ArticleThe Journal of physiology1999
Reduced glutathione inhibits beta-NAD+-activated non-selective cation currents in the CRI-G1 rat insulin-secreting cell line.
Article in The Journal of physiology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 15 citations in OpenAlex.
- Production of Ophthalmic Acid Using Engineered Escherichia coli.Applied and environmental microbiology · 2018Article
- Androgen and PARP-1 regulation of TRPM2 channels after ischemic injury.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2013Article
- Loss of glutathione homeostasis associated with neuronal senescence facilitates TRPM2 channel activation in cultured hippocampal pyramidal neurons.Molecular brain · 2012Article
- The role of TRPM channels in cell death.Pflugers Archiv : European journal of physiology · 2005Review
- Hydrogen-peroxide-induced toxicity of rat striatal neurones involves activation of a non-selective cation channel.The Journal of physiology · 2003Article
- Nitric oxide and thiol reagent modulation of Ca2+-activated K+ (BKCa) channels in myocytes of the guinea-pig taenia caeci.The Journal of physiology · 2000Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
1. Whole-cell voltage-clamp recordings were used to study the characteristics of a non-selective cation current, activated by intracellular beta-NAD+, present in CRI-G1 insulin-secreting cells. The monovalent cations Na+, K+ and Cs+ were equally permeant through this channel. 2. The magnitude of the beta-NAD+ current was dependent on the concentration of both beta-NAD+ and Ca2+ in the cell. The properties of the beta-NAD+-activated macroscopic current are similar to those of the beta-NAD+-activated non-selective cation channel (NSNAD) examined at the single channel level in this cell line. 3. The presence of intracellular reduced glutathione (GSH) inhibited the beta-NAD+-activated macroscopic current and the activity of the NSNAD channel in inside-out patch recordings. 4. The inhibition of beta-NAD+-activated currents by GSH is mimicked by its analogue ophthalmic acid but not by another thiol reducing agent dithiothreitol, indicating the presence of a specific GSH binding site present on the NSNAD channel or associated protein.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.