ArticlePflugers Archiv : European journal of physiology2009
PKC epsilon facilitates recovery of exocytosis after an exhausting stimulation.
Article in Pflugers Archiv : European journal of physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed, 10 citations in OpenAlex.
- A two-subpopulation model that reflects heterogeneity of large dense core vesicles in exocytosis.Cell cycle (Georgetown, Tex.) · 2022Article
- Linking cortical microtubule attachment and exocytosis.F1000Research · 2017Review
- Chemical analysis of single cells.Analytical chemistry · 2011Review
- An emerging role for IQGAP1 in regulating protein traffic.TheScientificWorldJournal · 2010Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It has been well documented that protein kinase Cs (PKCs) play multifaceted roles in regulating exocytosis of neurotransmitters and hormones. But the isoform-specific PKC effects are still poorly elucidated mainly because of the large variety of PKC isoforms and the dubious specificity of the commonly used pharmacological agents. In the present study, based on overexpression of wild-type or dominant negative PKC epsilon, we demonstrate in neuroendocrine PC12 cells that PKC epsilon, but not PKC alpha, facilitates recovery of exocytosis after an exhausting stimulation. Specifically, PKC epsilon mediates fast recovery of the extent of exocytosis in a phosphatidylinositol biphosphate-dependent manner, likely through enhancing the rate of vesicle delivery and reorganization of cortical actin network. In addition, PKC epsilon promotes fast recovery of vesicle release kinetics that is slowed after a strong stimulation. These experimental results may suggest a PKC-dependent mechanism relevant to the short-term plasticity of exocytosis in both neurons and neuroendocrine cells.
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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.