缺氧誘導因子（HIF）調節對缺氧的反應，并且由兩個亞基α和β組成。當細胞暴露于缺氧條件下時，HIF復合物（α和β亞基）被穩定并與DNA轉錄激活基因結合，這些基因與血管生成和葡萄糖代謝的細胞過程相關1。在正常條件下，HIF-α亞基被HIF-α脯氨酰羥化酶（HIF-PH）羥基化，導致HIF-α的泛素化和隨后的破壞2。DMOG（二甲基草酰甘氨酸）是HIF-α脯氨酰羥化酶（HIF-PH）的細胞滲透性競爭性抑制劑，在0.1和1 mM 3之間的濃度下導致HIF的穩定和隨后的血管生成和葡萄糖代謝。 K. Kondo等人（2001年）?！癏IF α靶向VHL介導的破壞脯氨酸羥基化：對O2傳感的影響?？茖W292（5516）：464-8.2）Jaakkola P. D。R. Mole等人（2001年）。“通過O2調節的脯氨酰羥基化將HIF-α靶向von Hippel-Lindau泛素化復合物?！翱茖W292（5516）：468-72.3）康明斯E。P. F. Seeballuck等人（2008年）。“羥化酶抑制劑二甲基草酰甘氨酸在結腸炎小鼠模型中具有保護作用?！癎astroenterology 134（1）：156-65.4）Glassford A. J. P. Yue等人（2007年）。“HIF-1調節脂肪細胞中缺氧和胰島素誘導的apelin表達?！懊绹韺W內分泌代謝雜志293（6）：E1590-6。
產品描述
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.
