HIF3A Antibody, HRP conjugated
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Description
Introduction to HIF3A and Its Antibody
Hypoxia-Inducible Factor 3 Alpha (HIF3A) is a transcriptional regulator involved in cellular responses to hypoxia, playing roles in angiogenesis, metabolism, and apoptosis . The HIF3A Antibody, HRP conjugated is a rabbit polyclonal antibody designed to detect HIF3A protein, conjugated with horseradish peroxidase (HRP) for enzymatic detection in assays like ELISA. This conjugation enables colorimetric or chemiluminescent detection of antigen-antibody complexes, enhancing sensitivity in quantitative analyses .
Molecular Weight and Detection
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Observed Molecular Weight: ~72 kDa in western blotting , consistent with the calculated molecular weight of HIF3A isoforms .
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Conjugate Function: HRP catalyzes the oxidation of substrates (e.g., TMB) to produce a colored product, enabling quantification in ELISA .
Cross-Reactivity and Specificity
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Potential Cross-Reactivity: Limited to species with high sequence homology (e.g., mouse or rat in other antibody variants) , but not confirmed for this HRP-conjugated product .
Recommended Dilutions
Research Validation
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Hypoxia-Induced Regulation: Studies using HIF3A antibodies (e.g., in western blotting) demonstrate that HIF3A mRNA and protein levels fluctuate under hypoxic conditions. For instance, HIF3A mRNA transiently decreases at 4 hours of hypoxia before rebounding .
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Cancer Research: HIF3A overexpression correlates with oncogenic phenotypes, including metastasis and radioresistance. Antibodies targeting HIF3A have been used to study its role in cervical cancer progression .
Key Studies
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Hypoxia-Dependent Expression
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Role in Cancer
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miRNA Regulation
Product Specs
Buffer
Preservative: 0.03% Proclin 300
Constituents: 50% Glycerol, 0.01M PBS, pH 7.4
Constituents: 50% Glycerol, 0.01M PBS, pH 7.4
Form
Liquid
Lead Time
Typically, we can ship the products within 1-3 business days after receiving your order. The delivery time may vary depending on the order method or location. For specific delivery times, please consult your local distributors.
Synonyms
Basic-helix-loop-helix-PAS protein MOP7 antibody; bHLHe17 antibody; Class E basic helix-loop-helix protein 17 antibody; HIF 3A antibody; HIF 3A4 antibody; HIF-3-alpha antibody; HIF3 alpha antibody; HIF3-alpha antibody; HIF3-alpha-1 antibody; HIF3A antibody; HIF3A_HUMAN antibody; Hypoxia Inducible Factor 3 alpha antibody; Hypoxia inducible factor 3 alpha subunit antibody; Hypoxia inducible factor three alpha antibody; Hypoxia-inducible factor 3-alpha antibody; Inhibitory PAS domain protein antibody; IPAS antibody; Member of PAS protein 7 antibody; MOP7 antibody; PAS domain-containing protein 7 antibody; PASD7 antibody
Target Names
HIF3A
Uniprot No.
Target Background
Function
HIF3A acts as a transcriptional regulator in the adaptive response to low oxygen tension. It functions as a regulator of hypoxia-inducible gene expression, inhibiting angiogenesis in hypoxic corneal cells. It plays a role in the development of the cardiorespiratory system and may also be involved in apoptosis.
HIF3A attenuates the ability of transcription factor HIF1A to bind to hypoxia-responsive elements (HRE) within the enhancer/promoter of hypoxia-inducible target genes, thereby inhibiting HRE-driven transcriptional activation. It also inhibits hypoxia-inducible ARNT-mediated gene expression.
HIF3A attenuates the ability of transcription factors HIF1A and EPAS1/HIF2A to bind to hypoxia-responsive elements (HRE) within the enhancer/promoter of hypoxia-inducible target genes, thus inhibiting HRE-driven transcriptional activation. It may act as a tumor suppressor and inhibit malignant cell transformation.
HIF3A attenuates the ability of transcription factor HIF1A to bind to hypoxia-responsive elements (HRE) located within the enhancer/promoter of hypoxia-inducible target genes, consequently inhibiting HRE-driven transcriptional activation.
HIF3A attenuates the ability of transcription factor HIF1A to bind to hypoxia-responsive elements (HRE) within the enhancer/promoter of hypoxia-inducible target genes, thereby inhibiting HRE-driven transcriptional activation. It also inhibits hypoxia-inducible ARNT-mediated gene expression.
HIF3A attenuates the ability of transcription factors HIF1A and EPAS1/HIF2A to bind to hypoxia-responsive elements (HRE) within the enhancer/promoter of hypoxia-inducible target genes, thus inhibiting HRE-driven transcriptional activation. It may act as a tumor suppressor and inhibit malignant cell transformation.
HIF3A attenuates the ability of transcription factor HIF1A to bind to hypoxia-responsive elements (HRE) located within the enhancer/promoter of hypoxia-inducible target genes, consequently inhibiting HRE-driven transcriptional activation.
