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Effects of the Calcium-Activated Chloride Channel Inhibitors T16Ainh-A01 and CaCCinh-A01 on Cardiac Fibroblast Function.

08:00 EDT 30th August 2018 | BioPortfolio

Summary of "Effects of the Calcium-Activated Chloride Channel Inhibitors T16Ainh-A01 and CaCCinh-A01 on Cardiac Fibroblast Function."

Calcium-activated chloride channels (CaCCs) regulate numerous physiological processes including cell proliferation, migration, and extracellular matrix secretion. T16Ainh-A01 and CaCCinh-A01 are selective inhibitors of CaCCs. But it is unknown whether these two compounds have functional effects on cardiac fibroblasts (CFs).

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Journal Details

This article was published in the following journal.

Name: Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology
ISSN: 1421-9778
Pages: 706-716

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Medical and Biotech [MESH] Definitions

A calcium release-activated calcium-like (CRAC-like) channel subunit which functions with STROMAL INTERACTION MOLECULE 1 to regulate cell calcium influx and increase (Ca2+)-selective current.

A stromal interaction molecule that functions in the regulation of calcium influx following depletion of intracellular calcium in the ENDOPLASMIC RETICULUM. It translocates to the plasma membrane upon calcium depletion where it activates the CALCIUM RELEASE ACTIVATED CALCIUM CHANNEL ORAI1.

A methylpyrrole-carboxylate from RYANIA that disrupts the RYANODINE RECEPTOR CALCIUM RELEASE CHANNEL to modify CALCIUM release from SARCOPLASMIC RETICULUM resulting in alteration of MUSCLE CONTRACTION. It was previously used in INSECTICIDES. It is used experimentally in conjunction with THAPSIGARGIN and other inhibitors of CALCIUM ATPASE uptake of calcium into SARCOPLASMIC RETICULUM.

The pore-forming subunits of large-conductance calcium-activated potassium channels. They form tetramers in CELL MEMBRANES.

The regulatory subunits of large-conductance calcium-activated potassium channels.

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