ArticleCell adhesion & migration
GIV/Girdin is a rheostat that fine-tunes growth factor signals during tumor progression.
Article in Cell adhesion & migration. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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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
42 citing papers in PubMed, 54 citations in OpenAlex.
- Girdin silencing enhances mebendazole-mediated anticancer activity: a combinatorial therapeutic strategy for ovarian cancer.Medical oncology (Northwood, London, England) · 2025Article
- Genome sequencing reveals CCDC88A variants in malformations of cortical development and immune dysfunction.Human molecular genetics · 2025Article
- Heterotrimeric G protein signaling without GPCRs: The Gα-binding-and-activating (GBA) motif.The Journal of biological chemistry · 2024Review
- Identification and screening of circular RNAs during adipogenic differentiation of ovine preadipocyte by RNA-seq.Journal of animal science · 2024Article
- Small-molecule targeting of GPCR-independent noncanonical G-protein signaling in cancer.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- GNAQ mutations drive port wine birthmark-associated Sturge-Weber syndrome: A review of pathobiology, therapies, and current models.Frontiers in human neuroscience · 2022Review
- CCDC88A Post-Transcriptionally Regulates VEGFFrontiers in immunology · 2022Article
- The Multifaceted Nature of Nucleobindin-2 in Carcinogenesis.International journal of molecular sciences · 2021Review
- GIV/Girdin promotes cell survival during endoplasmic reticulum stress.Molecular and cellular biochemistry · 2019Article
- Single-Cell Imaging of Metastatic Potential of Cancer Cells.iScience · 2018Article
- Membrane Recruitment of the Non-receptor Protein GIV/Girdin (Gα-interacting, Vesicle-associated Protein/Girdin) Is Sufficient for Activating Heterotrimeric G Protein Signaling.The Journal of biological chemistry · 2016Article
- Prognostic impact of total and tyrosine phosphorylated GIV/Girdin in breast cancers.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Article
- Regulation, Signaling, and Physiological Functions of G-Proteins.Journal of molecular biology · 2016Review
- Girdin (GIV) Expression as a Prognostic Marker of Recurrence in Mismatch Repair-Proficient Stage II Colon Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016Article
- Heterotrimeric G protein signaling via GIV/Girdin: Breaking the rules of engagement, space, and time.BioEssays : news and reviews in molecular, cellular and developmental biology · 2016Review
- The untapped potential of tyrosine-based G protein signaling.Pharmacological research · 2016Review
- Prognostic Impact of Modulators of G proteins in Circulating Tumor Cells from Patients with Metastatic Colorectal Cancer.Scientific reports · 2016Article
- Focal adhesions are foci for tyrosine-based signal transduction via GIV/Girdin and G proteins.Molecular biology of the cell · 2015Article
- Cyclin-dependent kinase 5 activates guanine nucleotide exchange factor GIV/Girdin to orchestrate migration-proliferation dichotomy.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Gα13 Stimulates the Tyrosine Phosphorylation of Ric-8A.Journal of molecular signaling · 2015Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
GIV/Girdin is a multidomain signaling molecule that enhances PI3K-Akt signals downstream of both G protein-coupled and growth factor receptors. We previously reported that GIV triggers cell migration via its C-terminal guanine-nucleotide exchange factor (GEF) motif that activates Gαi. Recently we discovered that GIV's C-terminus directly interacts with the epidermal growth factor receptor (EGFR), and when its GEF function is intact, a Gαi-GIV-EGFR signaling complex assembles. By coupling G proteins to growth factor receptors, GIV is uniquely poised to intercept the incoming receptor-initiated signals and modulate them via G protein intermediates. Subsequent work has revealed that expression of the highly specialized C-terminus of GIV undergoes a bipartite dysregulation during oncogenesis-full length GIV with an intact C-terminus is expressed at levels ~20-50-fold above normal in highly invasive cancer cells and metastatic tumors, but its C-terminus is truncated by alternative splicing in poorly invasive cancer cells and non-invasive tumors. The consequences of such dysregulation on graded signal transduction and cellular phenotypes in the normal epithelium and its implication during tumor progression are discussed herein. Based on the fact that GIV grades incoming signals initiated by ligand-activated receptors by linking them to cyclical activation of G proteins, we propose that GIV is a molecular rheostat for signal transduction.
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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.