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The protein encoded by HIF3A is the alpha-3 subunit of one of several alpha/beta-subunit heterodimeric transcription factors that regulate many adaptive responses to low oxygen tension (hypoxia).
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AA can protect cardiomyocytes against hypoxia-induced apoptosis through regulating the miR (Montrer MLXIP Kits ELISA)-1290/HIF3A/HIF-1alpha (Montrer HIF1A Kits ELISA) axis, and miR (Montrer MLXIP Kits ELISA)-1290 may be a potential target in the prevention of myocardial ischemia-reperfusion injury
NAP peptide prevents outer blood retinal barrier breakdown by reducing HIF1alpha (Montrer HIF1A Kits ELISA)/HIF2alpha (Montrer EPAS1 Kits ELISA), VEGF (Montrer VEGFA Kits ELISA)/VEGFRs, and increasing HIF3alpha expression Moreover it is able to reduce the percentage of apoptotic cells by modulating the expression of two death related genes, BAX (Montrer BAX Kits ELISA) and Bcl2 (Montrer BCL2 Kits ELISA).
HIF3A methylation was found in the association between the HIF3A rs3826795 polymorphism and alanine aminotransferase (Montrer ALT Kits ELISA) among obese children.
TIMP2 (Montrer TIMP2 Kits ELISA) suppression, in a hypoxic environment, was induced through a regulatory feedback circuit consisting of hypoxia-inducible factor (HIF) 1 alpha (Montrer HIF1A Kits ELISA), microRNA-210 (miR (Montrer MLXIP Kits ELISA)-210), and HIF-3alpha.
Results were discordant with those expected if HIF3A methylation has a causal effect on body mass index (BMI) & provided more evidence for causality in the reverse direction (i.e., an effect of BMI on HIF3A methylation); results also show a long-lasting intergenerational influence of maternal BMI on offspring methylation at this locus, which may confound associations between own adiposity & HIF3A methylation.
DNA methylation in HIF3A shares moderate correlation between adipose tissue and blood, and both are associated with BMI. In contrast, methylation in FASN is poorly correlated across tissues, but the DNA methylation in adipose tissue but not blood is highly associated with BMI
Reduced lifetimes of the donor were partially restored by coexpression of HIF-1alpha (Montrer HIF1A Kits ELISA) or Bcl-xL (Montrer BCL2L1 Kits ELISA), binding proteins of IPAS in the nucleus and mitochondria, respectively.
Results confirmed a positive association between BMI and HIF3A DNA promoter methylation in the blood. The tissue-specific results of HIF3A gene expression indicate that subcutaneous adipose tissue is the more functional tissue in which a low expression may adversely affect whole-body insulin (Montrer INS Kits ELISA) sensitivity.
Parkin (Montrer PARK2 Kits ELISA) is downregulated under hypoxia and that it interferes with HIF expression based on cellular oxygen tension.
This provides a compelling model for how hypoxia-induced miR (Montrer MLXIP Kits ELISA)-429 regulates the switch between HIF-1 (Montrer HIF1A Kits ELISA) adaptive responses to HIF-3 survival responses by rapidly decreasing HIF1A (Montrer HIF1A Kits ELISA) levels while simultaneously slowing the progression of HIF3A expression until the miR (Montrer MLXIP Kits ELISA)-429 levels drop below normoxic levels.
Phosphorylation of inhibitory PAS domain protein (IPAS) at Ser184 by MAPK-activated protein kinase 2 (MK2 (Montrer MAPKAPK2 Kits ELISA) or MAPKAPK2 (Montrer MAPKAPK2 Kits ELISA)) enhances the proapoptotic function of IPAS.
Report suggests that BV-2 microglial cells express HIF-3a under inflammatory conditions and that its activation differed from that of HIF-1a (Montrer HIF1A Kits ELISA)
mRNA of HIF-2alpha (Montrer EPAS1 Kits ELISA) and Ets-1 (Montrer ETS1 Kits ELISA) were significantly increased by HIF-3alpha ablation. Both factors activate the VE-cadherin (Montrer CDH5 Kits ELISA) gene, the transcriptional repression of these factors by HIF-3alpha is important for silencing the irrelevant expression of the VE-cadherin (Montrer CDH5 Kits ELISA) gene.
our data indicated that Tnni2K175del mutation led to abnormally increased hif3a and decreased vegf (Montrer VEGFA Kits ELISA) in bone, which explain, at least in part, the small body size of Tnni2K175del mice
Anoxia preconditioning increases anti-ischemic neuronal resistance which to a certain extent correlates with the changes of HIF-1alpha (Montrer HIF1A Kits ELISA) and HIF-3alpha expression.
alternative splicing and expression of IPAS is induced by hypoxia.
By generating mice with a targeted disruption of the NEPAS/HIF-3alpha locus, it was found that homozygous mutant mice, NEPAS/HIF-3alpha(-/-), were viable but displayed enlargement of the right ventricle and impaired lung remodeling.
Identity of third HIF alpha class member, HIF-3alpha. mRNA expression information by mouse MTN. Experimental proof of dimerization with ARNT/HIF-1beta (Montrer ARNT Kits ELISA).
The protein encoded by this gene is the alpha-3 subunit of one of several alpha/beta-subunit heterodimeric transcription factors that regulate many adaptive responses to low oxygen tension (hypoxia). 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. Multiple alternatively spliced transcript variants have been found for this gene.
, PAS domain-containing protein 7
, basic-helix-loop-helix-PAS protein MOP7
, class E basic helix-loop-helix protein 17
, hypoxia-inducible factor 3-alpha
, inhibitory PAS domain protein
, member of PAS protein 7
, hypoxia inducible factor three alpha
, neonatal and embryonic PAS
, HIF-3 alpha
, HIF3 alpha 1
, hypoxia inducible factor 3 alpha
, hypoxia inducible factor 3a
, hypoxia-inducible factor 3 alpha
, hypoxia-inducible factor 3 alpha subunit
, hypoxia inducible factor 3, alpha subunit
, hypoxia-inducible factor-3 alpha
, hypoxia-inducible factor 3-alpha-like