ArticlePsychopharmacology2011
Phospholipase C, Ca2+, and calmodulin signaling are required for 5-HT2A receptor-mediated transamidation of Rac1 by transglutaminase.
Article in Psychopharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.
- The Role of the Serotonergic System in Time Perception: A Systematic Review.International journal of molecular sciences · 2024Pooled it
- Neurotransmitters in cancer: how receptor signaling and posttranslational modifications modulate tumor progression and offer new therapeutic targets.Cell communication and signaling : CCS · 2026Review
- Partners in plasticity: serotonergic glial interactions in brain circuit remodeling.Frontiers in neuroscience · 2026Review
- Role of Serotonylation and SERT Posttranslational Modifications in Alzheimer's Disease Pathogenesis.Aging and disease · 2024Review
- Serotonin: an overlooked regulator of endocytosis and endosomal sorting?Biology open · 2022Article
- Pleiotropic Roles of Calmodulin in the Regulation of KRas and Rac1 GTPases: Functional Diversity in Health and Disease.International journal of molecular sciences · 2020Review
- Article
- Receptor-stimulated transamidation induces activation of Rac1 and Cdc42 and the regulation of dendritic spines.Neuropharmacology · 2017Article
- Ca2+ signaling in cytoskeletal reorganization, cell migration, and cancer metastasis.BioMed research international · 2015Review
- G-protein receptor kinase 5 regulates the cannabinoid receptor 2-induced up-regulation of serotonin 2A receptors.The Journal of biological chemistry · 2013Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
rationaleSerotonin and especially serotonin 2A (5-HT(2A)) receptor signaling are important in the etiology and treatment of schizophrenia and affective disorders. We previously reported a novel 5-HT(2A) receptor effector, increased transglutaminase (TGase)-catalyzed transamidation, and activation of the small G protein Rac1 in A1A1v cells, a rat embryonic cortical cell line.
objectivesIn this study, we explore the signaling pathway involved in 5-HT(2A) receptor-mediated Rac1 transamidation.
methodsA1A1v cells were pretreated with pharmacological inhibitors of phospholipase C (PLC) or calmodulin (CaM), and then stimulated by the 5-HT(2A) receptor agonist, 2,5-dimethoxy-4-iodoamphetamine (DOI). Intracellular Ca(2+) concentration and TGase-modified Rac1 transamidation were monitored. The effect of manipulation of intracellular Ca(2+) by a Ca(2+) ionophore or a chelating agent on Rac1 transamidation was also evaluated.
resultsIn cells pretreated with a PLC inhibitor U73122, DOI-stimulated increases in the intracellular Ca(2+) concentration and TGase-modified Rac1 were significantly attenuated as compared to those pretreated with U73343, an inactive analog. The membrane-permeant Ca(2+) chelator, BAPTA-AM strongly reduced TGase-catalyzed Rac1 transamidation upon DOI stimulation. Conversely, the Ca(2+) ionophore ionomycin, at a concentration that induced an elevation of cytosolic Ca(2+) to a level comparable to cells treated with DOI, produced an increase in TGase-modified Rac1 without 5-HT(2A) receptor activation. Moreover, the CaM inhibitor W-7, significantly decreased Rac1 transamidation in a dose-dependent manner in DOI-treated cells.
conclusionsThese results indicate that 5-HT(2A) receptor-coupled PLC activation and subsequent Ca(2+) and CaM signaling are necessary for TGase-catalyzed Rac1 transamidation, and an increase in intracellular Ca(2+) is sufficient to induce Rac1 transamidation.
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