March 1, 1998The Journal of General PhysiologyOpen Access

Effect of Bay K 8644 (−) and the β2a Subunit on Ca2+-dependent Inactivation in α1C Ca2+ Channels

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Population

Xenopus oocytes expressing the cloned alpha1C subunit of the rabbit cardiac Ca2+ channel, with and without…

Comparison

Coexpression of the beta2a subunit or addition… vs alpha1C subunit expressed alone without Bay K 8644

Design

Preclinical

Authors

FNFrancesca NocetiUniversity of California, Los Angeles RORiccardo OlceseUniversity of California, Los Angeles NQNa QinTianjin University of Technology

Discussion

Member takes

Implication

Preclinical channel data on Ca2+-dependent inactivation; leaves open native myocyte validation and any therapeutic relevance.

Structured PICO

Population

Xenopus oocytes expressing the cloned alpha1C subunit of the rabbit cardiac Ca2+ channel, with and without the accessory beta2a subunit

Intervention

Coexpression of the beta2a subunit or addition of dihydropyridine agonist Bay K 8644 (-)

Comparator

alpha1C subunit expressed alone without Bay K 8644 (-)

Outcome

Rates of Ca2+-dependent inactivation of Ca2+ currentssurrogate

The study demonstrates that the Ca2+ site for inactivation is in the alpha1C pore-forming subunit of the cardiac Ca2+ channel and is sensitive to both Ca2+ flux and open probability.

Cite This Study

Noceti et al. (1998) studied this question.

synapsesocial.com/papers/6a8ace5877493d51bfdebfe3 https://doi.org/10.1085/jgp.111.3.463

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Effect of Bay K 8644 (−) and the β2a Subunit on Ca2+-dependent Inactivation in α1C Ca2+ Channels

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Effect of Bay K 8644 (−) and the β2a Subunit on Ca2+-dependent Inactivation in α1C Ca2+ Channels

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider