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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). Additionally we are shipping HIF3A Kits (5) and HIF3A Proteins (4) and many more products for this protein.
Showing 10 out of 88 products:
Human Polyclonal HIF3A Primary Antibody for ICC, IF - ABIN250964
Forooghian, Razavi, Timms: Hypoxia-inducible factor expression in human RPE cells. in The British journal of ophthalmology 2007
Show all 6 Pubmed References
Human Polyclonal HIF3A Primary Antibody for ICC, IF - ABIN315681
Huang, Kapere Ochieng, Kempen, Munck, Swagemakers, van Ijcken, Grosveld, Tibboel, Rottier: Hypoxia inducible factor 3α plays a critical role in alveolarization and distal epithelial cell differentiation during mouse lung development. in PLoS ONE 2013
Human Polyclonal HIF3A Primary Antibody for WB - ABIN151687
Jackson, Zhang, Hadley, Rabbani, Zhang, Marks, Vujaskovic: Temporal expression of hypoxia-regulated genes is associated with early changes in redox status in irradiated lung. in Free radical biology & medicine 2012
Human Monoclonal HIF3A Primary Antibody for IHC, IHC (p) - ABIN4317485
Liu, Fang, Song, Jiang, He, Liu: Expression of hypoxia-inducible factor 3α in hepatocellular carcinoma and its association with other hypoxia-inducible factors. in Experimental and therapeutic medicine 2016
Human Polyclonal HIF3A Primary Antibody for IHC, WB - ABIN2778530
Lazrek, Goffard, Schanen, Karquel, Bocket, Lion, Devaux, Hedouin, Gosset, Hober: Detection of hepatitis C virus antibodies and RNA among medicolegal autopsy cases in Northern France. in Diagnostic microbiology and infectious disease 2006
Show all 2 Pubmed References
Mouse (Murine) Polyclonal HIF3A Primary Antibody for ELISA, WB - ABIN100475
Takeda, Ho, Takeda, Duan, Nagy, Fong: Placental but not heart defects are associated with elevated hypoxia-inducible factor alpha levels in mice lacking prolyl hydroxylase domain protein 2. in Molecular and cellular biology 2006
NAP peptide prevents outer blood retinal barrier breakdown by reducing HIF1alpha (show HIF1A Antibodies)/HIF2alpha (show EPAS1 Antibodies), VEGF (show VEGFA Antibodies)/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 (show BAX Antibodies) and Bcl2 (show BCL2 Antibodies).
HIF3A methylation was found in the association between the HIF3A rs3826795 polymorphism and alanine aminotransferase (show ALT Antibodies) among obese children.
TIMP2 (show TIMP2 Antibodies) suppression, in a hypoxic environment, was induced through a regulatory feedback circuit consisting of hypoxia-inducible factor (HIF) 1 alpha (show HIF1A Antibodies), microRNA-210 (miR (show MLXIP Antibodies)-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 (show HELLS Antibodies) in HIF3A shares moderate correlation between adipose tissue and blood, and both are associated with BMI. In contrast, methylation in FASN (show FASN Antibodies) is poorly correlated across tissues, but the DNA methylation (show HELLS Antibodies) in adipose tissue but not blood is highly associated with BMI
Reduced lifetimes of the donor were partially restored by coexpression of HIF-1alpha (show HIF1A Antibodies) or Bcl-xL (show BCL2L1 Antibodies), 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 (show INS Antibodies) sensitivity.
Parkin (show PARK2 Antibodies) 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 (show MLXIP Antibodies)-429 regulates the switch between HIF-1 (show HIF1A Antibodies) adaptive responses to HIF-3 survival responses by rapidly decreasing HIF1A (show HIF1A Antibodies) levels while simultaneously slowing the progression of HIF3A expression until the miR (show MLXIP Antibodies)-429 levels drop below normoxic levels.
The association between increased DNA methylation (show HELLS Antibodies) at HIF3A and increased adiposity is present in neonates.
Phosphorylation of inhibitory PAS domain protein (IPAS) at Ser184 by MAPK-activated protein kinase 2 (MK2 (show MAPKAPK2 Antibodies) or MAPKAPK2 (show MAPKAPK2 Antibodies)) 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 (show HIF1A Antibodies)
mRNA of HIF-2alpha (show EPAS1 Antibodies) and Ets-1 (show ETS1 Antibodies) were significantly increased by HIF-3alpha ablation. Both factors activate the VE-cadherin (show CDH5 Antibodies) gene, the transcriptional repression of these factors by HIF-3alpha is important for silencing the irrelevant expression of the VE-cadherin (show CDH5 Antibodies) gene.
our data indicated that Tnni2K175del mutation led to abnormally increased hif3a and decreased vegf (show VEGFA Antibodies) 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 (show HIF1A Antibodies) 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 (show ARNT Antibodies).
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