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一般描述
Isocitrate dehydrogenase 1 (IDH1) gene is located on human chromosome 2q33. IDH1 is present in the cytoplasm and peroxisomes. It is expressed at high levels in the mammalian liver. IDH1 consists of a C-terminal tripeptide peroxisome, that targets the signal one sequence.
生化/生理作用
Isocitrate dehydrogenase 1 (IDH1) help in the oxidative carboxylation of isocitrate to α-ketoglutarate, that results in the formation of reduced nicotinamide adenine dinucleotide phosphate (NADPH). It participates in lipid metabolism and glucose sensing. Suppressing IDH1 in pancreatic islets affects the insulin secretion, induced by glucose and leads to increase in lactate production.
单位定义
One unit corresponds to the amount of enzyme which converts 1.0 μmol DL-isocitrate to α-ketoglutarate per minute at pH 7.4 and 37 °C (NADP as cofactor).
外形
Supplied as a lyophilized powder containing Tris-HCl pH 8.0, trehalose, ammonium sulfate and DTT
储存分类代码
11 - Combustible Solids
WGK
WGK 2
闪点(°F)
Not applicable
闪点(°C)
Not applicable
法规信息
常规特殊物品
历史批次信息供参考:
Isocitrate dehydrogenase 1 codon 132 mutation is an important prognostic biomarker in gliomas
Journal of Clinical Oncology, 27(25), 4150-4154 (2009)
Mast cell tryptase and carboxypeptidase A expression in body fluid and gastrointestinal tract associated with drug-related fatal anaphylaxis
World Journal of Gastroenterology, 21(47), 13288-13288 (2015)
American journal of hematology, 89(2), 137-144 (2013-10-12)
Current information about clinical significance of IDH mutations in myelodysplastic syndromes (MDS), their association with other genetic alterations and the stability during disease progression is limited. In this study, IDH mutations were identified in 4.6% of 477 patients with MDS
Neuro-oncology, 15(9), 1114-1126 (2013-07-24)
Isocitrate dehydrogenase (IDH) enzymes have recently become a focal point for research aimed at understanding the biology of glioma. IDH1 and IDH2 are mutated in 50%-80% of astrocytomas, oligodendrogliomas, oligoastrocytomas, and secondary glioblastomas but are seldom mutated in primary glioblastomas.
Blood, 123(14), 2157-2160 (2014-01-25)
The JAK1/JAK2 inhibitor ruxolitinib produced significant reductions in splenomegaly and symptomatic burden and improved survival in patients with myelofibrosis (MF), irrespective of their JAK2 mutation status, in 2 phase III studies against placebo (COMFORT-I) and best available therapy (COMFORT-II). We
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