Facteur induit par l’hypoxie — Wikipédia

Vue d’ensemble

HIF1A hypoxia inducible factor 1 subunit alpha [ human]

This gene encodes the alpha subunit of transcription factor hypoxia-inducible factor-1 HIF-1, which is a heterodimer composed of an alpha and a beta subunit, HIF-1 functions as a master regulator of cellular and systemic homeostatic response to hypoxia by activating transcription of many genes, including those involved in energy metabolism, angiogenesis, apoptosis, and other genes whose

HIF-1α pathway: role, regulation and intervention for

HIF-1α is an oxygen sensitive subunit and its expression is induced under hypoxic conditions, In contrast, HIF-1β is constitutively expressed, HIF-1β is also known as aryl hydrocarbon nuclear translocator ARNT, because it was discovered before HIF-1α and was identified

Role of hypoxia-inducible factor HIF-1alpha versus HIF

Overexpression of hypoxia-inducible factors HIF, HIF-1alpha and HIF-2alpha, leads to the up-regulation of genes involved in proliferation, angiogenesis, and glucose metabolism and is associated with tumor progression in several cancers, However, the contribution of HIF-1alpha versus HIF-2alpha to …

HIF-1α pathway: role, regulation and intervention for

Hypoxia-inducible factor-1 HIF-1 has been recognized as an important cancer drug target, Many recent studies have provided convincing evidences of strong correlation between elevated levels of HIF-1 and tumor metastasis, angiogenesis, poor patient prognosis as well as tumor resistance therapy, It … HIF-1α pathway: role, regulation and intervention for cancer therapy Acta Pharm Sin B, 2015

Biology of HIF-1α

HIF-1 alpha is required for solid tumor formation and embryonic vascularization, EMBO J 1998; 17: 3005–3015, CAS Article Google Scholar 36, Thurston G, Suri C, Smith K

Hypoxia-inducible factor 1-alpha HIF-1α as a factor

Hypoxia-inducible factor 1-alpha HIF-1α as a factor mediating the relationship between obesity and heart failure with preserved ejection fraction Obes Rev, 2019 May;205:701-712, doi: 10,1111/obr,12828, Epub 2019 Mar 3, Authors Ian Warbrick 1 , Simon W Rabkin 1 Affiliation 1 Department of Medicine Cardiology, University of British Columbia, Vancouver, Canada, PMID: 30828970 DOI: 10,1111

Hypoxia-inducible factor

The alpha subunits of HIF are hydroxylated at conserved proline residues by HIF prolyl-hydroxylases, allowing their recognition and ubiquitination by the VHL E3 ubiquitin ligase, which labels them for rapid degradation by the proteasome, This occurs only in normoxic conditions, In hypoxic conditions, HIF prolyl-hydroxylase is inhibited, since it utilizes oxygen as a cosubstrate, Inhibition of

Hypoxia-Inducible Factor HIF-1 Regulatory Pathway and

HIF-1 is among the primary genes involved in the homeostatic process, which can increase vascularization in hypoxic areas such as localized ischemia and tumors, It is a transcription factor for dozens of target genes; HIF-1 is also essential for immunological responses and is a crucial physiological regulator of homeostasis, vascularization, and anaerobic metabolism, Furthermore, HIF-1 is

Hypoxia-Inducible Factor 1 and Cardiovascular Disease

Hypoxia-inducible factor 1 HIF-1 is a transcription factor that functions as a master regulator of oxygen homeostasis in all metazoan species, HIF-1 controls oxygen delivery, by regulating angiogenesis and vascular remodeling, and oxygen utilization, by regulating glucose metabolism and redox homeostasis, Analysis of animal models suggests that by activation of these homeostatic mechanisms

HIF3A

The alpha-3 subunit lacks the transactivation domain found in factors containing either the alpha-1 or alpha-2 subunits, It is thought that factors containing the alpha-3 subunit are negative regulators of hypoxia-inducible gene expression, At least three transcript variants encoding three different isoforms have been found for this gene, In rats, it plays a negative role in the adaptation to

mTOR- and HIF-1α-mediated aerobic glycolysis as metabolic

Inhibition of Akt, mTOR, or HIF-1α blocked monocyte induction of trained immunity, whereas the adenosine monophosphate-activated protein kinase activator metformin inhibited the innate immune response to fungal infection, Mice with a myeloid cell-specific defect in HIF-1α were unable to mount trained immunity against bacterial sepsis, Our results indicate that induction of aerobic glycolysis