CaMKII is a RIP3 substrate mediating ischemia- and oxidative stress–induced myocardial necroptosis-Reference-Cited by-同舟云学术

CaMKII is a RIP3 substrate mediating ischemia- and oxidative stress–induced myocardial necroptosis

Published:2016-01-04 Issue:2 Volume:22 Page:175-182
ISSN:1078-8956
Container-title:Nature Medicine
language:en
Short-container-title:Nat Med

Author:

Zhang Ting,Zhang Yan,Cui Mingyao^ORCID,Jin Li,Wang Yimei,Lv Fengxiang,Liu Yuli,Zheng Wen,Shang Haibao,Zhang Jun,Zhang Mao,Wu Hongkun,Guo Jiaojiao,Zhang Xiuqin,Hu Xinli,Cao Chun-Mei,Xiao Rui-Ping

Publisher

Springer Science and Business Media LLC

Subject

General Biochemistry, Genetics and Molecular Biology,General Medicine

Link

http://www.nature.com/articles/nm.4017.pdf

Reference55 articles.

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2. Whelan, R.S., Kaplinskiy, V. & Kitsis, R.N. Cell death in the pathogenesis of heart disease: mechanisms and significance. Annu. Rev. Physiol. 72, 19–44 (2010).

3. Cho, Y.S. et al. Phosphorylation-driven assembly of the RIP1-RIP3 complex regulates programmed necrosis and virus-induced inflammation. Cell 137, 1112–1123 (2009).

4. He, S. et al. Receptor interacting protein kinase-3 determines cellular necrotic response to TNF-α. Cell 137, 1100–1111 (2009).

5. Zhang, D.W. et al. RIP3, an energy metabolism regulator that switches TNF-induced cell death from apoptosis to necrosis. Science 325, 332–336 (2009).

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