ArticleMolecular and cellular biochemistry2010
Phospholipase D modulation by ceramide in senescence.
Article in Molecular and cellular biochemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 29 citations in OpenAlex.
- The Role of Neutral Sphingomyelinase-2 (NSM2) in the Control of Neutral Lipid Storage in T Cells.International journal of molecular sciences · 2024Article
- Rapid evaluation of 25 key sphingolipids and phosphosphingolipids in human plasma by LC-MS/MS.Analytical and bioanalytical chemistry · 2015Article
- Sphingolipids and lifespan regulation.Biochimica et biophysica acta · 2014Review
- Correlation between composition of the outer layer and phase asymmetry for vesicles ruptured by phospholipase D.The Journal of membrane biology · 2013Article
- p53 and Ceramide as Collaborators in the Stress Response.International journal of molecular sciences · 2013Article
- Effect of mixed-phospholipid layer on phospholipase D reaction-induced vesicle rupture.The Journal of membrane biology · 2012Article
- Effect of phospholipid bilayer phase asymmetry on phospholipase d reaction-induced vesicle rupture.The Journal of membrane biology · 2011Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Phospholipase D (PLD) has been implicated in mitotic regulation and has been shown to be defective in cells following replicative senescence. We examined the source of changes in PLD activity in senescent human umbilical vein endothelial cells and in human diploid fibroblasts. Using fractionated cell components we found that the cytosolic components were necessary for maximum PLD activation. In comparison to low-passage cells, senescent cells showed a profound lack of PLD activatability. By recombining fractionated components from senescent and low-passage cells, we found that in senescence the membrane component is defective in activating PLD implicating either the PLD enzyme itself or its interaction with PKC and/or ARF. The sphingolipid ceramide has been implicated in mediating senescence. Treatment with ceramide resulted in a decrease in PLD activity, implicating ceramide as the mediator of the inhibition.
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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.