Ablation of junctin or triadin is associated with increased cardiac injury following ischaemia/reperfusion | Zendy

Wenfeng Cai | Zendy; Tracy J. Pritchard | Zendy; Stela Florea | Zendy; Chi Keung Lam | Zendy; Peidong Han | Zendy; Xiaoyang Zhou | Zendy; Qunying Yuan | Zendy; Stephan E. Lehnart | Zendy; Paul D. Allen | Zendy; Evangelia G. Kranias | Zendy

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Ablation of junctin or triadin is associated with increased cardiac injury following ischaemia/reperfusion

Author(s) -

Wenfeng Cai,

Tracy J. Pritchard,

Stela Florea,

Chi Keung Lam,

Peidong Han,

Xiaoyang Zhou,

Qunying Yuan,

Stephan E. Lehnart,

Paul D. Allen,

Evangelia G. Kranias

Publication year - 2012

Publication title -

cardiovascular research

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.774

H-Index - 219

eISSN - 1755-3245

pISSN - 0008-6363

DOI - 10.1093/cvr/cvs119

Subject(s) - calsequestrin , ryanodine receptor , calpain , medicine , endoplasmic reticulum , endocrinology , biology , microbiology and biotechnology , chemistry , biochemistry , enzyme

Junctin and triadin are calsequestrin-binding proteins that regulate sarcoplasmic reticulum (SR) Ca(2+) release by interacting with the ryanodine receptor. The levels of these proteins are significantly down-regulated in failing human hearts. However, the significance of such decreases is currently unknown. Here, we addressed the functional role of these accessory proteins in the heart's responses to ischaemia/reperfusion (I/R) injury.

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