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- 克隆性:
单克隆
- 抗体英文名:
Anti-HIF-2α (Hypoxia
- 抗体名:
缺氧诱导因子2α 抗体
Transcription factor involved in the induction of oxygen regulated genes. Binds to core DNA sequence 5'-[AG]CGTG-3' within the hypoxia response element (HRE) of target gene promoters. Regulates the vascular endothelial growth factor (VEGF) expression and seems to be implicated in the development of blood vessels and the tubular system of lung. May also play a role in the formation of the endothelium that gives rise to the blood brain barrier. Potent activator of the Tie-2 tyrosine kinase expression. Activation requires recruitment of transcriptional coactivators such as CREBPB and probably EP300. Interaction with redox regulatory protein APEX seems to activate CTAD. Also known as Hypoxia-inducible factor -2α; Hypoxia-inducible factor 2 alpha; HIF-2 alpha; Endothelial PAS domain-containing protein 1; EPAS-1; HIF-1 alpha-like factor; MHLF; HIF-related factor; HRF; MOP2; Hif2a.
[SUBUNIT] Efficient DNA binding requires dimerization with another bHLH protein. Heterodimerizes with ARNT. Interacts with CREBPB.
[SUBCELLULAR LOCATION] Nucleus (Potential).
[TISSUE SPECIFICITY] Expressed in most tissues, with highest levels in lung, followed by heart, kidney, brain and liver. Predominantly expressed in endothelial cells. Also found in smooth muscle cells of the uterus, neurons, and brown adipose tissue. High expression in embryonic choroid plexus and kidney glomeruli.
[DEVELOPMENTAL STAGE] In day 11 embryo, expression is almost exclusively seen in endothelial cells of the intersegmental blood vessels separating the somites, the atrial and ventricular chambers of the heart, and the dorsal aorta. High expression also occurs in extraembryonic membranes. In the developing brain of day 13 embryo, endothelial cells of the highly vascularized choroid plexus contain high levels of EPAS1.
[PTM] In normoxia, is probably hydroxylated on Pro-405 and Pro-530 by EGLN1/PHD1, EGLN2/PHD2 and/or EGLN3/PHD3. The hydroxylated prolines promote interaction with VHL, initiating rapid ubiquitination and subsequent proteasomal degradation. Under hypoxia, proline hydroxylation is impaired and ubiquitination is attenuated, resulting in stabilization (By similarity).
[PTM] In normoxia, is hydroxylated on Asn-851 by HIF1AN thus probably abrogating interaction with CREBBP and EP300 and preventing transcriptional activation.
[ PTM] Phosphorylated on multiple sites in the CTAD.
[PTM] The iron and 2-oxoglutarate dependent 3-hydroxylation of asparagine is (S) stereospecific within HIF CTAD domains.
[SIMILARITY] Contains 1 basic helix-loop-helix (bHLH) domain.
[SIMILARITY] Contains 1 PAC (PAS-associated C-terminal) domain.
[SIMILARITY] Contains 2 PAS (PER-ARNT-SIM) domains
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缺氧诱导因子2α 抗体
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