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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 

The scaffold protein IB1/ JIP-1 is a critical mediator of cytokine-induced apoptosis in pancreatic beta cells.

In insulin-secreting cells, cytokines activate the c-Jun N-terminal kinase ( JNK), which contributes to a cell signaling towards apoptosis. The JNK activation requires the presence of the murine scaffold protein JNK-interacting protein 1 ( JIP-1) or human Islet-brain 1(IB1), which organizes MLK3, MKK7 and JNK for proper signaling specificity. Here, we used adenovirus-mediated gene transfer to modulate IB1/ JIP-1 cellular content in order to investigate the contribution of IB1/ JIP-1 to beta-cell survival. Exposure of the insulin-producing cell line INS-1 or isolated rat pancreatic islets to cytokines (interferon-gamma, tumor necrosis factor-alpha and interleukin-1beta) induced a marked reduction of IB1/ JIP-1 content and a concomitant increase in JNK activity and apoptosis rate. This JNK- induced pro-apoptotic program was prevented in INS-1 cells by overproducing IB1/ JIP-1 and this effect was associated with inhibition of caspase-3 cleavage. Conversely, reducing IB1/ JIP-1 content in INS-1 cells and isolated pancreatic islets induced a robust increase in basal and cytokine-stimulated apoptosis. In heterozygous mice carrying a selective disruption of the IB1/ JIP-1 gene, the reduction in IB1/ JIP-1 content in happloinsufficient isolated pancreatic islets was associated with an increased JNK activity and basal apoptosis. These data demonstrate that modulation of the IB1- JIP-1 content in beta cells is a crucial regulator of JNK signaling pathway and of cytokine-induced apoptosis.[1]

References

  1. The scaffold protein IB1/JIP-1 is a critical mediator of cytokine-induced apoptosis in pancreatic beta cells. Haefliger, J.A., Tawadros, T., Meylan, L., Gurun, S.L., Roehrich, M.E., Martin, D., Thorens, B., Waeber, G. J. Cell. Sci. (2003) [Pubmed]
 
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