缺氧诱导因子（HIF）调节对缺氧的反应，并且由两个亚基α和β组成。当细胞暴露于缺氧条件下时，HIF复合物（α和β亚基）被稳定并与DNA转录激活基因结合，这些基因与血管生成和葡萄糖代谢的细胞过程相关1。在正常条件下，HIF-α亚基被HIF-α脯氨酰羟化酶（HIF-PH）羟基化，导致HIF-α的泛素化和随后的破坏2。DMOG（二甲基草酰甘氨酸）是HIF-α脯氨酰羟化酶（HIF-PH）的细胞渗透性竞争性抑制剂，在0.1和1 mM 3之间的浓度下导致HIF的稳定和随后的血管生成和葡萄糖代谢。 K. Kondo等人（2001年）。“HIF α靶向VHL介导的破坏脯氨酸羟基化：对O2传感的影响。科学292（5516）：464-8.2）Jaakkola P. D。R. Mole等人（2001年）。“通过O2调节的脯氨酰羟基化将HIF-α靶向von Hippel-Lindau泛素化复合物。“科学292（5516）：468-72.3）康明斯E。P. F. Seeballuck等人（2008年）。“羟化酶抑制剂二甲基草酰甘氨酸在结肠炎小鼠模型中具有保护作用。“Gastroenterology 134（1）：156-65.4）Glassford A. J. P. Yue等人（2007年）。“HIF-1调节脂肪细胞中缺氧和胰岛素诱导的apelin表达。“美国生理学内分泌代谢杂志293（6）：E1590-6。
产品描述
Hypoxia Inducible Factor (HIF) regulates responses to hypoxia and is comprised of two subunits alpha and beta. Upon cellular exposure to hypoxic conditions the HIF complex (alpha and beta subunits) is stabilized and binds to DNA transcriptionally activating genes linked to the cellular processes of angiogenesis and glucose metabolism1. Under normal conditions the HIF-alpha subunit is hydroxylated by the enzyme HIF-alpha prolyl hydroxylase (HIF-PH) leading to ubiquitylation of HIF-alpha and subsequent destruction2. DMOG (dimethyloxalylglycine) is a cell permeable competitive inhibitor of HIF-alpha prolyl hydroxylase (HIF-PH) leading to the stabilization of HIF and subsequent angiogenesis and glucose metabolism at concentrations between 0.1 and 1 mM3 4References1) Ivan M. K. Kondo et al. (2001). "HIFalpha targeted for VHL-mediated destruction by proline hydroxylation: implications for O2 sensing." Science 292(5516): 464-8.2) Jaakkola P. D. R. Mole et al. (2001). "Targeting of HIF-alpha to the von Hippel-Lindau ubiquitylation complex by O2-regulated prolyl hydroxylation." Science 292(5516): 468-72.3) Cummins E. P. F. Seeballuck et al. (2008). "The hydroxylase inhibitor dimethyloxalylglycine is protective in a murine model of colitis." Gastroenterology 134(1): 156-65.4) Glassford A. J. P. Yue et al. (2007). "HIF-1 regulates hypoxia- and insulin-induced expression of apelin in adipocytes." Am J Physiol Endocrinol Metab 293(6): E1590-6.
