ArticleOncogene2000
Shp-2 mediates v-Src-induced morphological changes and activation of the anti-apoptotic protein kinase Akt.
Article in Oncogene, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 78 citations in OpenAlex.
- Tumor suppressor function of formyl peptide receptor 1 in gastrointestinal cancers: a focus on the underlying signaling.Frontiers in cell and developmental biology · 2025Review
- Role of Non-Receptor-Type Tyrosine Phosphatases in Brain-Related Diseases.Molecular neurobiology · 2023Review
- A Tale of Two States: Normal and Transformed, With and Without Rigidity Sensing.Annual review of cell and developmental biology · 2019Review
- PI3Kβ links integrin activation and PI(3,4)PMolecular biology of the cell · 2019Article
- In vivo efficacy of the AKT inhibitor ARQ 092 in Noonan Syndrome with multiple lentigines-associated hypertrophic cardiomyopathy.PloS one · 2017Article
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- 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
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- Deletion of SHP-2 in mesenchymal stem cells causes growth retardation, limb and chest deformity, and calvarial defects in mice.Disease models & mechanisms · 2013Article
- The tyrosine phosphatase SHP2 regulates focal adhesion kinase to promote EGF-induced lamellipodia persistence and cell migration.Molecular cancer research : MCR · 2013Article
- Novel functions of the phosphatase SHP2 in the DNA replication and damage checkpoints.PloS one · 2012Article
- Src homology domain 2-containing protein-tyrosine phosphatase-1 (SHP-1) binds and dephosphorylates G(alpha)-interacting, vesicle-associated protein (GIV)/Girdin and attenuates the GIV-phosphatidylinositol 3-kinase (PI3K)-Akt signaling pathway.The Journal of biological chemistry · 2011Article
- Development of severe skeletal defects in induced SHP-2-deficient adult mice: a model of skeletal malformation in humans with SHP-2 mutations.Disease models & mechanisms · 2011Article
- Rapamycin reverses hypertrophic cardiomyopathy in a mouse model of LEOPARD syndrome-associated PTPN11 mutation.The Journal of clinical investigation · 2011Article
- The protein tyrosine phosphatase SHP-2 is required for EGFRvIII oncogenic transformation in human glioblastoma cells.Experimental cell research · 2009Article
- Molecular mechanism for SHP2 in promoting HER2-induced signaling and transformation.The Journal of biological chemistry · 2009Article
- Role of Src signal transduction pathways in scatter factor-mediated cellular protection.The Journal of biological chemistry · 2009Article
- GRIM-19 inhibits v-Src-induced cell motility by interfering with cytoskeletal restructuring.Oncogene · 2009Article
- Global impact of oncogenic Src on a phosphotyrosine proteome.Journal of proteome research · 2008Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The protein-tyrosine phosphatase Shp-2 is a positive modulator of the Ras/mitogen-activated protein kinase pathway and a putative substrate of the transforming non-receptor tyrosine kinase v-Src. To characterize the role of Shp-2 in cellular transformation and signaling by v-Src, we expressed v-Src in normal and Shp-2-deficient mouse embryo fibroblasts. Expression of Shp-2 was found to be necessary for morphological transformation by v-Src: Shp-2+/+ cells became rounded or spindly upon v-Src expression, whereas Shp-2-deficient cells remained relatively flat. v-Src-induced reorganization of the actin cytoskeleton and the formation of podosomes were compromised in Shp-2-deficient cells. Shp-2 deficiency also reduced v-Src-induced activation of the anti-apoptotic protein kinase Akt. The reduced activation of Akt in Shp-2-deficient cells correlated with a reduction in the association of the p85 regulatory subunit of PI3-kinase with the adapter protein Cbl. Activation of PI3-kinase by v-Src may be mediated by the association of the adapter protein Cbl with the p85 subunit. Since activation of Akt is dependent on PI3-kinase, this suggests that the effect of Shp-2 on Akt activation may be mediated, at least in part, by its effects on the interaction between PI3-kinase and Cbl. The defect in activation of the Akt survival pathway also correlated with enhanced sensitivity of Shp-2-deficient cells to an apoptosis-inducing agent. These results implicate Shp-2 in v-Src-induced cytoskeletal reorganization and activation of the Akt cell survival pathway.
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