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Article

cJun N-terminal kinase (JNK) phosphorylation of serine 36 is critical for p66Shc activation.

Scientific reports - 12 Feb 2016

Khalid Sana, Drasche Astrid, Thurner Marco, Hermann Martin, Ashraf Muhammad Imtiaz, Fresser Friedrich, Baier Gottfried, Kremser Leopold, Lindner Herbert, Troppmair Jakob

Abstract excerpt

p66Shc-dependent ROS production contributes to many pathologies including ischemia/reperfusion injury (IRI) during solid organ transplantation. Inhibiting p66Shc activation may provide a novel therapeutic approach to prevent damage, which is poorly managed by antioxidants in vivo. Previous work suggested that pro-oxidant and a pro-apoptotic function of p66Shc required mitochondrial import, which depended on...

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Identifiers

PMID: 26868434
DOI: 10.1038/srep20930
PMCID: PMC4751440

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cJun N-terminal kinase (JNK) phosphorylation of serine 36 is critical for p66Shc activation.PMID 26868434Read ↗

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