Gene References Into Functions
- Data suggest an important role of miR-210 in sustaining HIF-1alpha activity via the suppression of HIF-3alpha, regulating cell growth and chemotherapeutic drug resistance in cholangiocarcinoma. PMID: 29953500
- AA can protect cardiomyocytes against hypoxia-induced apoptosis through regulating the miR-1290/HIF3A/HIF-1alpha axis. miR-1290 may be a potential target in the prevention of myocardial ischemia-reperfusion injury. PMID: 28686797
- NAP peptide prevents outer blood retinal barrier breakdown by reducing HIF1alpha/HIF2alpha, VEGF/VEGFRs, and increasing HIF3alpha expression. Additionally, it can reduce the percentage of apoptotic cells by modulating the expression of two death-related genes, BAX and Bcl2. PMID: 28436035
- HIF3A methylation was found in the association between the HIF3A rs3826795 polymorphism and alanine aminotransferase among obese children. PMID: 28754107
- TIMP2 suppression, in a hypoxic environment, was induced through a regulatory feedback circuit consisting of hypoxia-inducible factor (HIF) 1 alpha, microRNA-210 (miR-210), and HIF-3alpha. PMID: 27018975
- Results were discordant with those expected if HIF3A methylation has a causal effect on body mass index (BMI) and 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 and HIF3A methylation. PMID: 26861784
- 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. PMID: 26891033
- Reduced lifetimes of the donor were partially restored by coexpression of HIF-1alpha or Bcl-xL, binding proteins of IPAS in the nucleus and mitochondria, respectively. PMID: 28003430
- 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 sensitivity. PMID: 27594926
- Parkin is downregulated under hypoxia and that it interferes with HIF expression based on cellular oxygen tension. PMID: 26742768
- miR210 may be a negative regulator of the progression of osteoarthritis, which increases chondrocyte proliferation and prompts extracellular matrix deposition by directly targeting HIF3alpha. PMID: 26861791
- This provides a compelling model for how hypoxia-induced miR-429 regulates the switch between HIF-1 adaptive responses to HIF-3 survival responses by rapidly decreasing HIF1A levels while simultaneously slowing the progression of HIF3A expression until the miR-429 levels drop below normoxic levels. PMID: 26954587
- The association between increased DNA methylation at HIF3A and increased adiposity is present in neonates. PMID: 26011824
- Unsaturated fatty acids are high-affinity ligands of the C-terminal domain from the HIF-3alpha. PMID: 26237540
- HIF3A DNA Methylation Is Associated with Childhood Obesity and ALT. PMID: 26717317
- HIF3alpha has a transcriptional regulatory function, which negatively affects gene expression by competing with HIF1alpha and HIF2alpha in binding to transcriptional elements in target genes during hypoxia. (Review) PMID: 25936862
- Inverse association with hypertrophic markers in chondrogenic cells. PMID: 26174816
- A DNA methylation variant in HIF3A was associated with BMI changes through interactions with total or supplemental vitamin B2, vitamin B12, and folate. PMID: 26001398
- Here we provide evidence for the miRNA-mediated regulation of HIF3a by hypoxia-responsive miRNAs in STS, which may help to tightly regulate and fine-tune the hypoxic response. PMID: 24927770
- The Inhibitory Per/Arnt/Sim (PAS) domain protein (IPAS) is a splice variant of hypoxia-inducible factor (HIF)-3alpha, and possesses two entirely different functions. The results strongly suggest that IPAS is a nucleocytoplasmic shuttling protein. PMID: 24092767
- These findings highlight the importance of the hypoxia-sensing pathway and HIFs in clinical hematology. PMID: 24371328
- Were significantly upregulated in the HIF3alpha expressing lungs. PMID: 23451260
- The transcription of HIF-3alpha4 was silenced by the promoter DNA methylation in meningiomas, and inducible HIF-3alpha4 impaired angiogenesis, proliferation, and metabolism/oxidation in hypervascular meningiomas. PMID: 23485455
- Data indicate that the HIF-3alpha variants may have more versatile and specific roles in the regulation of the hypoxia response than previously anticipated. PMID: 21479871
- Cell-specific and hypoxia-dependent regulation of human HIF-3alpha. PMID: 21069422
- It is a negative regulator of tumorigenesis. (review) PMID: 21404626
- HIF3A is regulated by hypoxia in the developing human lung. PMID: 20551700
- Hypoxia upregulated transcription from all three alternative HIF-3alpha promoters. siRNA experiments showed that this induction is mediated specifically by HIF-1 and not by HIF-2. PMID: 20416395
- Multiple splice variants of the locus are targets of the von Hippel-Lindau E3 ubiquitin ligase complex. PMID: 12538644
- IPAS1 and IPAS2 inhibit angiogenesis by binding to and inhibiting HIF-1alpha and HIF-1beta. PMID: 16182248
- Findings suggest that HIF-3alpha, as a member of the HIF system, is complementary rather than redundant to HIF-1alpha induction in protection against hypoxic damage in alveolar epithelial cells. PMID: 16775626
- The expression of HIF-3alpha4 suppresses the growth of tumor xenografts in SCID mice. PMID: 17998805
- The findings shed light on a novel aspect of HIF-3alpha as a HIF-1 target gene and point to a possible role as a modulator of hypoxic gene induction. PMID: 19694616
- The splice isoform HIF-3alpha4 inhibits transcription of VEGF and GLUT1 by binding to and inhibiting HIF-1alpha and HIF-1beta. PMID: 16126907
Database Links
Subcellular Location
Nucleus. Cytoplasm. Nucleus speckle. Mitochondrion.
Tissue Specificity
Expressed in vascular cells (at protein level). Expressed in kidney. Expressed in lung epithelial cells. Expressed in endothelial cells (venous and arterial cells from umbilical cord and aortic endothelial cells) and in vascular smooth muscle cells (aorta
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