ArticleThe Biochemical journal1993
Effects of CoA and acyl-CoAs on GTP-dependent Ca2+ release and vesicle fusion in rat liver microsomal vesicles.
Article in The Biochemical journal, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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.
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Who cites it
8 citing papers in PubMed, 23 citations in OpenAlex.
- Article
- Slow kinetics of inositol 1,4,5-trisphosphate-induced Ca2+ release: is the release 'quantal' or 'non-quantal'?The Biochemical journal · 1997Article
- Role of long-chain fatty acyl-CoA esters in the regulation of metabolism and in cell signalling.The Biochemical journal · 1997Review
- Fatty acyl-CoA esters inhibit glucose-6-phosphatase in rat liver microsomes.The Biochemical journal · 1995Article
- Effects of CoA and acyl-CoA on Ca(2+)-permeability of endoplasmic-reticulum membranes from rat liver.The Biochemical journal · 1995Article
- A novel cycle involving fatty acyl-coenzyme A regulates asialoglycoprotein receptor activity in permeable hepatocytes.Molecular biology of the cell · 1994Article
- Calcium: its modulation in liver by cross-talk between the actions of glucagon and calcium-mobilizing agonists.The Biochemical journal · 1993Review
- CoA and fatty acyl-CoA derivatives mobilize calcium from a liver reticular pool.The Biochemical journal · 1993Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
(1) CoA (IC50 23 microM) and acyl-CoAs (IC50 values 15-18 microM) inhibit GTP-dependent vesicle fusion in rat liver microsomal vesicles. Acyl-CoAs of carbon chain length C8 and C20 are much less effective than acyl-CoAs of carbon chain length C14-C18. The effect of CoA is mimicked by dephospho-CoA, but not by desulpho-CoA. High acyl-CoA concentrations (50 microM) appear to favour formation of small vesicles (budding), while 50 microM CoA does not. (2) Low concentrations of CoA (EC50 2 microM) and palmitoyl-CoA (10 microM) cause re-accumulation of Ca2+ released in response to GTP. This re-accumulation is into an Ins(1,4,5)P3-sensitive compartment. By investigation of the effects of CoA and palmitoyl-CoA on the thapsigargin-induced passive leak rate of Ca2+, and on the latency of the mannose-6-phosphatase of the vesicles, we conclude that CoA and palmitoyl-CoA cause decreased vesicle permeability rather than stimulation of Ca2+ pumping activity. (3) It is suggested that GTP-induced membrane fusion in rat liver microsomes involves an as yet uncharacterized acylation-deacylation reaction which is required to produce complete vesicle sealing.
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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.