The small co-chaperone p23 overexpressing transgenic mouse

The Buck Institute for Research on Aging, 8001 Redwood Blvd, Novato, CA 94945, USA.
Journal of Neuroscience Methods (Impact Factor: 2.05). 09/2012; 212(2). DOI: 10.1016/j.jneumeth.2012.09.022
Source: PubMed


Studies from multiple laboratories have identified the roles of several ER stress-induced cell death modulators and effectors. Earlier, we described the role of p23 a small co-chaperone protein in preventing ER stress-induced cell death. p23 is cleaved by caspases at D142 to yield p19 (a 19kDa product) during ER stress-induced cell death. Mutation of the caspase cleavage site not only blocks formation of the 19kDa product but also attenuates the cell death process triggered by various ER stressors. Thus, uncleavable p23 (p23D142N) emerges as a reasonable candidate to test for potential inhibition of neurodegenerative disease phenotype that features misfolded proteins and ER stress. In the present work we report the generation of transgenic mouse lines that overexpress wild-type p23 or uncleavable p23 under the control of a ROSA promoter. These mice should prove useful for studying the role of p23 and/or uncleavable p23 in cellular stress-induced cell death.

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