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A pair of phospho-specific antibodies to PLN were first described in 1994. These have been in continual use by the entire cardiac excitation-contraction coupling research community since that time, and have underpinned a series of discoveries concerning the aetiology and potential management of heart failure. In the early days, research focused on defining the normal physiological situation in the heart and the role of PLN phosphorylation in the response to stress. PLN is a small transmembrane protein expressed in the sarcoplasmic reticulum (SR) of cardiac myocytes, which interacts with the Ca2+-pump of the SR and inhibits Ca2+ transport by this pump. This inhibition is relieved upon PLN phosphorylation at Ser-16 or Thr-17 sites, Ca2+-transport into the SR is accelerated and the contraction cycle quickens and generates more force. Read full article.
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