ArticleThe Journal of cell biology2008
Activation of Galphai3 triggers cell migration via regulation of GIV.
Article in The Journal of cell biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers.
What it found
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Who cites it
101 citing papers in PubMed, 152 citations in OpenAlex.
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- Essential strategies for the detection of constitutive and ligand-dependent Gi-directed activity of 7TM receptors using bioluminescence resonance energy transfer.bioRxiv : the preprint server for biology · 2024Article
- Identification of a coagulation-related gene signature for predicting prognosis in recurrent glioma.Discover oncology · 2024Article
- Iridium(III) carbene complexes as potent girdin inhibitors against metastatic cancers.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Growth factor-dependent phosphorylation of GαScience signaling · 2024Article
- Integrins regulate hERG1 dynamics by girdin-dependent Gαi3: signaling and modeling in cancer cells.Life science alliance · 2024Article
- hsa-miR-199b-3p suppresses osteosarcoma progression by targeting CCDC88A, inhibiting epithelial-to-mesenchymal transition, and Wnt/beta-catenin signaling pathway.Scientific reports · 2023Article
- Fine-tuning GPCR-mediated neuromodulation by biasing signaling through different G protein subunits.Molecular cell · 2023Article
- Regulation of DNA damage response by trimeric G-proteins.iScience · 2023Article
- Comprehensive analysis reveals the potential value of inflammatory response genes in the prognosis, immunity, and drug sensitivity of lung adenocarcinoma.BMC medical genomics · 2022Article
- DAPLE orchestrates apical actomyosin assembly from junctional polarity complexes.The Journal of cell biology · 2022Article
- The mechanism of Girdin in degenerative brain disease caused by high glucose stimulation.Frontiers in endocrinology · 2022Article
- Gαi protein subunit: A step toward understanding its non-canonical mechanisms.Frontiers in cell and developmental biology · 2022Review
- Article
- Hsa_circ_0076305 induces migration-proliferation dichotomy in gastric cancer.Oncology letters · 2021Article
- Receptor tyrosine kinases activate heterotrimeric G proteins via phosphorylation within the interdomain cleft of Gαi.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Revealing the Activity of Trimeric G-proteins in Live Cells with a Versatile Biosensor Design.Cell · 2020Article
41 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
During migration, cells must couple direction sensing to signal transduction and actin remodeling. We previously identified GIV/Girdin as a Galphai3 binding partner. We demonstrate that in mammalian cells Galphai3 controls the functions of GIV during cell migration. We find that Galphai3 preferentially localizes to the leading edge and that cells lacking Galphai3 fail to polarize or migrate. A conformational change induced by association of GIV with Galphai3 promotes Akt-mediated phosphorylation of GIV, resulting in its redistribution to the plasma membrane. Activation of Galphai3 serves as a molecular switch that triggers dissociation of Gbetagamma and GIV from the Gi3-GIV complex, thereby promoting cell migration by enhancing Akt signaling and actin remodeling. Galphai3-GIV coupling is essential for cell migration during wound healing, macrophage chemotaxis, and tumor cell migration, indicating that the Galphai3-GIV switch serves to link direction sensing from different families of chemotactic receptors to formation of the leading edge during cell migration.
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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.