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  • 1
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    Stress-dependent regulation of FOXO transcription factors by the SIRT1 deacetylase (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-02-21
    Description: The Sir2 deacetylase modulates organismal life-span in various species. However, the molecular mechanisms by which Sir2 increases longevity are largely unknown. We show that in mammalian cells, the Sir2 homolog SIRT1 appears to control the cellular response to stress by regulating the FOXO family of Forkhead transcription factors, a family of proteins that function as sensors of the insulin signaling pathway and as regulators of organismal longevity. SIRT1 and the FOXO transcription factor FOXO3 formed a complex in cells in response to oxidative stress, and SIRT1 deacetylated FOXO3 in vitro and within cells. SIRT1 had a dual effect on FOXO3 function: SIRT1 increased FOXO3's ability to induce cell cycle arrest and resistance to oxidative stress but inhibited FOXO3's ability to induce cell death. Thus, one way in which members of the Sir2 family of proteins may increase organismal longevity is by tipping FOXO-dependent responses away from apoptosis and toward stress resistance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brunet, Anne -- Sweeney, Lora B -- Sturgill, J Fitzhugh -- Chua, Katrin F -- Greer, Paul L -- Lin, Yingxi -- Tran, Hien -- Ross, Sarah E -- Mostoslavsky, Raul -- Cohen, Haim Y -- Hu, Linda S -- Cheng, Hwei-Ling -- Jedrychowski, Mark P -- Gygi, Steven P -- Sinclair, David A -- Alt, Frederick W -- Greenberg, Michael E -- NIHP30-HD18655/HD/NICHD NIH HHS/ -- P01 NS35138-17/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2004 Mar 26;303(5666):2011-5. Epub 2004 Feb 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neuroscience, Children's Hospital, and Department of Neurobiology, Center for Blood Research (CBR) Institute for Biomedical Research, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14976264" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Animals ; Apoptosis ; Cell Cycle ; Cell Line ; Cell Nucleus/metabolism ; Cells, Cultured ; Cerebellum/cytology ; Forkhead Transcription Factors ; Gene Expression Profiling ; Gene Expression Regulation ; Histone Deacetylases/genetics/*metabolism ; Humans ; Intracellular Signaling Peptides and Proteins ; Mice ; Mice, Knockout ; Neurons/cytology ; *Oxidative Stress ; Phosphorylation ; Proteins/genetics ; Recombinant Proteins/metabolism ; Sirtuin 1 ; Sirtuins/genetics/*metabolism ; Transcription Factors/genetics/*metabolism ; Transcription, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Noggin, cartilage morphogenesis, and joint formation in the mammalian skeleton (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-06-20
    Description: Noggin is a bone morphogenetic protein (BMP) antagonist expressed in Spemann's organizer. Murine Noggin is expressed in condensing cartilage and immature chondrocytes, as are many BMPs. In mice lacking Noggin, cartilage condensations initiated normally but developed hyperplasia, and initiation of joint development failed as measured by the expression of growth and differentiation factor-5. The maturation of cartilage and Hoxd expression were unaffected. Excess BMP activity in the absence of Noggin antagonism may enhance the recruitment of cells into cartilage, resulting in oversized growth plates; chondrocytes are also refractory to joint-inducing positional cues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brunet, L J -- McMahon, J A -- McMahon, A P -- Harland, R M -- GM49346/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1998 May 29;280(5368):1455-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cell Biology, Division of Biochemistry and Molecular Biology, University of California, Berkeley, CA 94720-3204, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9603738" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Morphogenetic Proteins/genetics/metabolism ; Carrier Proteins ; Cartilage/*embryology/*metabolism ; Chondrocytes/metabolism ; Embryo, Mammalian/metabolism ; Extremities/*embryology ; Gene Expression ; Growth Differentiation Factor 5 ; Growth Substances/genetics ; Homeodomain Proteins/genetics ; Joints/abnormalities/*embryology ; Mesoderm/metabolism ; Mice ; Mice, Knockout ; Morphogenesis ; Mutation ; Proteins/*genetics/*physiology ; Up-Regulation
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Crucial role for DNA ligase III in mitochondria but not in Xrcc1-dependent repair (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-03-11
    Description: Mammalian cells have three ATP-dependent DNA ligases, which are required for DNA replication and repair. Homologues of ligase I (Lig1) and ligase IV (Lig4) are ubiquitous in Eukarya, whereas ligase III (Lig3), which has nuclear and mitochondrial forms, appears to be restricted to vertebrates. Lig3 is implicated in various DNA repair pathways with its partner protein Xrcc1 (ref. 1). Deletion of Lig3 results in early embryonic lethality in mice, as well as apparent cellular lethality, which has precluded definitive characterization of Lig3 function. Here we used pre-emptive complementation to determine the viability requirement for Lig3 in mammalian cells and its requirement in DNA repair. Various forms of Lig3 were introduced stably into mouse embryonic stem (mES) cells containing a conditional allele of Lig3 that could be deleted with Cre recombinase. With this approach, we find that the mitochondrial, but not nuclear, Lig3 is required for cellular viability. Although the catalytic function of Lig3 is required, the zinc finger (ZnF) and BRCA1 carboxy (C)-terminal-related (BRCT) domains of Lig3 are not. Remarkably, the viability requirement for Lig3 can be circumvented by targeting Lig1 to the mitochondria or expressing Chlorella virus DNA ligase, the minimal eukaryal nick-sealing enzyme, or Escherichia coli LigA, an NAD(+)-dependent ligase. Lig3-null cells are not sensitive to several DNA-damaging agents that sensitize Xrcc1-deficient cells. Our results establish a role for Lig3 in mitochondria, but distinguish it from its interacting protein Xrcc1.