PTEN与肌管蛋白磷酸酶：从3-磷酸肌醇去磷酸化到疾病
PTEN and myotubularin phosphatases: from 3-phosphoinositide dephosphorylation to disease.
作者信息
Wishart Matthew J, Dixon Jack E
机构信息
Dept of Biological Chemistry, University of Michigan Medical School, Ann Arbor, MI 48109-0606, USA.
出版信息
Trends Cell Biol. 2002 Dec;12(12):579-85. doi: 10.1016/s0962-8924(02)02412-1.
The phosphatase and tensin homolog deleted on chromosome ten (PTEN) and myotubularin (MTM1) represent subfamilies of protein tyrosine phosphatases whose principal physiological substrates are D3-phosphorylated inositol phospholipids. As lipid phosphatases, PTEN- and MTM1-related (MTMR) proteins dephosphorylate the products of phosphoinositide 3-kinases and antagonize downstream effectors that utilize 3-phosphoinositides as ligands for protein targeting domains or allosteric activation. Here, we describe the cellular mechanisms of PTEN and MTMR function and their role in the etiology of cancer and other human diseases.
10号染色体缺失的磷酸酶及张力蛋白同源物（PTEN）和肌管素（MTM1）代表了蛋白质酪氨酸磷酸酶的亚家族，其主要生理底物是D3-磷酸化的肌醇磷脂。作为脂质磷酸酶，PTEN和MTM1相关（MTMR）蛋白使磷酸肌醇3激酶的产物去磷酸化，并拮抗利用3-磷酸肌醇作为蛋白质靶向结构域或变构激活配体的下游效应器。在此，我们描述了PTEN和MTMR功能的细胞机制及其在癌症和其他人类疾病病因学中的作用。
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