Reactive disulfides trigger Ca2+ release from sarcoplasmic reticulum via an oxidation reaction

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Reactive disulfides trigger Ca2+ release from sarcoplasmic reticulum via an oxidation reaction.

Reactive disulfide compounds (RDSs) with a pyridyl ring adjacent to the S-S bond such as 2,2'-dithiodipyridine (2,2'-DTDP), 4,4'-dithiodipyridine, and N-succinimidyl 3(2-pyridyldithio)propionate (SPDP) trigger Ca2+ release from sarcoplasmic reticulum (SR) vesicles. They are known to specifically oxidize free SH sites via a thiol-disulfide exchange reaction with the stoichiometric production of ...

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Heavy metal-induced Ca2+ release from sarcoplasmic reticulum.

Two distinct forms of Ca2+ release from isolated sarcoplasmic reticulum vesicles in response to additions of heavy metals (silver and mercurials) are described. One form of heavy metal-induced Ca2+ release involves the ruthenium red-sensitive Ca2+ release channel localized in terminal cisternae. The other form of heavy metal-induced Ca2+ release appears to involve all portions of the sarcoplasm...

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Characterization of Ca2+ release from the cardiac sarcoplasmic reticulum.

The characteristics of Ca2+ release in relation to Ca2+ binding were studied in sarcoplasmic reticulum vesicles isolated from canine myocardium. The Ca2+ binding appeared to be dependent on ATP as a 4 fold increase in Ca2+ binding was observed upon the addition of ATP. In the presence of a suboptimal ATP concentration (20 mumol/l; without ATP regenerating system) a rapid release of Ca2+ started...

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Sarcoplasmic reticulum Ca2+ refilling controls recovery from Ca2+-induced Ca2+ release refractoriness in heart muscle.

In cardiac muscle Ca2+-induced Ca2+ release (CICR) from the sarcoplasmic reticulum (SR) is initiated by Ca2+ influx via L-type Ca2+ channels. At present, the mechanisms underlying termination of SR Ca2+ release, which are required to ensure stable excitation-contraction coupling cycles, are not precisely known. However, the same mechanism leading to refractoriness of SR Ca2+ release could also ...

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Acidosis facilitates spontaneous sarcoplasmic reticulum Ca2+ release in rat myocardium

Previous studies have shown that acidosis increases myoplasmic [Ca2+] (Cai). We have investigated whether this facilitates spontaneous sarcoplasmic reticulum (SR) Ca2+ release and its functional sequelae. In unstimulated rat papillary muscles, exposure to an acid solution (produced by increasing the [CO2] of the perfusate from 5 to 20%) caused a rapid increase in the mean tissue Cai, as measure...

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ژورنال

عنوان ژورنال: Journal of Biological Chemistry

سال: 1989

ISSN: 0021-9258

DOI: 10.1016/s0021-9258(20)88246-5