Insulin-induced Effects on the Subcellular Localization of AKT1, AKT2 and AS160 in Rat Skeletal Muscle.
Insulin-induced Effects on the Subcellular Localization of AKT1, AKT2 and AS160 in Rat Skeletal Muscle.
复制标题
胰岛素诱导的对大鼠骨骼肌Akt1，Akt2和AS160亚细胞定位的影响。
DOI：
10.1038/srep39230
复制
发表时间：
2016-12-14
影响因子：
4.6
通讯作者：
Cartee GD
中科院分区：
文献类型：
--
作者：
Zheng X;Cartee GD
AKT1 and AKT2, the AKT isoforms that are highly expressed in skeletal muscle, have distinct and overlapping functions, with AKT2 more important for insulin-stimulated glucose metabolism. In adipocytes, AKT2 versus AKT1 has greater susceptibility for insulin-mediated redistribution from cytosolic to membrane localization, and insulin also causes subcellular redistribution of AKT Substrate of 160 kDa (AS160), an AKT2 substrate and crucial mediator of insulin-stimulated glucose transport. Although skeletal muscle is the major tissue for insulin-mediated glucose disposal, little is known about AKT1, AKT2 or AS160 subcellular localization in skeletal muscle. The major aim of this study was to determine insulin’s effects on the subcellular localization and phosphorylation of AKT1, AKT2 and AS160 in skeletal muscle. Rat skeletal muscles were incubated ex vivo ± insulin, and differential centrifugation was used to isolate cytosolic and membrane fractions. The results revealed that: 1) insulin increased muscle membrane localization of AKT2, but not AKT1; 2) insulin increased AKT2 phosphorylation in the cytosol and membrane fractions; 3) insulin increased AS160 localization to the cytosol and membranes; and 4) insulin increased AS160 phosphorylation in the cytosol, but not membranes. These results demonstrate distinctive insulin effects on the subcellular redistribution of AKT2 and its substrate AS160 in skeletal muscle.
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影响因子：
4.8
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Kane, S;Sano, H;Lienhard, GE
通讯作者：
Lienhard, GE
影响因子：
4.8
作者：
Sasaoka, T;Wada, T;Kobayashi, M
通讯作者：
Kobayashi, M
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通讯作者：
Ramm, Georg
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通讯作者：
Albiston, Anthony L.
影响因子：
29
作者：
Chen S;Wasserman DH;MacKintosh C;Sakamoto K
通讯作者：
Sakamoto K