1 nuclear protein abundance. Stimulation of AMPK destabilized cryptochromes and altered circadian rhythms, and mice in which the AMPK pathway was genetically disrupted showed alterations in peripheral clocks. Thus, phosphorylation by AMPK enables cryptochrome to transduce nutrient signals to circadian clocks in mammalian peripheral organs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2819106/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2819106/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lamia, Katja A -- Sachdeva, Uma M -- DiTacchio, Luciano -- Williams, Elliot C -- Alvarez, Jacqueline G -- Egan, Daniel F -- Vasquez, Debbie S -- Juguilon, Henry -- Panda, Satchidananda -- Shaw, Reuben J -- Thompson, Craig B -- Evans, Ronald M -- CA104838/CA/NCI NIH HHS/ -- DK057978/DK/NIDDK NIH HHS/ -- DK062434/DK/NIDDK NIH HHS/ -- DK080425/DK/NIDDK NIH HHS/ -- EY016807/EY/NEI NIH HHS/ -- P01 CA104838/CA/NCI NIH HHS/ -- P01 CA104838-05S1/CA/NCI NIH HHS/ -- P30 CA014195/CA/NCI NIH HHS/ -- R01 DK080425/DK/NIDDK NIH HHS/ -- R01 DK080425-03/DK/NIDDK NIH HHS/ -- R01 EY016807/EY/NEI NIH HHS/ -- R01 EY016807-03/EY/NEI NIH HHS/ -- R37 DK057978/DK/NIDDK NIH HHS/ -- R37 DK057978-31/DK/NIDDK NIH HHS/ -- T32 HL007439/HL/NHLBI NIH HHS/ -- T32 HL007439-27/HL/NHLBI NIH HHS/ -- T32-HL07439-27/HL/NHLBI NIH HHS/ -- U19 DK062434/DK/NIDDK NIH HHS/ -- U19 DK062434-08S19002/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Oct 16;326(5951):437-40. doi: 10.1126/science.1172156.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gene Expression Laboratory, the Salk Institute, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19833968" target="_blank"〉PubMed〈/a〉
    Keywords: AMP-Activated Protein Kinases/*metabolism ; ARNTL Transcription Factors ; Amino Acid Substitution ; Aminoimidazole Carboxamide/analogs & derivatives/pharmacology ; Animals ; Basic Helix-Loop-Helix Transcription Factors/genetics ; Cell Line ; Cell Nucleus/metabolism ; Cells, Cultured ; Circadian Rhythm/*physiology ; Cryptochromes ; Culture Media ; Flavoproteins/genetics/*metabolism ; Food ; Glucose/metabolism/pharmacology ; Humans ; Liver/*metabolism ; Mice ; Mutagenesis, Site-Directed ; Mutant Proteins/metabolism ; Phosphorylation ; Promoter Regions, Genetic ; Protein Stability ; Recombinant Fusion Proteins/metabolism ; Ribonucleotides/pharmacology ; Signal Transduction
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    Exchange of genetic material between cells in plant tissue grafts (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-05-02
    Description: Tissue grafting includes applications ranging from plant breeding to animal organ transplantation. Donor and recipient are generally believed to maintain their genetic integrity, in that the grafted tissues are joined but their genetic materials do not mix. We grafted tobacco plants from two transgenic lines carrying different marker and reporter genes in different cellular compartments, the nucleus and the plastid. Analysis of the graft sites revealed the frequent occurrence of cells harboring both antibiotic resistances and both fluorescent reporters. Our data demonstrate that plant grafting can result in the exchange of genetic information via either large DNA pieces or entire plastid genomes. This observation of novel combinations of genetic material has implications for grafting techniques and also provides a possible path for horizontal gene transfer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stegemann, Sandra -- Bock, Ralph -- New York, N.Y. -- Science. 2009 May 1;324(5927):649-51. doi: 10.1126/science.1170397.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max-Planck-Institut fur Molekulare Pflanzenphysiologie, Am Muhlenberg 1, D-14476 Potsdam-Golm, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19407205" target="_blank"〉PubMed〈/a〉
    Keywords: Breeding ; Cell Line ; Cell Nucleus/genetics ; Chloroplasts/genetics ; Drug Resistance/genetics ; *Gene Transfer, Horizontal ; *Genes, Plant ; Genes, Reporter ; Green Fluorescent Proteins/analysis ; Kanamycin/pharmacology ; Luminescent Proteins/analysis ; Plants, Genetically Modified ; Selection, Genetic ; Spectinomycin/pharmacology ; Tobacco/cytology/*genetics
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    Synaptic integration in tuft dendrites of layer 5 pyramidal neurons: a new unifying principle (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-08-08
