Ablation of junctin or triadin is associated with increased cardiac injury following ischaemia/reperfusion
2012 | journal article
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Ablation of junctin or triadin is associated with increased cardiac injury following ischaemia/reperfusion
Cai, W.-F.; Pritchard, T.; Florea, S.; Lam, C.-K.; Han, P.; Zhou, X. & Yuan, Q. et al. (2012)
Cardiovascular Research, 94(2) pp. 333-341. DOI: https://doi.org/10.1093/cvr/cvs119
Documents & Media
Details
- Authors
- Cai, Wen-Feng; Pritchard, Tracy; Florea, Stela; Lam, Chi-Kueng; Han, Peidong; Zhou, Xiaoyang; Yuan, Qunying; Lehnart, Stephan E. ; Allen, Paul D.; Kranias, Evangelia G.
- Abstract
- 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.
- Issue Date
- 2012
- Journal
- Cardiovascular Research
- ISSN
- 1755-3245
- eISSN
- 1755-3245
- Language
- English
