Inhibition of p66Shc-mediated mitochondrial apoptosis via targeting prolyl-isomerase Pin1 attenuates intestinal ischemia/reperfusion injury in rats

D Feng, J Yao, G Wang, Z Li, G Zu, Y Li, F Luo… - Clinical …, 2017 - portlandpress.com
Intestinal epithelial oxidative stress and apoptosis constitute key pathogenic mechanisms
underlying intestinal ischemia/reperfusion (I/R) injury. We previously reported that the
adaptor 66 kDa isoform of the adaptor molecule ShcA (p66Shc)-mediated pro-apoptotic
pathway was activated after intestinal I/R. However, the upstream regulators of the p66Shc
pathway involved in intestinal I/R remain to be fully identified. Here, we focused on the role
of a prolyl-isomerase, peptidyl–prolyl cis–trans isomerase (Pin1), in the regulation of p66Shc …

[PDF][PDF] page Inhibition of p66Shc-mediated mitochondrial apoptosis via targeting prolyl-isomerase Pin1 attenuates intestinal ischemia/reperfusion injury in rats.

D Feng, J Yao, G Wang, Z Li, G Zu, Y Li, F Luo, S Ning… - 2017 - researchgate.net
Intestinal epithelial oxidative stress and apoptosis constitute key pathogenic mechanisms
underlying intestinal ischemia/reperfusion (I/R) injury. We previously reported that the
adaptor p66Shc-mediated pro-apoptotic pathway was activated after intestinal I/R. However,
the upstream regulators of the p66Shc pathway involved in intestinal I/R remain to be fully
identified. Here, we focused on the role of a prolyl-isomerase, Pin1, in the regulation of
p66Shc activity during intestinal I/R. Intestinal I/R was induced in rats by superior mesenteric …
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