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From Full Text: We have recently demonstrated that 11 other poorly studied protein kinases that belong to the AMPK subfamily (NUAK1, NUAK2, BRSK1, BRSK2, QSK, SIK, QIK, MARK1, MARK2, MARK3, MARK4), are activated in vitro following phosphorylation of their T-loop threonine residues by LKB1 (16). We have also developed assays to measure the activities of the endogenous AMPK-related kinases and found that the activities of these enzymes are markedly reduced in LKB1-deficient fibroblasts or HeLa cells (16). These results imply that LKB1 functions as a master \"upstream\" protein kinase, regulating the activities of AMPK and the AMPK-related kinases. LKB1 and AMPK-related kinase activities have thus far been studied only in cultured cell lines and not in tissues of relevance to diabetes. Because the beneficial effects of exercise and metformin for type 2 diabetes are thought to be at least partly mediated through activation of AMPK, we sought to determine whether LKB1 and AMPK-related kinases are also regulated by muscle contraction and/or phenformin in rat skeletal muscles.
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2014-07-03T14:30:22.355+02:00
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