Ablation of triadin causes loss of cardiac Ca2+ release units, impaired excitation-contraction coupling, and cardiac arrhythmias

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Triadin overexpression stimulates excitation-contraction coupling and increases predisposition to cellular arrhythmia in cardiac myocytes.

Triadin 1 (TRD) is an integral membrane protein that associates with the ryanodine receptor (RyR2), calsequestrin (CASQ2) and junctin to form a macromolecular Ca signaling complex in the cardiac junctional sarcoplasmic reticulum (SR). To define the functional role of TRD, we examined the effects of adenoviral-mediated overexpression of the wild-type protein (TRD(WT)) or a TRD mutant lacking the...

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Calcium and cardiac excitation-contraction coupling.

gitudinal system of the SR, governing the Ca storage compartment with the highest recruitable amount of Ca in cardiac myocytes. The RyR are chemically coupled to L-type Ca channels via Ca, and a relatively small amount of Ca entering the cell via L-type Ca channels (depending on species or stimulation rate) activates a limited number of adjacent RyRs. This leads to Ca release from the SR, and a...

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Excitation Contraction Coupling in Cardiac Muscle

It is well established that excitation contraction (EC) coupling in cardiac myocytes is mediated by the entry of calcium ions (Ca 2 ) from the bathing medium into the cell cytoplasm (Fabiato, 1985), which then triggers calcium-induced calcium release (CICR) from the sarcoplasmic reticulum (SR). More recently, it was proposed that a second, quite separate, EC-coupling process, mediated by an eff...

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Calcium in Cardiac Excitation- Contraction Coupling

gitudinal system of the SR, governing the Ca storage compartment with the highest recruitable amount of Ca in cardiac myocytes. The RyR are chemically coupled to L-type Ca channels via Ca, and a relatively small amount of Ca entering the cell via L-type Ca channels (depending on species or stimulation rate) activates a limited number of adjacent RyRs. This leads to Ca release from the SR, and a...

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Excitation-contraction coupling and control of cardiac contractility.

EARLY WORK ON MUSCLE led to the discovery of the chemical basis for muscular contraction: The contractile protein actomyosin was discovered, ATP was established as the energy source for contraction, and the enzymatic activity required for utilization of ATP was localized to a portion of the actomyosin. Recent advances may offer insight into the control of muscular contraction, that is, the way ...

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ژورنال

عنوان ژورنال: Proceedings of the National Academy of Sciences

سال: 2009

ISSN: 0027-8424,1091-6490

DOI: 10.1073/pnas.0902919106