ArticlePflugers Archiv : European journal of physiology2012
Modulation of the hepatocyte rough endoplasmic reticulum single chloride channel by nucleotide-Mg2+ interaction.
Article in Pflugers Archiv : European journal of physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed, 2 citations in OpenAlex.
- New and notable ion-channels in the sarcoplasmic/endoplasmic reticulum: do they support the process of intracellular Ca²⁺ release?The Journal of physiology · 2015Review
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The effect of nucleotides on single chloride channels derived from rat hepatocyte rough endoplasmic reticulum vesicles incorporated into bilayer lipid membrane was investigated. The single chloride channel currents were measured in 200/50 mmol/l KCl cis/trans solutions. Adding 2.5 mM adenosine triphosphate (ATP) and adenosine diphosphate (ADP) did not influence channel activity. However, MgATP addition inhibited the chloride channels by decreasing the channel open probability (Po) and current amplitude, whereas mixture of Mg(2+) and ADP activated the chloride channel by increasing the Po and unitary current amplitude. According to the results, there is a novel regulation mechanism for rough endoplasmic reticulum (RER) Cl(-) channel activity by intracellular MgATP and mixture of Mg(2+) and ADP that would result in significant inhibition by MgATP and activation by mixture of Mg(2+) and ADP. These modulatory effects of nucleotide-Mg(2+) complexes on chloride channels may be dependent on their chemical structure configuration. It seems that Mg-nucleotide-ion channel interactions are involved to produce a regulatory response for RER chloride channels.
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