    Description: Tuft dendrites are the main target for feedback inputs innervating neocortical layer 5 pyramidal neurons, but their properties remain obscure. We report the existence of N-methyl-D-aspartate (NMDA) spikes in the fine distal tuft dendrites that otherwise did not support the initiation of calcium spikes. Both direct measurements and computer simulations showed that NMDA spikes are the dominant mechanism by which distal synaptic input leads to firing of the neuron and provide the substrate for complex parallel processing of top-down input arriving at the tuft. These data lead to a new unifying view of integration in pyramidal neurons in which all fine dendrites, basal and tuft, integrate inputs locally through the recruitment of NMDA receptor channels relative to the fixed apical calcium and axosomatic sodium integration points.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Larkum, Matthew E -- Nevian, Thomas -- Sandler, Maya -- Polsky, Alon -- Schiller, Jackie -- New York, N.Y. -- Science. 2009 Aug 7;325(5941):756-60. doi: 10.1126/science.1171958.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, University of Berne, Buhlplatz 5, 3012 Berne, Switzerland. matthew.larkum@gmail.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19661433" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Axons/physiology ; Calcium Signaling ; Computer Simulation ; Dendrites/*physiology ; Excitatory Postsynaptic Potentials ; In Vitro Techniques ; Models, Neurological ; N-Methylaspartate/metabolism ; Neocortex/cytology/*physiology ; Patch-Clamp Techniques ; Pyramidal Cells/*physiology ; Rats ; Rats, Wistar ; Receptors, N-Methyl-D-Aspartate/metabolism ; Sodium/metabolism ; Synapses/*physiology ; Synaptic Potentials
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    Cell-specific information processing in segregating populations of Eph receptor ephrin-expressing cells (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-12-17
    Description: Cells have self-organizing properties that control their behavior in complex tissues. Contact between cells expressing either B-type Eph receptors or their transmembrane ephrin ligands initiates bidirectional signals that regulate cell positioning. However, simultaneously investigating how information is processed in two interacting cell types remains a challenge. We implemented a proteomic strategy to systematically determine cell-specific signaling networks underlying EphB2- and ephrin-B1-controlled cell sorting. Quantitative mass spectrometric analysis of mixed populations of EphB2- and ephrin-B1-expressing cells that were labeled with different isotopes revealed cell-specific tyrosine phosphorylation events. Functional associations between these phosphotyrosine signaling networks and cell sorting were established with small interfering RNA screening. Data-driven network modeling revealed that signaling between mixed EphB2- and ephrin-B1-expressing cells is asymmetric and that the distinct cell types use different tyrosine kinases and targets to process signals induced by cell-cell contact. We provide systems- and cell-specific network models of contact-initiated signaling between two distinct cell types.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jorgensen, Claus -- Sherman, Andrew -- Chen, Ginny I -- Pasculescu, Adrian -- Poliakov, Alexei -- Hsiung, Marilyn -- Larsen, Brett -- Wilkinson, David G -- Linding, Rune -- Pawson, Tony -- MC_U117532048/Medical Research Council/United Kingdom -- MOP-6849/Canadian Institutes of Health Research/Canada -- New York, N.Y. -- Science. 2009 Dec 11;326(5959):1502-9. doi: 10.1126/science.1176615.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Samuel Lunenfeld Research Institute (SLRI), Mount Sinai Hospital, Toronto M5G 1X5, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20007894" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/metabolism ; Algorithms ; Cell Line ; Ephrin-B1/genetics/*metabolism ; Humans ; Ligands ; Mass Spectrometry ; Models, Biological ; PDZ Domains ; Phosphorylation ; Protein Binding ; Protein Interaction Domains and Motifs ; Protein-Tyrosine Kinases/metabolism ; Proteomics ; RNA, Small Interfering ; Receptor, EphB2/genetics/*metabolism ; *Signal Transduction ; Tyrosine/metabolism ; src Homology Domains
