ArticlePloS one2013
Cholecystokinin-mediated RhoGDI phosphorylation via PKCα promotes both RhoA and Rac1 signaling.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed, 26 citations in OpenAlex.
- Article
- Computationally designed sensors detect endogenous Ras activity and signaling effectors at subcellular resolution.Nature biotechnology · 2024Article
- The Role of Twist1 in Chronic Pancreatitis-Associated Pancreatic Stellate Cells.The American journal of pathology · 2024Article
- Article
- PLK1 phosphorylates RhoGDI1 and promotes cancer cell migration and invasion.Cancer cell international · 2024Article
- Review
- Histamine-induced biphasic activation of RhoA allows for persistent RhoA signaling.PLoS biology · 2020Article
- NADPH oxidase 1 mediates caerulein-induced pancreatic fibrosis in chronic pancreatitis.Free radical biology & medicine · 2020Article
- Review
- EphrinB1 promotes cancer cell migration and invasion through the interaction with RhoGDI1.Oncogene · 2018Article
- RCAD/BiP pathway is necessary for the proper synthesis of digestive enzymes and secretory function of the exocrine pancreas.American journal of physiology. Gastrointestinal and liver physiology · 2017Article
- Regulating Rho GTPases and their regulators.Nature reviews. Molecular cell biology · 2016Review
- Acinar cell-specific knockout of the PTHrP gene decreases the proinflammatory and profibrotic responses in pancreatitis.American journal of physiology. Gastrointestinal and liver physiology · 2014Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
RhoA and Rac1 have been implicated in the mechanism of CCK-induced amylase secretion from pancreatic acini. In all cell types studied to date, inactive Rho GTPases are present in the cytosol bound to the guanine nucleotide dissociation inhibitor RhoGDI. Here, we identified the switch mechanism regulating RhoGDI1-Rho GTPase dissociation and RhoA translocation upon CCK stimulation in pancreatic acini. We found that both Gα13 and PKC, independently, regulate CCK-induced RhoA translocation and that the PKC isoform involved is PKCα. Both RhoGDI1 and RhoGDI3, but not RhoGDI2, are expressed in pancreatic acini. Cytosolic RhoA and Rac1 are associated with RhoGDI1, and CCK-stimulated PKCα activation releases the complex. Overexpression of RhoGDI1, by binding RhoA, inhibits its activation, and thereby, CCK-induced apical amylase secretion. RhoA translocation is also inhibited by RhoGDI1. Inactive Rac1 influences CCK-induced RhoA activation by preventing RhoGDI1 from binding RhoA. By mutational analysis we found that CCK-induced PKCα phosphorylation on RhoGDI1 at Ser96 releases RhoA and Rac1 from RhoGDI1 to facilitate Rho GTPases signaling.
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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 Socratic graph.