Proteins associated with hypoxia play roles in sensing and responding to low oxygen levels, ensuring cellular adaptation and survival under conditions of reduced oxygen supply. Aside from HIF, other proteins contribute to various aspects of this process, including oxygen sensing, energy metabolism, apoptosis, and angiogenesis. AMPK is a key energy sensor that becomes activated in response to the decreased cellular ATP levels occurring during hypoxia. Activated AMPK promotes multiple metabolic adjustments to conserve energy and enhance cellular survival. It stimulates glycolysis, fatty acid oxidation, and autophagy to maintain ATP production and adapt to hypoxic conditions. Hypoxia-Inducible Factor Prolyl Hydroxylases (PHDs), although not hypoxia proteins per se, play a crucial role in oxygen sensing. PHDs hydroxylate HIF-α subunits in the presence of oxygen, marking them for degradation under normoxic conditions. During hypoxia, PHD activity is reduced, leading to HIF stabilization and activation. In response to hypoxia, Pyruvate Dehydrogenase Kinase (PDK) is upregulated to inhibit pyruvate dehydrogenase, reducing glucose oxidation in mitochondria. This metabolic shift conserves oxygen by promoting glycolysis, which generates ATP without the need for oxygen. BNIP3 (BCL2/adenovirus E1B 19kDa interacting protein 3) is a pro-apoptotic protein that becomes upregulated in response to hypoxia. It induces selective mitophagy (mitochondrial autophagy) to eliminate damaged mitochondria, helping cells survive under low oxygen conditions. Hypoxia also triggers the upregulation of VEGF, a key regulator of angiogenesis (formation of new blood vessels). Increased VEGF expression promotes the growth of new blood vessels to improve oxygen delivery to hypoxic tissues. In response to hypoxia, kidney cells release erythropoietin (EPO), a hormone that stimulates the production of red blood cells in the bone marrow. This enhances the oxygen-carrying capacity of the blood, aiding in tissue oxygenation. Hypoxia can similarly increase the expression of glucose transporters (GLUTs), such as GLUT1, to enhance glucose uptake by cells, thus providing a source of glycolytic energy even in the absence of abundant oxygen. Under hypoxic conditions, the tumour suppressor protein p53 can also become activated. Whilst primarily known for its role in cell cycle regulation and apoptosis, p53 also contributes to hypoxia-induced adaptive responses, such as autophagy and metabolic adjustments. Other adaptive genes are also altered in the adaptive hypoxic response. For example, Nuclear Factor-Erythroid 2-Related Factor 2 (NRF2), a transcription factor that regulates antioxidant responses is induced. During hypoxia, NRF2 upregulates genes involved in antioxidant defence, thereby promoting cell survival in low oxygen conditions. Similarly, Heme Oxygenase-1 (HO-1), an enzyme that plays a key role in cellular defence against oxidative stress, is upregulated during hypoxia. HO-1 breaks down heme, releasing carbon monoxide (CO), biliverdin, and iron. HO-1 induction during hypoxia helps mitigate oxidative damage and has anti-inflammatory and cytoprotective effects. Carbonic Anhydrase IX (CAIX) CAIX, an enzyme that helps regulate pH, is similarly upregulated in response to hypoxia and contributes to acid-base balance. Finally, adenosine is a purine nucleoside that accumulates during hypoxia due to reduced ATP breakdown. It acts as a signalling molecule, promoting vasodilation, and increasing blood flow to oxygen-deprived tissues, enhancing oxygen delivery. We provide a wide product range of research reagents for investigating hypoxia associated proteins, including CD73 antibodies, Carbonic Anhydrase IX antibodies, ORP150 antibodies, Kir6.2 antibodies, and CD73 ELISA Kits. Explore our full hypoxia associated proteins product range below and discover more, for less.