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  • 1
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    Neuronal activity-dependent cell survival mediated by transcription factor MEF2 (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-26
    Description: During mammalian development, electrical activity promotes the calcium-dependent survival of neurons that have made appropriate synaptic connections. However, the mechanisms by which calcium mediates neuronal survival during development are not well characterized. A transcription-dependent mechanism was identified by which calcium influx into neurons promoted cell survival. The transcription factor MEF2 was selectively expressed in newly generated postmitotic neurons and was required for the survival of these neurons. Calcium influx into cerebellar granule neurons led to activation of p38 mitogen-activated protein kinase-dependent phosphorylation and activation of MEF2. Once activated, MEF2 regulated neuronal survival by stimulating MEF2-dependent gene transcription. These findings demonstrate that MEF2 is a calcium-regulated transcription factor and define a function for MEF2 during nervous system development that is distinct from previously well-characterized functions of MEF2 during muscle differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mao, Z -- Bonni, A -- Xia, F -- Nadal-Vicens, M -- Greenberg, M E -- 5T32NS07112/NS/NINDS NIH HHS/ -- NS28829/NS/NINDS NIH HHS/ -- P30-HD18655/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1999 Oct 22;286(5440):785-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neuroscience, Department of Neurology, Children's Hospital and Department of Neurobiology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10531066" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Calcium/metabolism ; Calcium Channels, L-Type/metabolism ; Cell Differentiation ; Cell Survival ; Cells, Cultured ; Cerebellum/cytology/metabolism ; Cerebral Cortex/cytology/embryology/metabolism ; DNA-Binding Proteins/genetics/*metabolism ; Dimerization ; Immunohistochemistry ; MEF2 Transcription Factors ; Mitogen-Activated Protein Kinases/metabolism ; Mitosis ; Mutation ; Myogenic Regulatory Factors ; Neurons/*cytology/*metabolism ; Phosphorylation ; Rats ; Signal Transduction ; Transcription Factors/genetics/*metabolism ; *Transcription, Genetic ; Transfection ; 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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  • 2
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    Regulation of gliogenesis in the central nervous system by the JAK-STAT signaling pathway (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-10-23
    Description: A mechanism by which members of the ciliary neurotrophic factor (CNTF)-leukemia inhibitory factor cytokine family regulate gliogenesis in the developing mammalian central nervous system was characterized. Activation of the CNTF receptor promoted differentiation of cerebral cortical precursor cells into astrocytes and inhibited differentiation of cortical precursors along a neuronal lineage. Although CNTF stimulated both the Janus kinase-signal transducer and activator of transcription (JAK-STAT) and Ras-mitogen-activated protein kinase signaling pathways in cortical precursor cells, the JAK-STAT signaling pathway selectively enhanced differentiation of these precursors along a glial lineage. These findings suggest that cytokine activation of the JAK-STAT signaling pathway may be a mechanism by which cell fate is controlled during mammalian development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bonni, A -- Sun, Y -- Nadal-Vicens, M -- Bhatt, A -- Frank, D A -- Rozovsky, I -- Stahl, N -- Yancopoulos, G D -- Greenberg, M E -- NIHP30-HD 18655/HD/NICHD NIH HHS/ -- R01 CA43855/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1997 Oct 17;278(5337):477-83.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neuroscience, Children's Hospital, and Department of Neurobiology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9334309" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/metabolism ; Astrocytes/*cytology/drug effects/metabolism ; Cell Differentiation ; Cell Division ; Cell Lineage ; Cells, Cultured ; Cerebral Cortex/*cytology/embryology ; Ciliary Neurotrophic Factor ; Cytokine Receptor gp130 ; DNA-Binding Proteins/*metabolism ; Dimerization ; Glial Fibrillary Acidic Protein/biosynthesis ; Growth Inhibitors/metabolism/pharmacology ; *Interleukin-6 ; Janus Kinase 1 ; Leukemia Inhibitory Factor ; Leukemia Inhibitory Factor Receptor alpha Subunit ; Lymphokines/metabolism/pharmacology ; Membrane Glycoproteins/metabolism ; Nerve Growth Factors/pharmacology ; Nerve Tissue Proteins/metabolism/pharmacology ; Platelet-Derived Growth Factor/pharmacology ; Protein-Tyrosine Kinases/*metabolism ; Rats ; Receptor Protein-Tyrosine Kinases/metabolism ; Receptor, Ciliary Neurotrophic Factor ; Receptors, Cytokine/metabolism ; Receptors, Nerve Growth Factor/metabolism ; Receptors, OSM-LIF ; STAT1 Transcription Factor ; STAT3 Transcription Factor ; *Signal Transduction ; Stem Cells/cytology ; Trans-Activators/*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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
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