ArticleThe Journal of cell biology1997
Phospholipase D stimulates release of nascent secretory vesicles from the trans-Golgi network.
Article in The Journal of cell biology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 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
83 citing papers in PubMed, 253 citations in OpenAlex.
- Golgi retention of KIT in gastrointestinal stromal tumour cells is phospholipase D activity-dependent.Scientific reports · 2025Article
- Arfs on the Golgi: four conductors, one orchestra.Frontiers in molecular biosciences · 2025Review
- Article
- A secretory phospholipase D hydrolyzes phosphatidylcholine to suppress rice heading time.PLoS genetics · 2021Article
- Mammalian phospholipase D: Function, and therapeutics.Progress in lipid research · 2020Review
- Integrated Analysis of Transcriptomic and Proteomics Data Reveals the Induction Effects of Rotenoid Biosynthesis ofInternational journal of molecular sciences · 2018Article
- Protein Kinase C-epsilon in Membrane Delivery during Phagocytosis.Journal of immunological sciences · 2018Article
- Ethylene Regulates Differential Growth via BIG ARF-GEF-Dependent Post-Golgi Secretory Trafficking in Arabidopsis.The Plant cell · 2017Article
- Astrocyte-derived phosphatidic acid promotes dendritic branching.Scientific reports · 2016Article
- Journey to the cell surface--the central role of the trans-Golgi network in plants.Protoplasma · 2015Review
- Genome-Wide Association Studies of the Human Gut Microbiota.PloS one · 2015Article
- Article
- Modulation of Insulin Sensitivity of Hepatocytes by the Pharmacological Downregulation of Phospholipase D.International journal of endocrinology · 2015Article
- Sphingomyelin synthase 2, but not sphingomyelin synthase 1, is involved in HIV-1 envelope-mediated membrane fusion.The Journal of biological chemistry · 2014Article
- Phospholipase D is involved in the formation of Golgi associated clathrin coated vesicles in human parotid duct cells.PloS one · 2014Article
- Components of the CtBP1/BARS-dependent fission machinery.Histochemistry and cell biology · 2013Review
- Targeting the chameleon: a focused look at α-synuclein and its roles in neurodegeneration.Molecular neurobiology · 2013Review
- The lipidome and proteome of oil bodies from Helianthus annuus (common sunflower).Journal of chemical biology · 2013Article
- Involvement of diacylglycerol kinase γ in modulation of iNOS synthesis in Golgi apparatus of vascular endothelial cells.Naunyn-Schmiedeberg's archives of pharmacology · 2012Article
- PLD1 Negatively Regulates Dendritic Branching.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
23 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Phospholipase D (PLD) is a phospholipid hydrolyzing enzyme whose activation has been implicated in mediating signal transduction pathways, cell growth, and membrane trafficking in mammalian cells. Several laboratories have demonstrated that small GTP-binding proteins including ADP-ribosylation factor (ARF) can stimulate PLD activity in vitro and an ARF-activated PLD activity has been found in Golgi membranes. Since ARF-1 has also been shown to enhance release of nascent secretory vesicles from the TGN of endocrine cells, we hypothesized that this reaction occurred via PLD activation. Using a permeabilized cell system derived from growth hormone and prolactin-secreting pituitary GH3 cells, we demonstrate that immunoaffinity-purified human PLD1 stimulated nascent secretory vesicle budding from the TGN approximately twofold. In contrast, a similarly purified but enzymatically inactive mutant form of PLD1, designated Lys898Arg, had no effect on vesicle budding when added to the permeabilized cells. The release of nascent secretory vesicles from the TGN was sensitive to 1% 1-butanol, a concentration that inhibited PLD-catalyzed formation of phosphatidic acid. Furthermore, ARF-1 stimulated endogenous PLD activity in Golgi membranes approximately threefold and this activation correlated with its enhancement of vesicle budding. Our results suggest that ARF regulation of PLD activity plays an important role in the release of nascent secretory vesicles from the TGN.
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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.