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Egln3  -  egl-9 family hypoxia-inducible factor 3

Mus musculus

Synonyms: 2610021G09Rik, AI505553, AI648162, Egl nine homolog 3, HIF-PH3, ...
 
 
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High impact information on Egln3

  • Additionally, overexpression of SM-20, under conditions where cell death is blocked by a general caspase inhibitor, did not result in widespread release of cytochrome c from mitochondria [1].
  • An amino-terminal truncated form of SM-20 was not restricted to mitochondria but instead localized throughout the cytosol and nucleus [1].
  • Similar results were obtained with the nonfusing mouse C25 myoblast line, suggesting that SM-20 upregulation is a consequence of biochemical differentiation and is fusion independent [2].
  • SM-20 is a novel growth factor-responsive gene regulated during skeletal muscle development and differentiation [2].
  • Differentiation by serum withdrawal was associated with a marked induction of SM-20 mRNA and the expression of high levels of SM-20 antigen in myotubes [2].
 

Biological context of Egln3

  • We have now examined SM-20 expression during differentiation of cultured skeletal myoblasts and during skeletal myogenesis in vivo [2].
  • SM-20 is a novel, evolutionarily conserved "early response" gene originally cloned from a rat aortic smooth muscle cell (SMC) cDNA library [2].
  • During mouse embryogenesis, SM-20 was first observed at 8.5E in the dermomyotomal cells of the rostral somites [2].
  • These results indicate that SM-20 is a novel mitochondrial protein that may be an important mediator of neurotrophin-withdrawal-mediated cell death [1].
 

Anatomical context of Egln3

  • Low levels of SM-20 mRNA and protein were expressed in proliferating mouse C2C12 myoblasts [2].
  • The rat orthologue of EGLN3 (SM-20) exhibits tissue-restricted expression, is induced by growth factors in cultured vascular smooth muscle, and is up-regulated during myogenesis [3].
 

Associations of Egln3 with chemical compounds

  • SM-20 encodes a cytoplasmic protein, which is induced by platelet-derived growth factor and angiotensin II in cultured SMC and is upregulated in intimal SMC of atherosclerotic plaques and injured arteries [2].
 

Analytical, diagnostic and therapeutic context of Egln3

  • SM-20 immunofluorescence was present in the cytoplasm in a punctate pattern that colocalized with cytochrome oxidase I and with mitochondria-selective dyes [1].

References

  1. SM-20 is a novel mitochondrial protein that causes caspase-dependent cell death in nerve growth factor-dependent neurons. Lipscomb, E.A., Sarmiere, P.D., Freeman, R.S. J. Biol. Chem. (2001) [Pubmed]
  2. SM-20 is a novel growth factor-responsive gene regulated during skeletal muscle development and differentiation. Moschella, M.C., Menzies, K., Tsao, L., Lieb, M.A., Kohtz, J.D., Kohtz, D.S., Taubman, M.B. Gene Expr. (1999) [Pubmed]
  3. Mammalian EGLN genes have distinct patterns of mRNA expression and regulation. Lieb, M.E., Menzies, K., Moschella, M.C., Ni, R., Taubman, M.B. Biochem. Cell Biol. (2002) [Pubmed]
 
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