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• W1993460435 abstract "The Cdk4–pRb–E2F1 pathway is shown to have a role in insulin secretion in b cells by controlling the expression of a subunit of the K+ATP channel through E2F1 binding to its promoter. CDK4–pRB–E2F1 cell-cycle regulators are robustly expressed in non-proliferating β cells, suggesting that besides the control of β-cell number the CDK4–pRB–E2F1 pathway has a role in β-cell function. We show here that E2F1 directly regulates expression of Kir6.2, which is a key component of the KATP channel involved in the regulation of glucose-induced insulin secretion. We demonstrate, through chromatin immunoprecipitation analysis from tissues, that Kir6.2 expression is regulated at the promoter level by the CDK4–pRB–E2F1 pathway. Consistently, inhibition of CDK4, or genetic inactivation of E2F1, results in decreased expression of Kir6.2, impaired insulin secretion and glucose intolerance in mice. Furthermore we show that rescue of Kir6.2 expression restores insulin secretion in E2f1−/− β cells. Finally, we demonstrate that CDK4 is activated by glucose through the insulin pathway, ultimately resulting in E2F1 activation and, consequently, increased expression of Kir6.2. In summary we provide evidence that the CDK4–pRB–E2F1 regulatory pathway is involved in glucose homeostasis, defining a new link between cell proliferation and metabolism." @default.
• W1993460435 created "2016-06-24" @default.
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• W1993460435 date "2009-07-13" @default.
• W1993460435 modified "2023-10-17" @default.
• W1993460435 title "The CDK4–pRB–E2F1 pathway controls insulin secretion" @default.
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• W1993460435 doi "https://doi.org/10.1038/ncb1915" @default.
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