MedicineMolecular BiologyOncologyApoptosisGene ExpressionMolecular OncologyCancer Cell SignalingGlial Cell Molecular BiologyGlial Gene ExpressionGlioblastomaOncogenic Signaling PathwaysCell Growth RegulationCell Survival AssaysCrispr-cas9 KnockoutErk SignalingGlioblastoma Cell SignalingPotential FunctionsPrimary CellsProtein Expression Levels
. In human glioma tissues and cells, Ninj2 co-immunoprecipitated with multiple receptor tyrosine kinases (EGFR, PDGFRβ and FGFR), required for downstream Akt and Erk activation. Akt and Erk activation was potently inhibited by Ninj2 shRNA or knockout, but enhanced with ectopic Ninj2 overexpression in glioma cells. In summary, we show that Ninj2 overexpression promotes glioma cell growth.
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