Recombinant Mouse Hypoxia-Inducible Factor 1-Alpha (Hif1a), N-His

In mice, Hypoxia-Inducible Factor 1-Alpha (Hif1a) is a crucial transcription factor that plays a vital role in the cellular response to hypoxia. Under normal oxygen conditions, Hif1a is rapidly degraded, but in hypoxic conditions, it stabilizes and activates the expression of numerous genes related to angiogenesis, metabolic reprogramming, and cell survival. Hif1a is expressed in various mouse tissues, including the kidneys and heart, and is often overexpressed in many cancers. It forms the Hif1 transcription factor complex with Hif1β, regulating genes involved in angiogenesis, erythropoiesis, and metabolism. For example, Hif1a promotes the expression of vascular endothelial growth factor (VEGF), aiding in the formation of new blood vessels to improve tissue oxygen supply. Additionally, Hif1a is used in mouse models to study various diseases, such as ischemic diseases and cancers, and modulating its activity can influence cell metabolism and survival, offering potential therapeutic targets for related diseases. In mouse cartilage, Hif1a suppresses NF-κB signaling, exerting anti-catabolic effects and maintaining the integrity of articular cartilage. In diabetes research, Hif1a plays a significant role in β cell function, with reduced levels affecting β cell function and reserve, while increased levels can improve insulin secretion and glucose tolerance.