LKB1 and AMPK differentially regulate pancreatic β-cell identity.

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2014

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info:eu-repo/semantics/altIdentifier/doi/10.1096/fj.14-257667

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info:eu-repo/semantics/altIdentifier/pmid/25070369

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info:eu-repo/semantics/altIdentifier/eissn/1530-6860

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info:eu-repo/semantics/altIdentifier/urn/urn:nbn:ch:serval-BIB_8F808B5B27DA9

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M. Kone et al., « LKB1 and AMPK differentially regulate pancreatic β-cell identity. », Serveur académique Lausannois, ID : 10.1096/fj.14-257667


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Fully differentiated pancreatic β cells are essential for normal glucose homeostasis in mammals. Dedifferentiation of these cells has been suggested to occur in type 2 diabetes, impairing insulin production. Since chronic fuel excess ("glucotoxicity") is implicated in this process, we sought here to identify the potential roles in β-cell identity of the tumor suppressor liver kinase B1 (LKB1/STK11) and the downstream fuel-sensitive kinase, AMP-activated protein kinase (AMPK). Highly β-cell-restricted deletion of each kinase in mice, using an Ins1-controlled Cre, was therefore followed by physiological, morphometric, and massive parallel sequencing analysis. Loss of LKB1 strikingly (2.0-12-fold, E

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