Published in Gene Therapy Weekly, February 12th, 2004
"In many types of heart failure cardiac myocyte Ca2+ handling is abnormal because of downregulation of key Ca2+-handling proteins like sarco(endo) plasmic reticulum Ca2+- ATPase (SERCA) 2a and ryanodine receptor (RyR) 2. The alteration in SERCA2a and RyR2 expression results in altered cytosolic Ca2+ transients, leading to abnormal contraction. Sorcin is an EF-hand protein that confers the property of caffeine-activated intracellular Ca2+ release in nonmuscle cells by interacting with RyR2," researchers in the United States report.
"To determine whether sorcin could...
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