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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). De plus, nous expédions HIF3A Kits (7) et HIF3A Protéines (4) et beaucoup plus de produits pour cette protéine.
Showing 10 out of 97 products:
Human Polyclonal HIF3A Primary Antibody pour ICC, IF - ABIN250964
Forooghian, Razavi, Timms: Hypoxia-inducible factor expression in human RPE cells. dans The British journal of ophthalmology 2007
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Human Polyclonal HIF3A Primary Antibody pour 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. dans Diagnostic microbiology and infectious disease 2006
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Human Polyclonal HIF3A Primary Antibody pour 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. dans Free radical biology & medicine 2012
Human Polyclonal HIF3A Primary Antibody pour 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. dans PLoS ONE 2013
Human Monoclonal HIF3A Primary Antibody pour 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. dans Experimental and therapeutic medicine 2016
Mouse (Murine) Polyclonal HIF3A Primary Antibody pour 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. dans Molecular and cellular biology 2006
AA can protect cardiomyocytes against hypoxia-induced apoptosis through regulating the miR (Montrer MLXIP Anticorps)-1290/HIF3A/HIF-1alpha (Montrer HIF1A Anticorps) axis, and miR (Montrer MLXIP Anticorps)-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 Anticorps)/HIF2alpha (Montrer EPAS1 Anticorps), VEGF (Montrer VEGFA Anticorps)/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 Anticorps) and Bcl2 (Montrer BCL2 Anticorps).
HIF3A methylation was found in the association between the HIF3A rs3826795 polymorphism and alanine aminotransferase (Montrer ALT Anticorps) among obese children.
TIMP2 (Montrer TIMP2 Anticorps) suppression, in a hypoxic environment, was induced through a regulatory feedback circuit consisting of hypoxia-inducible factor (HIF) 1 alpha (Montrer HIF1A Anticorps), microRNA-210 (miR (Montrer MLXIP Anticorps)-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 (Montrer HELLS Anticorps) in HIF3A shares moderate correlation between adipose tissue and blood, and both are associated with BMI. In contrast, methylation in FASN (Montrer FASN Anticorps) is poorly correlated across tissues, but the DNA methylation (Montrer HELLS Anticorps) 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 Anticorps) or Bcl-xL (Montrer BCL2L1 Anticorps), 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 Anticorps) sensitivity.
Parkin (Montrer PARK2 Anticorps) 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 Anticorps)-429 regulates the switch between HIF-1 (Montrer HIF1A Anticorps) adaptive responses to HIF-3 survival responses by rapidly decreasing HIF1A (Montrer HIF1A Anticorps) levels while simultaneously slowing the progression of HIF3A expression until the miR (Montrer MLXIP Anticorps)-429 levels drop below normoxic levels.
Phosphorylation of inhibitory PAS domain protein (IPAS) at Ser184 by MAPK-activated protein kinase 2 (MK2 (Montrer MAPKAPK2 Anticorps) or MAPKAPK2 (Montrer MAPKAPK2 Anticorps)) 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 Anticorps)
mRNA of HIF-2alpha (Montrer EPAS1 Anticorps) and Ets-1 (Montrer ETS1 Anticorps) were significantly increased by HIF-3alpha ablation. Both factors activate the VE-cadherin (Montrer CDH5 Anticorps) gene, the transcriptional repression of these factors by HIF-3alpha is important for silencing the irrelevant expression of the VE-cadherin (Montrer CDH5 Anticorps) gene.
our data indicated that Tnni2K175del mutation led to abnormally increased hif3a and decreased vegf (Montrer VEGFA Anticorps) 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 Anticorps) 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 Anticorps).
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
, hypoxia-inducible factor 3-alpha-like