ArticleMolecular biology of the cell2006
Gab1 is required for cell cycle transition, cell proliferation, and transformation induced by an oncogenic met receptor.
Article in Molecular biology of the cell, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 36 citations in OpenAlex.
- Spindle Cell Tumors with aInternational journal of molecular sciences · 2026Article
- Identification of Novel Gene Signature Predicting Lymph Node Metastasis in Papillary Thyroid Cancer via Bioinformatics Analysis and in vitro Validation.International journal of general medicine · 2025Article
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- The Role of GAB1 in Cancer.Cancers · 2023Review
- PAK4, a target of miR-9-5p, promotes cell proliferation and inhibits apoptosis in colorectal cancer.Cellular & molecular biology letters · 2019Article
- Cholinergic Grb2-Associated-Binding Protein 1 Regulates Cognitive Function.Cerebral cortex (New York, N.Y. : 1991) · 2018Article
- Host response during Yersinia pestis infection of human bronchial epithelial cells involves negative regulation of autophagy and suggests a modulation of survival-related and cellular growth pathways.Frontiers in microbiology · 2015Article
- Article
- Profiling phospho-signaling networks in breast cancer using reverse-phase protein arrays.Oncogene · 2013Article
- Acquired substrate preference for GAB1 protein bestows transforming activity to ERBB2 kinase lung cancer mutants.The Journal of biological chemistry · 2013Article
- Article
- Gab docking proteins in cardiovascular disease, cancer, and inflammation.International journal of inflammation · 2013Article
- Novel role of proline-rich nonreceptor tyrosine kinase 2 in vascular wall remodeling after balloon injury.Arteriosclerosis, thrombosis, and vascular biology · 2012Article
- The signaling adaptor GAB1 regulates cell polarity by acting as a PAR protein scaffold.Molecular cell · 2012Article
- Gab adapter proteins as therapeutic targets for hematologic disease.Advances in hematology · 2012Article
- Distinct requirements for Gab1 in Met and EGF receptor signaling in vivo.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- Haloperidol induces the nuclear translocation of phosphatidylinositol 3'-kinase to disrupt Akt phosphorylation in PC12 cells.Journal of psychiatry & neuroscience : JPN · 2007Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
We have shown previously that either Grb2- or Shc-mediated signaling from the oncogenic Met receptor Tpr-Met is sufficient to trigger cell cycle progression in Xenopus oocytes. However, direct binding of these adaptors to Tpr-Met is dispensable, implying that another Met binding partner mediates these responses. In this study, we show that overexpression of Grb2-associated binder 1 (Gab1) promotes cell cycle progression when Tpr-Met is expressed at suboptimal levels. This response requires that Gab1 possess an intact Met-binding motif, the pleckstrin homology domain, and the binding sites for phosphatidylinositol 3-kinase and tyrosine phosphatase SHP-2, but not the Grb2 and CrkII/phospholipase Cgamma binding sites. Importantly, we establish that Gab1-mediated signals are critical for cell cycle transition promoted by the oncogenic Met and fibroblast growth factor receptors, but not by progesterone, the natural inducer of cell cycle transition in Xenopus oocytes. Moreover, Gab1 is essential for Tpr-Met-mediated morphological transformation and proliferation of fibroblasts. This study provides the first evidence that Gab1 is a key binding partner of the Met receptor for induction of cell cycle progression, proliferation, and oncogenic morphological transformation. This study identifies Gab1 and its associated signaling partners as potential therapeutic targets to impair proliferation or transformation of cancer cells in human malignancies harboring a deregulated Met receptor.
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