CaMKIIδ subtypes differentially regulate infarct formation following ex vivo myocardial ischemia/reperfusion through NF-κB and TNF-α

Deletion of Ca(2+/)calmodulin-dependent protein kinase II delta (CaMKIIδ) has been shown to protect against in vivo ischemia/reperfusion (I/R) injury. It remains unclear which CaMKIIδ isoforms and downstream mechanisms are responsible for the salutary effects of CaMKIIδ gene deletion. In this study...

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Publié dans:J Mol Cell Cardiol
Auteurs principaux: Gray, Charles B.B., Suetomi, Takeshi, Xiang, Sunny, Mishra, Shikha, Blackwood, Erik A., Glembotski, Christopher C., Miyamoto, Shigeki, Westenbrink, B. Daan, Brown, Joan Heller
Format: Artigo
Langue:Inglês
Publié: 2017
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Article
Accès en ligne:https://ncbi.nlm.nih.gov/pmc/articles/PMC5564300/
https://ncbi.nlm.nih.gov/pubmed/28077321
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1016/j.yjmcc.2017.01.002
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