Loss of insulin-secreting pancreatic cells through apoptosis contributes to the progression of type 2 diabetes, but underlying mechanisms remain elusive. Here, we identify a pathway in which the cell death inhibitor ARC paradoxically becomes a killer during diabetes.
While cytoplasmic ARC maintains survival of insulin-producing pancreatic cells, McKimpson et al. show that a pool of ARC relocates to the nucleus during diabetes where it paradoxically triggers cell death.
Conversion of the death inhibitor ARC to a killer activates pancreatic beta cell death in diabetes.The activity-regulated cytoskeleton-associated protein, Arc/Arg3.1, influences mouse cocaine self-administration.
W. M. McKimpson, Y. Chen, J. A. Irving, M. Zheng, J. Weinberger, W. L. W. Tan, Z. Tiang, A. M. Jagger, S. C. Chua Jr., J. E. Pessin, R. S. Foo, D. A. Lomas, R. N. Kitsis, Conversion of the death inhibitor ARC to a killer activates pancreatic cell death in diabetes.
Thrombin, a serine protease, plays a central role in hemostasis by converting soluble plasma fibrinogen into an insoluble fibrin clot and by promoting platelet aggregation.Conversion of the death inhibitor ARC to a killer activates pancreatic cell death in diabetes.
Conversion of the death inhibitor ARC to a killer activates pancreatic cell...
