CaMKII is a RIP3 substrate mediating ischemia- and oxidative stress–induced myocardial necroptosis
By Tingting Zhang, Yan Zhang, Mingyao Cui, Li Jin, Yimei Wang, Fengxiang Lv, Yuli Liu, Wen Zheng, Haibao Shang, Jun Zhang and 7 more. Nature Medicine, 2016
729 citations recorded by the source corpus.
Subfields: Molecular Biology, Pathology and Forensic Medicine
View Paper: https://www.semanticscholar.org/paper/212ac383d63161c3ef5cc9422b682ffeec9a9497
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In Molecular Biology
- D. Tang
- R. Kang
- Guido Kroemer
- Xin Chen
- Christopher P. Baines
- Ronald J. Korthuis
- Theodore J Kalogeris
- M. Krenz
In Pathology and Forensic Medicine
- D. Tang
- R. Kang
- M. Krenz
- Guido Kroemer
- Ronald J. Korthuis
- Christopher P. Baines
- Theodore J Kalogeris
Citations in the corpus
- Ferroptosis in infection, inflammation, and immunity (2021, background): “However, other RCD subroutines, such as necroptosis, also contribute to the development of IRI in kidney (Linkermann et al., 2013) and heart (Zhang et al., 2016).”
- Necroptosis: Mechanisms and Relevance to Disease (2016, neutral): “Moreover, Ripk3 −/− (but not Mlkl −/− ) mice are less prone to develop a rheumatoid arthritis–like syndrome in response to serum from K/BxN transgenic mice as compared with their WT littermates (52), whereas Ripk3 −/− hearts are less likely to be rejected from WT hosts than are Ripk3 +/− organs, esp”
- Ferroptosis as a target for protection against cardiomyopathy (2019, background): “However, unlike the previous finding (13), we observed that Ca calmodulin-dependent protein kinase (CaMKII) inhibition using KN-93 showed little effect on DOX-induced mortality either by single KN-93 treatment or cotreatment with Fer-1 (Fig.”
- Ischemia/Reperfusion (2016, positive): “demonstrated in RIP3-deficient mice, where it was also shown that RIP3 induced the activation of CaMKII via phosphorylation at Thr287 in response to I/R (909).”
- Mitochondria-dependent ferroptosis plays a pivotal role in doxorubicin cardiotoxicity (2020, neutral): “of DIC in the mice used in previous studies (3, 4), and no mice in our study died even at the 1-month period during which we monitored DIC progression.”