Anti-HIF-1 alpha Polyclonal Antibody is a Rabbit antibody targeting HIF-1 alpha. Anti-HIF-1 alpha Polyclonal Antibody can be used in FCM,ICC/IF.

IgG

Human (predicted:Mouse,Rat,Chicken,Pig)

1. The HepG2 (H) (treated with 500uM CoCl2 for 6 hours) cells were fixed with 4% PFA (10 min at room temperature) and then permeabilized with 90% ice-cold methanol for 20 min at-20°C,the cells then were incubated in 5% BSA to block non-specific protein-protein interactions (30 min at room temperature). Primary Antibody (green): Rabbit Anti-HIF-1 Alpha antibody (TMAB-00855): 1 μg/10^6 cells; Secondary Antibody (white blue): Goat anti-Rabbit IgG-FITC: 1 μg/test. Isotype Control (orange): Rabbit IgG. Blank control (black): PBS.
2. 4% Paraformaldehyde-fixed HepG2 (treated with 500uM CoCl2 for 6 hours)(H) cell; Triton X-100 at RT for 20 min; Antibody incubation with (HIF-1 Alpha) polyclonal Antibody, unconjugated (TMAB-00855) 1:100, 90 min at 37°C; followed by conjugated Goat Anti-Rabbit IgG antibody (green) at 37°C for 90 min, DAPI (blue) was used to stain the cell nucleus. PBS instead of the primary antibody was used as the blank control.

ICC/IF: 1:50-200; FCM: 1μg/Test

Polyclonal

KLH conjugated synthetic peptide: middle of human HIF-1 Alpha

Human

HIF1A

Hypoxia-inducible factor 1-alpha

HIF,Hydroxylases,HIF,Jumonji containing proteins,Methylation

Functions as a master transcriptional regulator of theadaptive response to hypoxia. Under hypoxic conditions activatesthe transcription of over 40 genes, including, erythropoietin,glucose transporters, glycolytic enzymes, vascular endothelialgrowth factor, and other genes whose protein products increaseoxygen delivery or facilitate metabolic adaptation to hypoxia.Plays an essential role in embryonic vascularization, tumorangiogenesis and pathophysiology of ischemic disease. Binds to coreDNA sequence 5'-[AG]CGTG-3' within the hypoxia response element(HRE) of target gene promoters. Activation requires recruitment oftranscriptional coactivators such as CREBPB and EP300. Activity isenhanced by interaction with both, NCOA1 or NCOA2. Interaction withredox regulatory protein APEX seems to activate CTAD andpotentiates activation by NCOA1 and CREBBP.