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    Crystal structure of the nuclear export receptor CRM1 in complex with Snurportin1 and RanGTP (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-04-25
    Description: CRM1 mediates nuclear export of numerous unrelated cargoes, which may carry a short leucine-rich nuclear export signal or export signatures that include folded domains. How CRM1 recognizes such a variety of cargoes has been unknown up to this point. Here we present the crystal structure of the SPN1.CRM1.RanGTP export complex at 2.5 angstrom resolution (where SPN1 is snurportin1 and RanGTP is guanosine 5' triphosphate-bound Ran). SPN1 is a nuclear import adapter for cytoplasmically assembled, m(3)G-capped spliceosomal U snRNPs (small nuclear ribonucleoproteins). The structure shows how CRM1 can specifically return the cargo-free form of SPN1 to the cytoplasm. The extensive contact area includes five hydrophobic residues at the SPN1 amino terminus that dock into a hydrophobic cleft of CRM1, as well as numerous hydrophilic contacts of CRM1 to m(3)G cap-binding domain and carboxyl-terminal residues of SPN1. The structure suggests that RanGTP promotes cargo-binding to CRM1 solely through long-range conformational changes in the exportin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Monecke, Thomas -- Guttler, Thomas -- Neumann, Piotr -- Dickmanns, Achim -- Gorlich, Dirk -- Ficner, Ralf -- New York, N.Y. -- Science. 2009 May 22;324(5930):1087-91. doi: 10.1126/science.1173388. Epub 2009 Apr 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Abteilung fur Molekulare Strukturbiologie, Institut fur Mikrobiologie und Genetik, GZMB, Georg-August-Universitat Gottingen, Justus-von-Liebig-Weg 11, 37077 Gottingen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19389996" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Crystallography, X-Ray ; Guanosine Triphosphate/metabolism ; Humans ; Hydrophobic and Hydrophilic Interactions ; Karyopherins/*chemistry/metabolism ; Mice ; Models, Molecular ; Protein Binding ; Protein Conformation ; Protein Structure, Secondary ; Protein Structure, Tertiary ; RNA Cap-Binding Proteins/*chemistry/metabolism ; Receptors, Cytoplasmic and Nuclear/*chemistry/metabolism ; beta Karyopherins/metabolism ; ran GTP-Binding Protein/*chemistry/metabolism
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    Nuclear hormone receptor regulation of microRNAs controls developmental progression (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-04-04
    Description: In response to small-molecule signals such as retinoids or steroids, nuclear receptors activate gene expression to regulate development in different tissues. MicroRNAs turn off target gene expression within cells by binding complementary regions in messenger RNA transcripts, and they have been broadly implicated in development and disease. Here we show that the Caenorhabditis elegans nuclear receptor DAF-12 and its steroidal ligand directly activate promoters of let-7 microRNA family members to down-regulate the microRNA target hbl-1, which drives progression of epidermal stem cells from second to third larval stage patterns of cell division. Conversely, the receptor without the ligand represses microRNA expression during developmental arrest. These findings identify microRNAs as components of a hormone-coupled molecular switch that shuts off earlier developmental programs to allow for later ones.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2757405/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2757405/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bethke, Axel -- Fielenbach, Nicole -- Wang, Zhu -- Mangelsdorf, David J -- Antebi, Adam -- GM077201/GM/NIGMS NIH HHS/ -- R01 GM077201/GM/NIGMS NIH HHS/ -- R01 GM077201-03/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Apr 3;324(5923):95-8. doi: 10.1126/science.1164899.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Huffington Center on Aging, Department of Molecular and Cellular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19342589" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Genetically Modified ; Caenorhabditis elegans/cytology/genetics/*growth & development/*metabolism ; Caenorhabditis elegans Proteins/genetics/*metabolism ; Cell Line ; Cholestenes/*metabolism ; DNA-Binding Proteins/genetics/metabolism ; Down-Regulation ; Gene Expression Regulation, Developmental ; Genes, Helminth ; Humans ; Ligands ; MicroRNAs/*genetics ; Mutation ; RNA, Helminth/genetics/metabolism ; Receptors, Cytoplasmic and Nuclear/genetics/*metabolism ; Response Elements ; Signal Transduction ; Transcription Factors/genetics/metabolism ; Transfection ; Up-Regulation
