Inhibition of AMP-Activated Protein Kinase Protects Pancreatic β-Cells From Cytokine-Mediated Apoptosis and CD8+ T-Cell–Induced Cytotoxicity
Author(s) -
Audrey Riboulet-Chavey,
Frédérique Diraison,
L. Khai Siew,
F. Susan Wong,
Guy A. Rutter
Publication year - 2007
Publication title -
diabetes
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.219
H-Index - 330
eISSN - 1939-327X
pISSN - 0012-1797
DOI - 10.2337/db07-0993
Subject(s) - ampk , cytotoxic t cell , protein kinase a , apoptosis , pancreatic islets , biology , nod mice , islet , cancer research , amp activated protein kinase , microbiology and biotechnology , chemistry , endocrinology , kinase , insulin , biochemistry , in vitro
Apoptotic destruction of insulin-producing pancreatic beta-cells is involved in the etiology of both type 1 and type 2 diabetes. AMP-activated protein kinase (AMPK) is a sensor of cellular energy charge whose sustained activation has recently been implicated in pancreatic beta-cell apoptosis and in islet cell death posttransplantation. Here, we examine the importance of beta-cell AMPK in cytokine-induced apoptosis and in the cytotoxic action of CD8(+) T-cells.
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