ArticleOncogene2005
The SH2-domian-containing inositol 5-phosphatase (SHIP)-2 binds to c-Met directly via tyrosine residue 1356 and involves hepatocyte growth factor (HGF)-induced lamellipodium formation, cell scattering and cell spreading.
Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 59 citations in OpenAlex.
- The power of five - inositol polyphosphate 5-phosphatase gene mutations at the intersection of development and disease.FEBS letters · 2026Review
- The HGF/MET Axis in Advanced Prostate Cancer: From Context-Dependent Biology to Biomarker-Driven Therapeutic Strategies.Cancers · 2026Review
- Identifying Qingkailing ingredients-dependent mesenchymal-epithelial transition factor-axiation "π" structuring module with angiogenesis and neurogenesis effects.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2024Article
- Structural Insights into the Binding Propensity of Human SHIP2 SH2 to Oncogenic CagA Isoforms fromInternational journal of molecular sciences · 2022Article
- Met-Controlled Allosteric Module of Neural Generation as A New Therapeutic Target in Rodent Brain Ischemia.Chinese journal of integrative medicine · 2021Article
- PTEN and Other PtdIns(3,4,5)PInternational journal of molecular sciences · 2020Review
- Solution structure of SHIP2 SH2 domain and its interaction with a phosphotyrosine peptide from c-MET.Archives of biochemistry and biophysics · 2018Article
- Functional Genome-wide Screen Identifies Pathways Restricting Central Nervous System Axonal Regeneration.Cell reports · 2018Article
- Coupling an EML4-ALK-centric interactome with RNA interference identifies sensitizers to ALK inhibitors.Science signaling · 2016Article
- Suppression of SHIP2 contributes to tumorigenesis and proliferation of gastric cancer cells via activation of Akt.Journal of gastroenterology · 2016Article
- Targeting MACC1 by RNA interference inhibits proliferation and invasion of bladder urothelial carcinoma in T24 cells.International journal of clinical and experimental pathology · 2015Article
- Physiological Signaling and Structure of the HGF Receptor MET.Biomedicines · 2014Review
- Opsismodysplasia resulting from an insertion mutation in the SH2 domain, which destabilizes INPPL1.American journal of medical genetics. Part A · 2014Article
- Evidence for SH2 domain-containing 5'-inositol phosphatase-2 (SHIP2) contributing to a lymphatic dysfunction.PloS one · 2014Article
- High SHIP2 expression indicates poor survival in colorectal cancer.Disease markers · 2014Article
- Targeting the epithelial to mesenchymal transition in glioblastoma: the emerging role of MET signaling.OncoTargets and therapy · 2014Review
- High expression of inositol polyphosphate phosphatase-like 1 associates with unfavorable survival in hepatocellular carcinoma.International journal of clinical and experimental pathology · 2013Article
- The SH2-domain-containing inositol 5-phosphatase (SHIP) limits the motility of neutrophils and their recruitment to wounds in zebrafish.Journal of cell science · 2012Article
- An overview of the c-MET signaling pathway.Therapeutic advances in medical oncology · 2011Article
- LyGDI, a novel SHIP-interacting protein, is a negative regulator of FcγR-mediated phagocytosis.PloS one · 2011Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recently, evidence has been accumulating that inositol and phosphatidylinositol polyphosphate play important roles in a variety of signal transduction systems including membrane traffic, actin cytoskeleton rearrangement and cell motility. In this paper, we show for the first time that the SH2-domain-containing inositol 5-phosphatase (SHIP)-2 binds directly to the hepatocyte growth factor (HGF/SF) receptor, c-Met, via phosphotyrosine 1356. HGF induces the breakdown of cell junctions and the dispersion of colonies of epithelial cells including MDCK cells. Whereas only few lamellipodia are observed in MDCK cells 2 min after stimulation with HGF, both SHIP-2- and SHIP-1-overexpressing cells form large, broad lamellipodia. The number of lamellipodia is 2-4-fold greater than that of mock-transfected MDCK cells in the same time period and SHIP is found to colocalize with actin at the leading edge. Furthermore, overexpression of a catalytic inactive mutant of SHIP-2 suppresses HGF-potentiated cell scattering and cell spreading, although these mutant-expressing cells form enhanced number of lamellipodia 2 min after HGF stimulation. Interestingly, cells expressing a mutant lacking the proline-rich domain of SHIP-2 at the C-terminal form few lamellipodia, but still spread and scatter upon stimulation with HGF at a reduced rate. These data suggest that phosphatase activity is required for HGF-mediated cell spreading and scattering but not for alteration of lamellipodium formation, while the proline-rich region influences lamellipodium formation. Furthermore, treatment with 10 microM of phosphatidylinositol 3 (PI3) kinase inhibitor, LY294002, abrogates HGF-induced cell scattering of SHIP-2-overexpressing cells but not parental HEK293 cells, suggesting that a balance between PI3 kinase and SHIP is important for cell motility.
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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.