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    Neuroscience. Nuclear power for axonal growth (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-10-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Subang, M C -- Richardson, P M -- New York, N.Y. -- Science. 2009 Oct 9;326(5950):238-9. doi: 10.1126/science.1181038.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Bone and Joint Research, Barts and the London School of Medicine, Charterhouse Square, London EC1M 6BQ, UK. m.c.subang@qmul.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19815761" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*physiology/ultrastructure ; Cell Nucleus/*metabolism ; Cytoskeleton/metabolism ; Growth Cones/*physiology/ultrastructure ; Hippocampus/cytology/embryology ; Intercellular Signaling Peptides and Proteins/metabolism ; Kruppel-Like Transcription Factors/genetics/*metabolism ; Mice ; Nerve Regeneration ; Nerve Tissue Proteins/metabolism ; Rats ; Retinal Ganglion Cells/cytology ; Transcription Factors/metabolism ; Transcription, Genetic
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    The dynamic control of kiss-and-run and vesicular reuse probed with single nanoparticles (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-02-14
    Description: Vesicular secretion of neurotransmitter is essential for neuronal communication. Kiss-and-run is a mode of membrane fusion and retrieval without the full collapse of the vesicle into the plasma membrane and de novo regeneration. The importance of kiss-and-run during efficient neurotransmission has remained in doubt. We developed an approach for loading individual synaptic vesicles with single quantum dots. Their size and pH-dependent photoluminescence change allowed us to distinguish kiss-and-run from full-collapse fusion and to track single vesicles through multiple rounds of kiss-and-run and reuse, without perturbing vesicle cycling. Kiss-and-run dominated at the beginning of stimulus trains, reflecting the preference of vesicles with high release probability. Its incidence was increased by rapid firing, a response appropriate to shape the kinetics of neurotransmission during a wide range of firing patterns.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2696197/" 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/PMC2696197/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Qi -- Li, Yulong -- Tsien, Richard W -- K99 DA025143/DA/NIDA NIH HHS/ -- K99 DA025143-01A1/DA/NIDA NIH HHS/ -- R01 MH064070/MH/NIMH NIH HHS/ -- R01 MH064070-08/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2009 Mar 13;323(5920):1448-53. doi: 10.1126/science.1167373. Epub 2009 Feb 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Physiology, Stanford University, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19213879" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Electric Stimulation ; Hippocampus/cytology ; Hydrogen-Ion Concentration ; Ion Transport ; Luminescence ; *Membrane Fusion ; Neurons/*physiology ; Neurotransmitter Agents/metabolism ; Presynaptic Terminals/physiology ; Quantum Dots ; Rats ; Rats, Sprague-Dawley ; Synaptic Membranes/physiology ; *Synaptic Transmission ; Synaptic Vesicles/*physiology
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    A functional genomics approach reveals CHE as a component of the Arabidopsis circadian clock (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-03-17
