HIF1A Monoclonal Antibody (mgc3), Invitrogen™

Description

MA1-516 detects hypoxia-inducible factor 1 alpha (HIF-1 alpha) from human, non-human primate, bovine, mouse and porcine cells. This antibody does not cross-react with ARNT or the related HIF-2 alpha. MA1-516 has been successfully used in Western blot, immunofluorescence, immunoprecipitation, immunocytochemistry, and gel shift procedures. By Western blot, this antibody detects an ∽116 kDa protein representing HIF-1 alpha after hypoxic induction in COS cells. Immunofluorescence staining of HIF-1 alpha in COS-7 cells with MA1-516 yields nuclear staining after exposing cells to 1% oxygen for 4 hours. In gel shift assays, MA1-516 has been successfully used only with mouse HIF-1 alpha. Antibodies to this protein (and modification) were previously sold as part of a Thermo Scientific Cellomics High Content Screening Kit. This replacement antibody is now recommended for researchers who need an antibody for high content cell based assays. It has been thoroughly tested and validated for cellular immunofluorescence (IF) applications. Further optimization including the selection of the most appropriate fluorescent Dylight conjugated secondary antibody may have to be performed for your high content assay.

HIF1-alpha (HIF1A) is a subunit of HIF1, which is a transcription factor found in mammalian cells cultured under reduced oxygen tension. HIF-1 is a heterodimer consisting of an alpha and beta subunit, both belonging to the basic-helix-loop-helix Per-aryl hydrocarbon receptor nuclear translocator-Sim (PAS) family of transcription factors. HIF1 functions as a transcriptional regulator of the adaptive response to hypoxia. Under hypoxic conditions, HIF-1 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. HIF1-alpha regulates hypoxia-mediated apoptosis, cell proliferation and tumor angiogenesis. Hypoxia which induces p53 protein accumulation, directly interacts with HIF1-alpha and reduces hypoxia-induced expression of HIF1-alpha by promoting MDM2-mediated ubiquitination and proteasomal degradation under hypoxic conditions. Recent studies suggest that induction of NOX4 by HIF1-alpha contributes to maintain ROS levels after hypoxia and hypoxia-induced proliferation. In humans, it is located on the q arm of chromosome 14. The C-terminal of HIF1A binds to p300. p300/CBP-HIF complexes participate in the induction of hypoxia-responsive genes, including VEGF. Hypoxia contributes significantly to the pathophysiology of major categories of human disease, including myocardial and cerebral ischemia, cancer, pulmonary hypertension, congenital heart disease and chronic obstructive pulmonary disease.