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.Heterodimerizes with ARNT, heterodimer binds to core DNA sequence 5'-TACGTG-3' within the hypoxia response element (HRE) of target gene promoters.
HIF-1 alpha, also known as HIF1A, contains 1 basic helix-loop-helix (bHLH) domain, 1 PAC (PAS-associated C-terminal) domain, and 2 PAS (PER-ARNT-SIM) domains. It is one of the two subunits of Hypoxia-inducible factor-1 (HIF1). HIF1 is a transcription factor found in mammalian cells cultured under reduced oxygen tension that plays an essential role in cellular and systemic homeostatic responses to hypoxia. HIF1 is a heterodimer composed of an alpha subunit and a beta subunit. The beta subunit has been identified as the aryl hydrocarbon receptor nuclear translocator (ARNT). HIF-1 alpha is expressed in most tissues with the highest levels in the kidney and heart. It is 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. HIF-1 alpha functions as a master transcriptional regulator of the adaptive response to hypoxia. Under hypoxic conditions, it 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. HIF1A plays an essential role in embryonic vascularization, tumor angiogenesis, and the pathophysiology of ischemic disease. HIF-1 alpha binds to core DNA sequence 5'-[AG]CGTG-3' within the hypoxia response element (HRE) of target gene promoters. Activation requires the recruitment of transcriptional coactivators such as CREBPB and EP300.
Ubiquitin-Conjugating Enzyme E2 K (UBE2K) belongs to the E2 Ubiquitin-Conjugating Enzyme family. UBE2K is highly expressed in the brain; with highest levels found in cortex and striatum; and at lower levels in cerebellum and brainstem. UBE2K may mediate foam cell formation by the suppression of apoptosis of lipid-bearing macrophages through ubiquitination and subsequence degradation of p53/TP53. UBE2K is associated with the selective degradation of short-lived and abnormal proteins; such as the endoplasmic reticulum-associated degradation (ERAD) of misfolded lumenal proteins. In addition; UBE2K is involved in Alzheimer's disease; Huntington's disease and antigen processing through its interaction with huntingtin; and MHC-heavy chain proteins.
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