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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). Zusätzlich bieten wir Ihnen HIF3A Kits (5) und HIF3A Proteine (4) und viele weitere Produktgruppen zu diesem Protein an.
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Human Polyclonal HIF3A Primary Antibody für ICC, IF - ABIN250964
Forooghian, Razavi, Timms: Hypoxia-inducible factor expression in human RPE cells. in The British journal of ophthalmology 2007
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Mouse (Murine) Polyclonal HIF3A Primary Antibody für 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
Human Polyclonal HIF3A Primary Antibody für 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 Polyclonal HIF3A Primary Antibody für 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 für 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
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Human Monoclonal HIF3A Primary Antibody für 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
Report suggests that BV-2 microglial cells express HIF-3a under inflammatory conditions and that its activation differed from that of HIF-1a (zeige HIF1A Antikörper)
mRNA of HIF-2alpha (zeige EPAS1 Antikörper) and Ets-1 (zeige ETS1 Antikörper) were significantly increased by HIF-3alpha ablation. Both factors activate the VE-cadherin (zeige CDH5 Antikörper) gene, the transcriptional repression of these factors by HIF-3alpha is important for silencing the irrelevant expression of the VE-cadherin (zeige CDH5 Antikörper) gene.
our data indicated that Tnni2K175del mutation led to abnormally increased hif3a and decreased vegf 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 (zeige HIF1A Antikörper) 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 (zeige ARNT Antikörper).
HIF3A methylation was found in the association between the HIF3A rs3826795 polymorphism and alanine aminotransferase (zeige ALT Antikörper) among obese children.
TIMP2 (zeige TIMP2 Antikörper) suppression, in a hypoxic environment, was induced through a regulatory feedback circuit consisting of hypoxia-inducible factor (HIF) 1 alpha (zeige HIF1A Antikörper), microRNA-210 (miR (zeige MLXIP Antikörper)-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 (zeige HELLS Antikörper) in HIF3A shares moderate correlation between adipose tissue and blood, and both are associated with BMI. In contrast, methylation in FASN (zeige FASN Antikörper) is poorly correlated across tissues, but the DNA methylation (zeige HELLS Antikörper) in adipose tissue but not blood is highly associated with BMI
Reduced lifetimes of the donor were partially restored by coexpression of HIF-1alpha (zeige HIF1A Antikörper) or Bcl-xL (zeige BCL2L1 Antikörper), 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 (zeige INS Antikörper) sensitivity.
Parkin (zeige PARK2 Antikörper) 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 (zeige MLXIP Antikörper)-429 regulates the switch between HIF-1 (zeige HIF1A Antikörper) adaptive responses to HIF-3 survival responses by rapidly decreasing HIF1A (zeige HIF1A Antikörper) levels while simultaneously slowing the progression of HIF3A expression until the miR (zeige MLXIP Antikörper)-429 levels drop below normoxic levels.
The association between increased DNA methylation (zeige HELLS Antikörper) at HIF3A and increased adiposity is present in neonates.
HIF3A DNA Methylation Is Associated with Childhood Obesity and ALT
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.
hypoxia inducible factor 3, alpha subunit
, hypoxia-inducible factor 3 alpha subunit
, hypoxia-inducible factor 3-alpha
, hypoxia-inducible factor-3 alpha
, hypoxia-inducible factor 3-alpha-like
, basic-helix-loop-helix-PAS protein MOP7
, hypoxia inducible factor three alpha
, inhibitory PAS domain protein
, member of PAS protein 7
, neonatal and embryonic PAS
, HIF-3 alpha
, HIF3 alpha 1
, hypoxia inducible factor 3 alpha
, hypoxia inducible factor 3a
, hypoxia-inducible factor 3 alpha
, PAS domain-containing protein 7
, class E basic helix-loop-helix protein 17