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| FARRELL,EMILY F; ANTARAMIAN,ANAID; BENKUSKY,NANCY; ZHU,XINSHENG; RUEDA,ANGÉLICA; GÓMEZ,ANA M; VALDIVIA,HÉCTOR H. |
| Activation of Ca2+ release channels/ryanodine receptors (RyR) by the inward Ca2+ current (I Ca) gives rise to Ca2+-induced Ca2+ release (CICR), the amplifying Ca2+ signaling mechanism that triggers contraction of the heart. CICR, in theory, is a high-gain, self-regenerating process, but an unidentified mechanism stabilizes it in vivo. Sorcin, a 21.6 kDa Ca2+-binding protein, binds to cardiac RyRs with high affinity and completely inhibits channel activity. Sorcin significantly inhibits both the spontaneous activity of RyRs in quiescent cells (visualized as Ca2+ sparks) and the I Ca-triggered activity of RyRs that gives rise to [Ca2+]i transients. Since sorcin decreases the amplitude of the [Ca2+]i transient without affecting the amplitude of I Ca, the... |
| Tipo: Journal article |
Palavras-chave: Sorcin; Ryanodine receptors; CICR; Dihydropyridine receptor; Sarcoplasmic reticulum. |
| Ano: 2004 |
URL: http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602004000400015 |
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