    Description: Transcriptional feedback loops constitute the molecular circuitry of the plant circadian clock. In Arabidopsis, a core loop is established between CCA1 and TOC1. Although CCA1 directly represses TOC1, the TOC1 protein has no DNA binding domains, which suggests that it cannot directly regulate CCA1. We established a functional genomic strategy that led to the identification of CHE, a TCP transcription factor that binds specifically to the CCA1 promoter. CHE is a clock component partially redundant with LHY in the repression of CCA1. The expression of CHE is regulated by CCA1, thus adding a CCA1/CHE feedback loop to the Arabidopsis circadian network. Because CHE and TOC1 interact, and CHE binds to the CCA1 promoter, a molecular linkage between TOC1 and CCA1 gene regulation is established.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4259050/" 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/PMC4259050/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pruneda-Paz, Jose L -- Breton, Ghislain -- Para, Alessia -- Kay, Steve A -- GM56006/GM/NIGMS NIH HHS/ -- GM67837/GM/NIGMS NIH HHS/ -- R01 GM056006/GM/NIGMS NIH HHS/ -- R01 GM067837/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2009 Mar 13;323(5920):1481-5. doi: 10.1126/science.1167206.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Cell and Developmental Biology, Division of Biological Sciences, University of California San Diego, La Jolla, CA 92093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19286557" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Arabidopsis/genetics/metabolism/*physiology ; Arabidopsis Proteins/chemistry/*genetics/*metabolism ; Binding Sites ; Biological Clocks/*genetics ; Cell Nucleus/metabolism ; Circadian Rhythm/*genetics ; DNA-Binding Proteins/genetics/metabolism ; Feedback, Physiological ; *Gene Expression Regulation, Plant ; Genes, Plant ; Genomics ; Molecular Sequence Data ; Plants, Genetically Modified ; Promoter Regions, Genetic ; Repressor Proteins/chemistry/*genetics/*metabolism ; Transcription Factors/*genetics/metabolism ; Transcription, Genetic
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    Rhes, a striatal specific protein, mediates mutant-huntingtin cytotoxicity (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-06-06
    Description: Huntington's disease (HD) is caused by a polyglutamine repeat in the protein huntingtin (Htt) with mutant Htt (mHtt) expressed throughout the body and similarly in all brain regions. Yet, HD neuropathology is largely restricted to the corpus striatum. We report that the small guanine nucleotide-binding protein Rhes, which is localized very selectively to the striatum, binds physiologically to mHtt. Using cultured cells, we found Rhes induces sumoylation of mHtt, which leads to cytotoxicity. Thus, Rhes-mHtt interactions can account for the localized neuropathology of HD.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2745286/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2745286/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Subramaniam, Srinivasa -- Sixt, Katherine M -- Barrow, Roxanne -- Snyder, Solomon H -- DA00074/DA/NIDA NIH HHS/ -- MH18501/MH/NIMH NIH HHS/ -- R37 MH018501/MH/NIMH NIH HHS/ -- R37 MH018501-40/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2009 Jun 5;324(5932):1327-30. doi: 10.1126/science.1172871.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19498170" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Death ; Cell Line ; Cell Survival ; Corpus Striatum/metabolism ; GTP-Binding Proteins/*metabolism ; Humans ; Mice ; Mice, Transgenic ; Mutant Proteins/metabolism ; Nerve Tissue Proteins/chemistry/*metabolism ; Nuclear Proteins/chemistry/*metabolism ; PC12 Cells ; RNA Interference ; Rats ; Recombinant Fusion Proteins/metabolism ; SUMO-1 Protein/genetics/metabolism ; Small Ubiquitin-Related Modifier Proteins/metabolism ; Substrate Specificity
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    Mechanoenzymatic cleavage of the ultralarge vascular protein von Willebrand factor (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-06-06
    Description: Von Willebrand factor (VWF) is secreted as ultralarge multimers that are cleaved in the A2 domain by the metalloprotease ADAMTS13 to give smaller multimers. Cleaved VWF is activated by hydrodynamic forces found in arteriolar bleeding to promote hemostasis, whereas uncleaved VWF is activated at lower, physiologic shear stresses and causes thrombosis. Single-molecule experiments demonstrate that elongational forces in the range experienced by VWF in the vasculature unfold the A2 domain, and only the unfolded A2 domain is cleaved by ADAMTS13. In shear flow, tensile force on a VWF multimer increases with the square of multimer length and is highest at the middle, providing an efficient mechanism for homeostatic regulation of VWF size distribution by force-induced A2 unfolding and cleavage by ADAMTS13, as well as providing a counterbalance for VWF-mediated platelet aggregation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2753189/" 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/PMC2753189/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Xiaohui -- Halvorsen, Kenneth -- Zhang, Cheng-Zhong -- Wong, Wesley P -- Springer, Timothy A -- HL-48675/HL/NHLBI NIH HHS/ -- P01 HL048675/HL/NHLBI NIH HHS/ -- P01 HL048675-16/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2009 Jun 5;324(5932):1330-4. doi: 10.1126/science.1170905.