ELISA/assay

Mouse Hypoxia-inducible factor 1-alpha ELISA Kit

MBS2881121

48-Strip-Wells

355 USD

ELISA Kit

Mouse Hypoxia-inducible factor 1-alpha ELISA Kit

[Hypoxia-inducible factor 1-alpha]

[Hypoxia-inducible factor 1-alpha; HIF-1-alpha; HIF1-alpha; ARNT-interacting protein; Hif1a]

[hypoxia-inducible factor 1-alpha isoform 1; Hypoxia-inducible factor 1-alpha; hypoxia-inducible factor 1-alpha; hypoxia inducible factor 1, alpha subunit; ARNT-interacting protein]

[Hif1a]

[Hif1a; Hif1a; MOP1; bHLHe78; AA959795; HIF1alpha; HIF1-alpha; HIF-1-alpha; HIF-1-alpha; HIF1-alpha]

HIF1A_MOUSE

Mouse

837

Recombinant and natural Pig Heat shock 70 kDa protein 6

For long term storage, please store the entire kit at -20 degree C.

Typical Testing Data/Standard Curve (for reference only)

Samples: Serum, Plasma, Tissue Homogenates, Cell Culture Supernates Or Other Biological Fluids. Detection Range: 31.2 pg/mL-2000 pg/mL. Sensitivity: <7.7 pg/mL

Intra-assay Precision: Intra-Assay CV: <=5.6%. Inter-assay Precision: Inter-Assay CV: <=9.4%

Intended Uses: This immunoassay kit allows for the in vitro quantitative determination of target antigen concentrations in serum, plasma, tissue homogenates, cell culture supernates or other biological fluids. Principle of the Assay: The microtiter plate provided in this kit has been pre-coated with an antibody specific to target antigen. Standards or samples are then added to the appropriate microtiter plate wells with a biotin-conjugated antibody preparation specific for target antigen and then avidin conjugated to Horseradish Peroxidase (HRP) is added to each microplate well and incubated. Then a TMB substrate solution is added to each well. Only those wells that contain target antigen, biotin-conjugated antibody and enzyme-conjugated Avidin will exhibit a change in color. The enzyme-substrate reaction is terminated by the addition of a sulphuric acid solution and the color change is measured spectrophotometrically at a wavelength of 450 nm +/- 2 nm. The concentration of target antigen in the samples is then determined by comparing the O.D. of the samples to the standard curve.

927028881

NP_001300848.1

NM_001313919.1

Q61221

91,874 Da

Adipogenesis Pathway (198299); Cellular Response To Hypoxia Pathway (1324507); Cellular Responses To Stress Pathway (1324506); Central Carbon Metabolism In Cancer Pathway (1060315); Central Carbon Metabolism In Cancer Pathway (1084231); Choline Metabolism In Cancer Pathway (1060314); Choline Metabolism In Cancer Pathway (1084232); HIF-1 Signaling Pathway (695223); Oxygen-dependent Asparagine Hydroxylation Of Hypoxia-inducible Factor Alpha Pathway (1324509); Oxygen-dependent Proline Hydroxylation Of Hypoxia-inducible Factor Alpha Pathway (1324510)

This gene encodes the alpha subunit which, along with the beta subunit, forms a heterodimeric transcription factor that regulates the cellular and developmental response to reduced oxygen tension. The transcription factor has been shown to regulate genes involved in several biological processes, including erythropoiesis and angiogenesis which aid in increased delivery of oxygen to hypoxic regions. The transcription factor also plays a role in the induction of genes involved in cell proliferation and survival, energy metabolism, apoptosis, and glucose and iron metabolism. Alternative splicing results in multiple transcript variants encoding different isoforms. [provided by RefSeq, Sep 2015]

