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Transient activation of PKC results in long-lasting detrimental effects on systolic [Ca(2+)](i) in cardiomyocytes by altering actin cytoskeletal dynamics and T-tubule integrity
AIMS: Protein kinase C (PKC) isozymes contribute to the development of heart failure through dysregulation of Ca(2+) handling properties and disruption of contractile function in cardiomyocytes. However, the mechanisms by which PKC activation leads to Ca(2+) dysfunction are incompletely understood....
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| Vydáno v: | J Mol Cell Cardiol |
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| Hlavní autoři: | , , , , , , , |
| Médium: | Artigo |
| Jazyk: | Inglês |
| Vydáno: |
2018
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| Témata: | |
| On-line přístup: | https://ncbi.nlm.nih.gov/pmc/articles/PMC5839099/ https://ncbi.nlm.nih.gov/pubmed/29307535 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1016/j.yjmcc.2018.01.003 |
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