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immune Disease Institute, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19498171" target="_blank"〉PubMed〈/a〉
    Keywords: ADAM Proteins/*metabolism ; Binding Sites ; Blood Coagulation/physiology ; *Hemostasis ; Humans ; Kinetics ; *Mechanical Phenomena ; Optical Tweezers ; Platelet Aggregation ; Protein Conformation ; Protein Folding ; Protein Multimerization ; Protein Structure, Tertiary ; Stress, Mechanical ; Thermodynamics ; von Willebrand Factor/*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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  • 97
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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
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 98
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    HIN-200 proteins regulate caspase activation in response to foreign cytoplasmic DNA (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-01-10
    Description: The mammalian innate immune system is activated by foreign nucleic acids. Detection of double-stranded DNA (dsDNA) in the cytoplasm triggers characteristic antiviral responses and macrophage cell death. Cytoplasmic dsDNA rapidly activated caspase 3 and caspase 1 in bone marrow-derived macrophages. We identified the HIN-200 family member and candidate lupus susceptibility factor, p202, as a dsDNA binding protein that bound stably and rapidly to transfected DNA. Knockdown studies showed p202 to be an inhibitor of DNA-induced caspase activation. Conversely, the related pyrin domain-containing HIN-200 factor, AIM2 (p210), was required for caspase activation by cytoplasmic dsDNA. This work indicates that HIN-200 proteins can act as pattern recognition receptors mediating responses to cytoplasmic dsDNA.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roberts, Tara L -- Idris, Adi -- Dunn, Jasmyn A -- Kelly, Greg M -- Burnton, Carol M -- Hodgson, Samantha -- Hardy, Lani L -- Garceau, Valerie -- Sweet, Matthew J -- Ross, Ian L -- Hume, David A -- Stacey, Katryn J -- New York, N.Y. -- Science. 2009 Feb 20;323(5917):1057-60. doi: 10.1126/science.1169841. Epub 2009 Jan 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The University of Queensland, Institute for Molecular Bioscience, QLD 4072, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19131592" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caspase 1/*metabolism ; Caspase 3/*metabolism ; Cell Line ; Cytoplasm/*metabolism ; DNA/immunology/*metabolism ; DNA-Binding Proteins/isolation & purification/metabolism ; Enzyme Activation ; Immunity, Innate ; Intracellular Signaling Peptides and Proteins/chemistry/genetics/isolation & ; purification/*metabolism ; Macrophages/immunology/*metabolism ; Membrane Proteins/chemistry/genetics/*metabolism ; Mice ; Mice, Inbred Strains ; RNA, Small Interfering ; Receptors, Pattern Recognition/*metabolism ; Symporters ; Transfection
    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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  • 99
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    Cytosolic viral sensor RIG-I is a 5'-triphosphate-dependent translocase on double-stranded RNA (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-01-03
