The small co-chaperone p23 overexpressing transgenic mouse.

Junli Zhang, Patricia Spilman, Sylvia Chen, Olivia Gorostiza, Alex Matalis, Kayvan Niazi, Dale E Bredesen, Rammohan V Rao

Journal of neuroscience methods 2013 Jan 30

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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 19 kDa product) during ER stress-induced cell death. Mutation of the caspase cleavage site not only blocks formation of the 19 kDa 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. Copyright © 2012 Elsevier B.V. All rights reserved.

Citation

Junli Zhang, Patricia Spilman, Sylvia Chen, Olivia Gorostiza, Alex Matalis, Kayvan Niazi, Dale E Bredesen, Rammohan V Rao. The small co-chaperone p23 overexpressing transgenic mouse. Journal of neuroscience methods. 2013 Jan 30;212(2):190-4