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We report right here activation of PP2A in typical rat islands and insulin-secreting INS-1 832/13 cells under the discomfort of hyperglycemic problems. Small conflicting RNA-mediated knockdown of the catalytic subunit of PP2A noticeably undermined glucose-induced activation of PP2A. HG, however not nonmetabolizable 3-O-methyl glucose or mannitol, considerably promoted the methylation of PP2Ac at its C-terminal Leu-309, recommending a novel function for this posttranslational adjustment in glucose-induced activation of PP2A. Furthermore, knockdown of the cytosolic leucine carboxymethyl transferase 1, which carboxymethylates PP2Ac, substantially undermined PP2A activation under HG conditions. In addition, HG problems considerably increased the expression of B55α, a regulatory subunit of PP2A, which has been linked in islet disorder under conditions of oxidative anxiety and diabetic issues. Based on these findings, we conclude that exposure of the island β-cell to HG causes accelerated PP2A signaling pathway, causing loss in glucose-induced insulin secretion.
Source link: https://doi.org/10.1210/en.2013-1773
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