    Description: Retinoic acid inducible-gene I (RIG-I) is a cytosolic multidomain protein that detects viral RNA and elicits an antiviral immune response. Two N-terminal caspase activation and recruitment domains (CARDs) transmit the signal, and the regulatory domain prevents signaling in the absence of viral RNA. 5'-triphosphate and double-stranded RNA (dsRNA) are two molecular patterns that enable RIG-I to discriminate pathogenic from self-RNA. However, the function of the DExH box helicase domain that is also required for activity is less clear. Using single-molecule protein-induced fluorescence enhancement, we discovered a robust adenosine 5'-triphosphate-powered dsRNA translocation activity of RIG-I. The CARDs dramatically suppress translocation in the absence of 5'-triphosphate, and the activation by 5'-triphosphate triggers RIG-I to translocate preferentially on dsRNA in cis. This functional integration of two RNA molecular patterns may provide a means to specifically sense and counteract replicating viruses.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3567915/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3567915/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Myong, Sua -- Cui, Sheng -- Cornish, Peter V -- Kirchhofer, Axel -- Gack, Michaela U -- Jung, Jae U -- Hopfner, Karl-Peter -- Ha, Taekjip -- CA82057/CA/NCI NIH HHS/ -- R01 GM065367/GM/NIGMS NIH HHS/ -- R01-GM065367/GM/NIGMS NIH HHS/ -- U19 AI083025/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Feb 20;323(5917):1070-4. doi: 10.1126/science.1168352. Epub 2009 Jan 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Genomic Biology, University of Illinois at Urbana-Champaign, 1206 West Gregory Drive, Champaign, IL 61801, USA. smyong@uiuc.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19119185" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/*metabolism ; Animals ; Cell Line ; Cytosol/metabolism ; DEAD-box RNA Helicases/chemistry/genetics/*metabolism ; Kinetics ; Nucleic Acid Heteroduplexes ; Protein Structure, Tertiary ; RNA/metabolism ; RNA, Double-Stranded/*metabolism ; RNA, Viral/metabolism ; Receptors, Pattern Recognition/chemistry/genetics/*metabolism ; Signal Transduction ; Temperature
    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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  • 100
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    Genetic code supports targeted insertion of two amino acids by one codon (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-01-10
    Description: Strict one-to-one correspondence between codons and amino acids is thought to be an essential feature of the genetic code. However, we report that one codon can code for two different amino acids with the choice of the inserted amino acid determined by a specific 3' untranslated region structure and location of the dual-function codon within the messenger RNA (mRNA). We found that the codon UGA specifies insertion of selenocysteine and cysteine in the ciliate Euplotes crassus, that the dual use of this codon can occur even within the same gene, and that the structural arrangements of Euplotes mRNA preserve location-dependent dual function of UGA when expressed in mammalian cells. Thus, the genetic code supports the use of one codon to code for multiple amino acids.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3088105/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3088105/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Turanov, Anton A -- Lobanov, Alexey V -- Fomenko, Dmitri E -- Morrison, Hilary G -- Sogin, Mitchell L -- Klobutcher, Lawrence A -- Hatfield, Dolph L -- Gladyshev, Vadim N -- AI058054/AI/NIAID NIH HHS/ -- GM061603/GM/NIGMS NIH HHS/ -- GM065204/GM/NIGMS NIH HHS/ -- R01 GM061603/GM/NIGMS NIH HHS/ -- R01 GM061603-04S2/GM/NIGMS NIH HHS/ -- ZIA BC010767-03/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2009 Jan 9;323(5911):259-61. doi: 10.1126/science.1164748.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Redox Biology Center, University of Nebraska, Lincoln, NE 68588, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19131629" target="_blank"〉PubMed〈/a〉
    Keywords: 3' Untranslated Regions ; Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; Codon/*genetics ; Codon, Terminator/*genetics ; Cysteine/*genetics/metabolism ; Euplotes/chemistry/*genetics ; *Genetic Code ; Humans ; Molecular Sequence Data ; Mutation ; Protozoan Proteins/biosynthesis/chemistry/genetics ; RNA, Protozoan/genetics/metabolism ; RNA, Transfer, Amino Acid-Specific/chemistry/genetics ; RNA, Transfer, Cys/chemistry/genetics ; Recombinant Fusion Proteins/metabolism ; Selenocysteine/*genetics/metabolism ; Selenoproteins/biosynthesis/chemistry/*genetics
    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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