HIF1A: a master transcriptional regulator of the adaptive response to hypoxia. Under hypoxic conditions, activates the transcription of over 40 genes, including erythropoietin, glucose transporters, glycolytic enzymes, vascular endothelial growth factor, HILPDA, and other genes whose protein products increase oxygen delivery or facilitate metabolic adaptation to hypoxia. Plays an essential role in embryonic vascularization, tumor angiogenesis and pathophysiology of ischemic disease. Binds to core DNA sequence 5'-[AG]CGTG-3' within the hypoxia response element (HRE) of target gene promoters. Activation requires recruitment of transcriptional coactivators such as CREBPB and EP300. Activity is enhanced by interaction with both, NCOA1 or NCOA2. Interaction with redox regulatory protein APEX seems to activate CTAD and potentiates activation by NCOA1 and CREBBP. Involved in the axonal distribution and transport of mitochondria in neurons during hypoxia. Interacts with the HIF1A beta/ARNT subunit; heterodimerization is required for DNA binding. Interacts with COPS5; the interaction increases the transcriptional activity of HIF1A through increased stability. Interacts with EP300 (via TAZ-type 1 domains); the interaction is stimulated in response to hypoxia and inhibited by CITED2. Interacts with CREBBP (via TAZ-type 1 domains). Interacts with NCOA1, NCOA2, APEX and HSP90. Interacts (hydroxylated within the ODD domain) with VHLL (via beta domain); the interaction, leads to polyubiquitination and subsequent HIF1A proteasomal degradation. During hypoxia, sumoylated HIF1A also binds VHL; the interaction promotes the ubiquitination of HIF1A. Interacts with SENP1; the interaction desumoylates HIF1A resulting in stabilization and activation of transcription. Interacts (Via the ODD domain) with ARD1A; the interaction appears not to acetylate HIF1A nor have any affect on protein stability, during hypoxia. Interacts with RWDD3; the interaction enhances HIF1A sumoylation. Interacts with TSGA10. Interacts with RORA (via the DNA binding domain); the interaction enhances HIF1A transcription under hypoxia through increasing protein stability. Interaction with PSMA7 inhibits the transactivation activity of HIF1A under both normoxic and hypoxia- mimicking conditions. Interacts with USP20. Interacts with RACK1; promotes HIF1A ubiquitination and proteasome- mediated degradation. Interacts (via N-terminus) with USP19. Under reduced oxygen tension. Induced also by various receptor-mediated factors such as growth factors, cytokines, and circulatory factors such as PDGF, EGF, FGF2, IGF2, TGFB1, HGF, TNF, IL1B, angiotensin-2 and thrombin. However, this induction is less intense than that stimulated by hypoxia. Repressed by HIPK2 and LIMD1. Expressed in most tissues with highest levels in kidney and heart. Overexpressed in the majority of common human cancers and their metastases, due to the presence of intratumoral hypoxia and as a result of mutations in genes encoding oncoproteins and tumor suppressors. 2 isoforms of the human protein are produced by alternative splicing. Protein type: Transcription factor; DNA-binding; Autophagy. Cellular Component: cytoplasm; cytosol; nuclear speck; nucleus; transcription factor complex. Molecular Function: DNA binding; enzyme binding; histone acetyltransferase binding; histone deacetylase binding; Hsp90 protein binding; nuclear hormone receptor binding; protein binding; protein complex binding; protein dimerization activity; protein heterodimerization activity; protein kinase binding; RNA polymerase II transcription factor activity, enhancer binding; sequence-specific DNA binding; transcription factor activity; transcription factor binding; ubiquitin protein ligase binding. Biological Process: angiogenesis; axon transport of mitochondrion; B-1 B cell homeostasis; blood vessel development; blood vessel morphogenesis; camera-type eye morphogenesis; cartilage development; cell differentiation; cellular iron ion homeostasis; cerebral cortex development; collagen metabolic process; connective tissue replacement during inflammatory response; digestive tract morphogenesis; elastin metabolic process; embryonic hemopoiesis; embryonic placenta development; epithelial to mesenchymal transition; glucose homeostasis; heart looping; hemoglobin biosynthetic process; lactate metabolic process; lactation; muscle maintenance; negative regulation of apoptosis; negative regulation of bone mineralization; negative regulation of growth; negative regulation of neuron apoptosis; negative regulation of ossification; negative regulation of TOR signaling pathway; negative regulation of transcription from RNA polymerase II promoter; negative regulation of vasoconstriction; neural crest cell migration; neural fold elevation formation; oxygen homeostasis; positive regulation of apoptosis; positive regulation of autophagy; positive regulation of cell proliferation; positive regulation of erythrocyte differentiation; positive regulation of gluconeogenesis; positive regulation of hormone biosynthetic process; positive regulation of macroautophagy; positive regulation of neuroblast proliferation; positive regulation of smooth muscle cell proliferation; positive regulation of transcription from RNA polymerase II promoter; positive regulation of transcription, DNA-dependent; positive regulation of vascular endothelial growth factor receptor signaling pathway; regulation of catalytic activity; regulation of cell proliferation; regulation of gene expression; regulation of glycolysis; regulation of transcription from RNA polymerase II promoter in response to oxidative stress; regulation of transcription, DNA-dependent; regulation of transforming growth factor-beta2 production; response to hypoxia; response to muscle activity; signal transduction; transcription, DNA-dependent; vasculature development; visual learning

48-Strip-Wells

355 USD

96-Strip-Wells

475

5x96-Strip-Wells

2030

10x96-Strip-Wells

3700