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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Gene Review: 

Mef2d  -  myocyte enhancer factor 2D

Rattus norvegicus

Synonyms: Myocyte-specific enhancer factor 2D
 
 
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High impact information on Mef2d

  • The kinase(s) that phosphorylates MEF2D during apoptosis is currently unknown [1].
  • Lithium also attenuated MEF2D hyperphosphorylation and apoptosis induced by calcineurin inhibition under depolarizing conditions, a GSK-3 beta-independent model of neuronal death [1].
  • These results demonstrate that the kinase that phosphorylates and inhibits the pro-survival function of MEF2D in cerebellar granule neurons is a novel lithium target distinct from GSK-3 beta [1].
  • Concurrently, lithium suppressed the hyperphosphorylation and caspase-mediated degradation of MEF2D [1].
  • Removal of depolarization induces hyperphosphorylation of MEF2D on serine/threonine residues, resulting in its decreased DNA binding and susceptibility to caspases [1].
 

Biological context of Mef2d

  • These results suggest that IGF-I can prolong the time of commitment to irreversible cell death and enhance the recovery of neurons subjected to an acute apoptotic stimulus by preserving the activity of the pro-survival factor MEF2D [2].
 

Regulatory relationships of Mef2d

  • However, IGF-I significantly blocked the degradation of MEF2D [2].
 

Other interactions of Mef2d

  • IGF-I administered during the apoptotic insult did not prevent the hyperphosphorylation of MEF2D and consequential loss of DNA binding [2].

References

  1. A myocyte enhancer factor 2D (MEF2D) kinase activated during neuronal apoptosis is a novel target inhibited by lithium. Linseman, D.A., Cornejo, B.J., Le, S.S., Meintzer, M.K., Laessig, T.A., Bouchard, R.J., Heidenreich, K.A. J. Neurochem. (2003) [Pubmed]
  2. Insulin-like growth factor-I suppresses degradation of the pro-survival transcription factor myocyte enhancer factor 2D (MEF2D) during neuronal apoptosis. Butts, B.D., Linseman, D.A., Le, S.S., Laessig, T.A., Heidenreich, K.A. Horm. Metab. Res. (2003) [Pubmed]
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