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3261757/" 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/PMC3261757/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Simsek, Deniz -- Furda, Amy -- Gao, Yankun -- Artus, Jerome -- Brunet, Erika -- Hadjantonakis, Anna-Katerina -- Van Houten, Bennett -- Shuman, Stewart -- McKinnon, Peter J -- Jasin, Maria -- CA21765/CA/NCI NIH HHS/ -- ES019566/ES/NIEHS NIH HHS/ -- GM54668/GM/NIGMS NIH HHS/ -- NS37956/NS/NINDS NIH HHS/ -- P30 CA008748/CA/NCI NIH HHS/ -- R01 ES019566/ES/NIEHS NIH HHS/ -- R01 GM054668/GM/NIGMS NIH HHS/ -- R01 GM054668-12/GM/NIGMS NIH HHS/ -- R01 GM054668-12S1/GM/NIGMS NIH HHS/ -- R01 GM063611/GM/NIGMS NIH HHS/ -- R01 NS037956/NS/NINDS NIH HHS/ -- R01 NS037956-13/NS/NINDS NIH HHS/ -- England -- Nature. 2011 Mar 10;471(7337):245-8. doi: 10.1038/nature09794.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Developmental Biology Program, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21390132" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biocatalysis ; Cell Survival ; DNA Damage ; DNA Ligases/chemistry/deficiency/genetics/*metabolism ; *DNA Repair ; DNA, Mitochondrial/*metabolism ; DNA-Binding Proteins/*metabolism ; Embryonic Stem Cells/metabolism ; Genes, Essential ; Genetic Complementation Test ; Humans ; Mice ; Mitochondria/*enzymology/*genetics/pathology ; Protein Structure, Tertiary ; Sister Chromatid Exchange/drug effects
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 4
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    Neurodevelopment. Parasympathetic ganglia derive from Schwann cell precursors (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-06-14
    Description: Neural crest cells migrate extensively and give rise to most of the peripheral nervous system, including sympathetic, parasympathetic, enteric, and dorsal root ganglia. We studied how parasympathetic ganglia form close to visceral organs and what their precursors are. We find that many cranial nerve-associated crest cells coexpress the pan-autonomic determinant Paired-like homeodomain 2b (Phox2b) together with markers of Schwann cell precursors. Some give rise to Schwann cells after down-regulation of PHOX2b. Others form parasympathetic ganglia after being guided to the site of ganglion formation by the nerves that carry preganglionic fibers, a parsimonious way of wiring the pathway. Thus, cranial Schwann cell precursors are the source of parasympathetic neurons during normal development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Espinosa-Medina, I -- Outin, E -- Picard, C A -- Chettouh, Z -- Dymecki, S -- Consalez, G G -- Coppola, E -- Brunet, J-F -- P01 HD036379/HD/NICHD NIH HHS/ -- R01 DK067826/DK/NIDDK NIH HHS/ -- R21 DA023643/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 2014 Jul 4;345(6192):87-90. doi: 10.1126/science.1253286. Epub 2014 Jun 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut de Biologie de l'Ecole Normale Superieure, Inserm U1024, and CNRS UMR 8197, 75005 Paris, France. ; Department of Genetics, Harvard Medical School, Boston, MA 02115, USA. ; Division of Neuroscience, San Raffaele Scientific Institute, Milan, Italy. ; Institut de Biologie de l'Ecole Normale Superieure, Inserm U1024, and CNRS UMR 8197, 75005 Paris, France. jfbrunet@biologie.ens.fr.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24925912" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Basic Helix-Loop-Helix Transcription Factors/genetics/metabolism ; Cranial Nerves/cytology/metabolism ; Down-Regulation ; Ganglia, Parasympathetic/cytology/*embryology ; Homeodomain Proteins/genetics/*metabolism ; Mice ; Mice, Knockout ; Nerve Tissue Proteins/genetics/metabolism ; Neural Crest/cytology/metabolism ; Neural Stem Cells/*cytology ; Neurogenesis/genetics/*physiology ; Neurons/*cytology ; Schwann Cells/*cytology ; Transcription Factors/genetics/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 5
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    Identification of MAP kinase domains by redirecting stress signals into growth factor responses (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-06-14
    Description: Mitogen-activated protein kinase (MAPK) cascades, termed MAPK modules, channel extracellular signals into specific cellular responses. Chimeric molecules were constructed between p38 and p44 MAPKs, which transduce stress and growth factor signals, respectively. A discrete region of 40 residues located in the amono-terminal p38MAPK lobe directed the specificity of response to extracellular signals, whereas the p44MAPK chimera, expressed in vivo, redirected stress signals into early mitogenic responses, demonstrating the functional independence of these domains.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brunet, A -- Pouyssegur, J -- New York, N.Y. -- Science. 1996 Jun 14;272(5268):1652-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre de Biochemie-CNRS, UMR134, Parc Valrose, Faculte des Sciences, Nice, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8658140" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Anisomycin/pharmacology ; Binding Sites ; Calcium-Calmodulin-Dependent Protein Kinases/genetics/*metabolism ; Cell Division ; Cell Line ; Cricetinae ; Cricetulus ; Enzyme Activation ; Gene Expression Regulation ; Genes, fos ; Growth Substances/metabolism ; Mice ; Mitogen-Activated Protein Kinase 3 ; *Mitogen-Activated Protein Kinases ; Molecular Sequence Data ; Phosphorylation/drug effects ; Protein Kinases/metabolism ; Protein-Serine-Threonine Kinases/metabolism ; Recombinant Fusion Proteins/genetics/metabolism ; Ribosomal Protein S6 Kinases ; Signal Transduction ; Sorbitol/pharmacology ; Substrate Specificity ; p38 Mitogen-Activated Protein Kinases
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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