ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2008
Phosphorylation of SNAP-25 at Ser187 mediates enhancement of exocytosis by a phorbol ester in INS-1 cells.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 66 citations in OpenAlex.
- Phosphorylation of SNAP-25 at Ser187 is enhanced following its cleavage by Botulinum Neurotoxin Serotype A, promoting the dominant-negative effect of the resulting fragment.PLoS pathogens · 2025Article
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- Endogenous hydrogen peroxide positively regulates secretion of a gut-derived peptide in neuroendocrine potentiation of the oxidative stress response inbioRxiv : the preprint server for biology · 2024Article
- SNAP23 decreases insulin secretion by competitively inhibiting the interaction between SNAP25 and STX1A.Bioscience reports · 2023Article
- Plantainoside D Reduces Depolarization-Evoked Glutamate Release from Rat Cerebral Cortical Synaptosomes.Molecules (Basel, Switzerland) · 2023Article
- SerFrontiers in cell and developmental biology · 2021Article
- Diverse exocytic pathways for mast cell mediators.Biochemical Society transactions · 2018Review
- Application of High-Throughput Assays to Examine Phospho-Modulation of the Late Steps of Regulated Exocytosis.High-throughput · 2017Article
- Regulation of insulin exocytosis by calcium-dependent protein kinase C in beta cells.Cell calcium · 2017Review
- Regulator of G-protein signaling Gβ5-R7 is a crucial activator of muscarinic M3 receptor-stimulated insulin secretion.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
- Myosin phosphatase and RhoA-activated kinase modulate neurotransmitter release by regulating SNAP-25 of SNARE complex.PloS one · 2017Article
- Phosphorylation of residues inside the SNARE complex suppresses secretory vesicle fusion.The EMBO journal · 2016Article
- Pancreatic regulation of glucose homeostasis.Experimental & molecular medicine · 2016Review
- Synaptotagmin-7 phosphorylation mediates GLP-1-dependent potentiation of insulin secretion from β-cells.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- SRC family kinase inhibitors antagonize the toxicity of multiple serotypes of botulinum neurotoxin in human embryonic stem cell-derived motor neurons.Neurotoxicity research · 2015Article
- Article
- Netrin-G/NGL complexes encode functional synaptic diversification.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- MicroRNA-7a regulates pancreatic β cell function.The Journal of clinical investigation · 2014Article
- Article
- Phospholipase C-related but catalytically inactive protein (PRIP) modulates synaptosomal-associated protein 25 (SNAP-25) phosphorylation and exocytosis.The Journal of biological chemistry · 2012Article
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Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
Abstract
Activation of diacylglycerol (DAG) signaling pathways with phorbol esters dramatically enhances Ca2+-triggered exocytosis from both endocrine cells and neurons, however the relevant targets of DAG are controversial. A possible effector mechanism for this signaling pathway is phosphorylation of SNAP-25 (25 kDa synaptosome-associated protein) at Ser187 by PKC. Here, we investigated the role of Ser187 in the enhancement of exocytosis by the phorbol ester PMA (phorbol 12-myristate 13-acetate). We used patch-clamp measurements of membrane capacitance together with photorelease of caged-Ca2+ and membrane depolarization to study exocytosis. Expression of the nonphosphorylatable S187C SNAP-25 mutant did not attenuate the enhancement of exocytosis by PMA in either bovine chromaffin cells or the INS-1 insulin-secreting cell line. To test the effects of Ser187 mutations under conditions in which the endogenous SNAP-25 is disabled, we expressed botulinum toxin serotype E to cleave SNAP-25 in INS-1 cells. Coexpression of a toxin-resistant mutant (TR), but not wild-type SNAP-25, was able to rescue PMA-modulated exocytosis. Coexpression of the toxin with the TR-S187C SNAP-25 mutant was able to completely block the enhancement of exocytosis by PMA in response to photoelevation of [Ca2+]i to low microM levels or to a depolarizing train. The phospho-mimetic S187E mutation enhanced the small, fast burst of exocytosis evoked by photelevation of Ca2+, but, like PMA, had smaller effects on exocytosis evoked by a depolarizing train. This work supports the hypothesis that phosphorylation of Ser187 of SNAP-25 by PKC is a key step in the enhancement of exocytosis by DAG.
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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 Socratic graph.