ArticleThe Journal of biological chemistry2016
Protein Kinase D and Gβγ Subunits Mediate Agonist-evoked Translocation of Protease-activated Receptor-2 from the Golgi Apparatus to the Plasma Membrane.
Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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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
17 citing papers in PubMed, 22 citations in OpenAlex.
- Update on protease-activated receptor 2 in inflammatory and autoimmune dermatological diseases.Frontiers in immunology · 2024Review
- Gβγ signaling regulates microtubule-dependent control of Golgi integrity.Cellular signalling · 2023Article
- Non-canonical Golgi-compartmentalized Gβγ signaling: mechanisms, functions, and therapeutic targets.Trends in pharmacological sciences · 2023Review
- Protease-activated receptors in health and disease.Physiological reviews · 2023Review
- Characterization of lipoprotein lipase storage vesicles in 3T3-L1 adipocytes.Journal of cell science · 2022Article
- Mice expressing fluorescent PARProceedings of the National Academy of Sciences of the United States of America · 2022Article
- The olfactory receptor OR51E2 activates ERK1/2 through the Golgi-localized Gβγ-PI3Kγ-ARF1 pathway in prostate cancer cells.Frontiers in pharmacology · 2022Article
- Gβγ regulates mitotic Golgi fragmentation and G2/M cell cycle progression.Molecular biology of the cell · 2021Article
- Protease-Activated Receptors - Key Regulators of Inflammatory Bowel Diseases Progression.Journal of inflammation research · 2021Review
- Regulation of Osteoclast Differentiation at Multiple Stages by Protein Kinase D Family Kinases.International journal of molecular sciences · 2020Article
- Protein kinase D and Gβγ mediate sustained nociceptive signaling by biased agonists of protease-activated receptor-2.The Journal of biological chemistry · 2019Article
- Targeting G protein-coupled receptor signalling by blocking G proteins.Nature reviews. Drug discovery · 2018Review
- Protease-activated receptor-2 in endosomes signals persistent pain of irritable bowel syndrome.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- A Rho signaling network links microtubules to PKD controlled carrier transport to focal adhesions.eLife · 2018Article
- Inducible Inhibition of Gβγ Reveals Localization-dependent Functions at the Plasma Membrane and Golgi.The Journal of biological chemistry · 2017Article
- Gβγ translocation to the Golgi apparatus activates ARF1 to spatiotemporally regulate G protein-coupled receptor signaling to MAPK.The Journal of biological chemistryArticle
- G protein βγ translocation to the Golgi apparatus activates MAPK via p110γ-p101 heterodimers.The Journal of biological chemistryArticle
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Agonist-evoked endocytosis of G protein-coupled receptors has been extensively studied. The mechanisms by which agonists stimulate mobilization and plasma membrane translocation of G protein-coupled receptors from intracellular stores are unexplored. Protease-activated receptor-2 (PAR2) traffics to lysosomes, and sustained protease signaling requires mobilization and plasma membrane trafficking of PAR2 from Golgi stores. We evaluated the contribution of protein kinase D (PKD) and Gβγ to this process. In HEK293 and KNRK cells, the PAR2 agonists trypsin and 2-furoyl-LIGRLO-NH2 activated PKD in the Golgi apparatus, where PKD regulates protein trafficking. PAR2 activation induced translocation of Gβγ, a PKD activator, to the Golgi apparatus, determined by bioluminescence resonance energy transfer between Gγ-Venus and giantin-Rluc8. Inhibitors of PKD (CRT0066101) and Gβγ (gallein) prevented PAR2-stimulated activation of PKD. CRT0066101, PKD1 siRNA, and gallein all inhibited recovery of PAR2-evoked Ca(2+) signaling. PAR2 with a photoconvertible Kaede tag was expressed in KNRK cells to examine receptor translocation from the Golgi apparatus to the plasma membrane. Irradiation of the Golgi region (405 nm) induced green-red photo-conversion of PAR2-Kaede. Trypsin depleted PAR2-Kaede from the Golgi apparatus and repleted PAR2-Kaede at the plasma membrane. CRT0066101 inhibited PAR2-Kaede translocation to the plasma membrane. CRT0066101 also inhibited sustained protease signaling to colonocytes and nociceptive neurons that naturally express PAR2 and mediate protease-evoked inflammation and nociception. Our results reveal a major role for PKD and Gβγ in agonist-evoked mobilization of intracellular PAR2 stores that is required for sustained signaling by extracellular proteases.
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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.