ReviewMolecular and cellular biochemistry
Cell signalling through phospholipid breakdown.
Review in Molecular and cellular biochemistry. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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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
10 citing papers in PubMed, 44 citations in OpenAlex.
- Influence of Dietary Polar Lipid Supplementation on Memory and Longitudinal Brain Development.Nutrients · 2021Article
- Growth factors regulate phospholipid biosynthesis in human fibroblast-like synoviocytes obtained from osteoarthritic knees.Scientific reports · 2017Article
- Chronic lithium treatment decreases brain phospholipase A2 activity.Neurochemical research · 1998Article
- Article
- Time-course changes in content and fatty acid composition of phosphatidic acid from rat thymocytes during concanavalin A stimulation.The Biochemical journal · 1995Article
- Angiotensin II induces phosphatidic acid formation in neonatal rat cardiac fibroblasts: evaluation of the roles of phospholipases C and D.Molecular and cellular biochemistry · 1994Article
- The effect of lidocaine on de novo phospholipid biosynthesis in the isolated hamster heart.Lipids · 1994Article
- Serine and ethanolamine incorporation into different plasmalogen pools: subcellular analyses of phosphoglyceride synthesis in cultured glioma cells.Neurochemical research · 1994Article
- Hyperpolarization induced by K+ channel openers inhibits Ca2+ influx and Ca2+ release in coronary artery.Cardiovascular drugs and therapy · 1993Article
- Stimulation by phospholipids of a protein-tyrosine-phosphatase containing two src homology 2 domains.Proceedings of the National Academy of Sciences of the United States of America · 1993Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
There is much evidence that G-proteins transduce the signal from receptors for Ca(2+)-mobilizing agonists to the phospholipase C that catalyzes the hydrolysis of phosphoinositides. However, the specific G-proteins involved have not been identified. We have recently purified a 42 kDa protein from liver that activates phosphoinositide phospholipase C and cross-reacts with antisera to a peptide common to G-protein alpha-subunits. It is proposed that this protein is the alpha-subunit of the G-protein that regulates the phospholipase in this tissue. Ca(2+)-mobilizing agonists and certain growth factors also promote the hydrolysis of phosphatidylcholine through the activation of phospholipases C and D in many cell types. This yields a larger amount of diacylglycerol for a longer time than does the hydrolysis of inositol phospholipids. Consequently phosphatidylcholine breakdown is probably a major factor in long-term regulation of protein kinase C. The functions of phosphatidic acid produced by phospholipase D are speculative, but there is evidence that it is a major source of diacylglycerol in many cell types. The regulation of phosphatidylcholine phospholipases is multiple and involves direct activation by G-proteins, and regulation by Ca2+, protein kinase C and perhaps growth factor receptor tyrosine kinases.
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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.