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Gene Review

Egln3  -  egl-9 family hypoxia-inducible factor 3

Rattus norvegicus

Synonyms: Egl nine homolog 3, HIF-PH3, HIF-prolyl hydroxylase 3, HPH-3, Hypoxia-inducible factor prolyl hydroxylase 3, ...
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Disease relevance of Egln3

  • Recent findings show a homology of SM-20 with enzymes involved in the regulation of hypoxia inducible factor 1 [1].
  • Hypoxia-inducible factor (HIF)-alpha subunits (HIF-1alpha, HIF-2alpha and HIF-3alpha), which play a pivotal role during the development of hypoxia-induced pulmonary hypertension (HPH), are regulated through post-translational hydroxylation by their three prolyl hydroxylase domain-containing proteins (PHD1, PHD2 and PHD3) [2].

High impact information on Egln3


Biological context of Egln3


Anatomical context of Egln3

  • Analysis of cytochrome c in cytosolic and mitochondria-enriched subcellular fractions revealed that induction of SM-20 led to the accumulation of cytochrome c in the cytosol [5].
  • To further evaluate the mechanism by which SM-20 promotes cell death, we developed a PC12-derived cell line in which SM-20 expression can be induced by addition of doxycycline to the culture medium [5].
  • A rabbit polyclonal antibody was generated against a peptide sequence of SM-20 and detected a major band of the predicted size of 40 kd and a second 33-kd band that likely represents a processed form present in mitochondria [1].

Associations of Egln3 with chemical compounds

  • Cycloheximide induces high levels of SM-20 mRNA and superinduces it in the presence of serum, suggesting that the increase in SM-20 mRNA levels is not dependent on protein synthesis and is part of the primary response to growth agonists [3].
  • Expression of SM-20 also increases during neuronal death caused by cytosine arabinoside or the phosphatidylinositol 3-kinase inhibitor LY294002 [7].

Regulatory relationships of Egln3


Other interactions of Egln3


Analytical, diagnostic and therapeutic context of Egln3


  1. Angiotensin II's antiproliferative effects mediated through AT2-receptors depend on down-regulation of SM-20. Wolf, G., Harendza, S., Schroeder, R., Wenzel, U., Zahner, G., Butzmann, U., Freeman, R.S., Stahl, R.A. Lab. Invest. (2002) [Pubmed]
  2. Differential and reciprocal regulation between hypoxia-inducible factor-alpha subunits and their prolyl hydroxylases in pulmonary arteries of rat with hypoxia-induced hypertension. Chen, Y.R., Dai, A.G., Hu, R.C., Jiang, Y.L. Acta Biochim. Biophys. Sin. (Shanghai) (2006) [Pubmed]
  3. Identification of a novel growth factor-responsive gene in vascular smooth muscle cells. Wax, S.D., Rosenfield, C.L., Taubman, M.B. J. Biol. Chem. (1994) [Pubmed]
  4. Angiotensin II induces hypoxia-inducible factor-1 alpha in PC 12 cells through a posttranscriptional mechanism: role of AT2 receptors. Wolf, G., Schroeder, R., Stahl, R.A. American journal of nephrology. (2004) [Pubmed]
  5. Induction of SM-20 in PC12 cells leads to increased cytochrome c levels, accumulation of cytochrome c in the cytosol, and caspase-dependent cell death. Straub, J.A., Lipscomb, E.A., Yoshida, E.S., Freeman, R.S. J. Neurochem. (2003) [Pubmed]
  6. Regulation of the SM-20 prolyl hydroxylase gene in smooth muscle cells. Menzies, K., Liu, B., Kim, W.J., Moschella, M.C., Taubman, M.B. Biochem. Biophys. Res. Commun. (2004) [Pubmed]
  7. Expression of the SM-20 gene promotes death in nerve growth factor-dependent sympathetic neurons. Lipscomb, E.A., Sarmiere, P.D., Crowder, R.J., Freeman, R.S. J. Neurochem. (1999) [Pubmed]
  8. Identification and partial characterization of differentially expressed mRNAs in normal human endometria and endometrial carcinomas by differential display RT-PCR. Foca, C., Rice, G.E., Quinn, M.A., Moses, E.K. Mol. Hum. Reprod. (2000) [Pubmed]
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