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Anti-HIF-1α (K377) Antibody

品牌：Antibodies

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規(guī)格：50μl

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Anti-HIF-1α (K377) Antibody

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Overview

Name:	Anti-HIF-1α (K377) Antibody See all HIF-1α primary antibodies
Description:	Rabbit polyclonal antibody to HIF-1α (K377)
Specificity:	HIF-1α (K377) pAb detects endogenous levels of HIF-1α protein.
Applications:	WB, IHC
Reactivity:	Human, Mouse, Rat
Immunogen:	Synthetic peptide, corresponding to amino acids 345-398 of Human HIF-1α.
Host:	Rabbit
Clonality:	Polyclonal
Conjugate:	Unconjugated
Molecular Weight:	~ 90, 120 kDa
Purity:	The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen and the purity is > 95% (by SDS-PAGE).
Product Form:	1 mg/ml in Phosphate buffered saline (PBS) with 0.05% sodium azide, approx. pH 7.2.

Target

Function:	Functions as a master transcriptional regulator of the adaptive response to hypoxia. Under hypoxic conditions, activates the transcription of over 40 genes, including erythropoietin, glucose transporters, glycolytic enzymes, vascular endothelial growth factor, HILPDA, and other genes whose protein products increase oxygen delivery or facilitate metabolic adaptation to hypoxia. Plays an essential role in embryonic vascularization, tumor angiogenesis and pathophysiology of ischemic disease. Binds to core DNA sequence 5'-[AG]CGTG-3' within the hypoxia response element (HRE) of target gene promoters. Activation requires recruitment of transcriptional coactivators such as CREBBP and EP300. Activity is enhanced by interaction with both, NCOA1 or NCOA2. Interaction with redox regulatory protein APEX seems to activate CTAD and potentiates activation by NCOA1 and CREBBP. Involved in the axonal distribution and transport of mitochondria in neurons during hypoxia.
Tissue Specificity:	Expressed in most tissues with highest levels in kidney and heart. Overexpressed in the majority of common human cancers and their metastases, due to the presence of intratumoral hypoxia and as a result of mutations in genes encoding oncoproteins and tumor suppressors. A higher level expression seen in pituitary tumors as compared to the pituitary gland.
Post-Translational Modification:	In normoxia, is hydroxylated on Pro-402 and Pro-564 in the oxygen-dependent degradation domain (ODD) by EGLN1/PHD2 and EGLN2/PHD1. EGLN3/PHD3 has also been shown to hydroxylate Pro-564. The hydroxylated prolines promote interaction with VHL, initiating rapid ubiquitination and subsequent proteasomal degradation. Deubiquitinated by USP20. Under hypoxia, proline hydroxylation is impaired and ubiquitination is attenuated, resulting in stabilization.
Cellular Location:	Cytoplasm. Nucleus. Nucleus speckle. Colocalizes with HIF3A in the nucleus and speckles (By similarity). Cytoplasmic in normoxia, nuclear translocation in response to hypoxia (PubMed:9822602).