ArticleThe Journal of general physiology2004
Sensitivity of volume-regulated anion current to cholesterol structural analogues.
Article in The Journal of general physiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
30 citing papers in PubMed, 78 citations in OpenAlex.
- Physiology of the volume-sensitive/regulatory anion channel VSOR/VRAC: part 2: its activation mechanisms and essential roles in organic signal release.The journal of physiological sciences : JPS · 2024Review
- Cholesterol regulation of mechanosensitive ion channels.Frontiers in cell and developmental biology · 2024Review
- PI(4,5)PAdvances in experimental medicine and biology · 2023Article
- Zwitterions Layer at but Do Not Screen Electrified Interfaces.The journal of physical chemistry. B · 2022Article
- Inward Rectifier Potassium Channels: Membrane Lipid-Dependent Mechanosensitive Gates in Brain Vascular Cells.Frontiers in cardiovascular medicine · 2022Review
- Comparative docking analysis of cholesterol analogs to ion channels to discriminate between stereospecific binding vs. stereospecific response.Channels (Austin, Tex.) · 2019Article
- Effect of sterol structure on ordered membrane domain (raft) stability in symmetric and asymmetric vesicles.Biochimica et biophysica acta. Biomembranes · 2019Article
- Constitutive boost of a KProceedings of the National Academy of Sciences of the United States of America · 2018Article
- Challenges and approaches to understand cholesterol-binding impact on membrane protein function: an NMR view.Cellular and molecular life sciences : CMLS · 2018Review
- Hypotonic Challenge of Endothelial Cells Increases Membrane Stiffness with No Effect on Tether Force.Biophysical journal · 2018Article
- The effect of sterol structure upon clathrin-mediated and clathrin-independent endocytosis.Journal of cell science · 2017Article
- Reduced membrane cholesterol limits pulmonary endothelial CaAmerican journal of physiology. Heart and circulatory physiology · 2017Article
- Biophysics and Physiology of the Volume-Regulated Anion Channel (VRAC)/Volume-Sensitive Outwardly Rectifying Anion Channel (VSOR).Pflugers Archiv : European journal of physiology · 2016Review
- Review
- Identification of a cholesterol-binding pocket in inward rectifier K(+) (Kir) channels.Biophysical journal · 2014Article
- Cholesterol binding to ion channels.Frontiers in physiology · 2014Review
- Distant cytosolic residues mediate a two-way molecular switch that controls the modulation of inwardly rectifying potassium (Kir) channels by cholesterol and phosphatidylinositol 4,5-bisphosphate (PI(4,5)P(2)).The Journal of biological chemistry · 2012Article
- Large conductance, calcium- and voltage-gated potassium (BK) channels: regulation by cholesterol.Pharmacology & therapeutics · 2012Review
- Article
- Cholesterol sensitivity of KIR2.1 is controlled by a belt of residues around the cytosolic pore.Biophysical journal · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Depletion of membrane cholesterol and substitution of endogenous cholesterol with its structural analogues was used to analyze the mechanism by which cholesterol regulates volume-regulated anion current (VRAC) in endothelial cells. Depletion of membrane cholesterol enhanced the development of VRAC activated in a swelling-independent way by dialyzing the cells either with GTPgammaS or with low ionic strength solution. Using MbetaCD-sterol complexes, 50-80% of endogenous cholesterol was substituted with a specific analogue, as verified by gas-liquid chromatography. The effects of cholesterol depletion were reversed by the substitution of endogenous cholesterol with its chiral analogue, epicholesterol, or with a plant sterol, beta-sitosterol, two analogues that mimic the effect of cholesterol on the physical properties of the membrane bilayer. Alternatively, when cholesterol was substituted with coprostanol that has only minimal effect on the membrane physical properties it resulted in VRAC enhancement, similar to cholesterol depletion. In summary, our data show that these channels do not discriminate between the two chiral analogues of cholesterol, as well as between the two cholesterols and beta-sitosterol, but discriminate between cholesterol and coprostanol. These observations suggest that endothelial VRAC is regulated by the physical properties of the membrane.
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What OpenQuestion holds
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.