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• W1569363665 startingPage "820" @default.
• W1569363665 abstract "Abstract We have characterized the cell cycle deficit of a novel TrkA receptor mutant (TrkAS3) that fails to support nerve growth factor (NGF)‐dependent cell cycle arrest and neurite outgrowth. TrkAS3 receptors fail to support an NGF‐dependent increase in the expression of cyclin D1 and the cell cycle inhibitor, p21 Waf1/Cip1 , two important regulators of G 1 /S transition, and do not down‐regulate expression of the G 2 /M phase marker, cdc2/cdk1, or the S phase marker, proliferating cell nuclear antigen. Moreover, NGF‐activated TrkAS3 receptors do not down‐regulate cyclin‐dependent kinase 4 phosphorylation of the retinoblastoma protein, essential for G 1 arrest, in comparison to NGF‐activated wild‐type TrkA. Collectively these data indicate that TrkAS3 receptors fail to support NGF‐dependent G 1 arrest. Interestingly, ectopic expression of regulators of G 1 /S arrest, such as cyclin D1 or inhibitors of cell cycle (p21 Waf1/Cip1 , p16 INK4A ), or the fibroblast growth factor (FGF) receptor substrate‐2 (FRS2) in cells expressing TrkAS3 reconstitutes NGF‐dependent neurite outgrowth. Collectively, these data suggest a model in which NGF‐stimulated TrkA‐dependent activation of FRS2 supports neurite outgrowth through a mechanism that likely involves the induction of p21 Waf1/Cip1 expression and the arrest of cells at G 1 /S." @default.
• W1569363665 created "2016-06-24" @default.
• W1569363665 creator A5007109487 @default.
• W1569363665 creator A5012787721 @default.
• W1569363665 date "2002-05-07" @default.
• W1569363665 modified "2023-10-13" @default.
• W1569363665 title "Overexpression of the signaling adapter FRS2 reconstitutes the cell cycle deficit of a nerve growth factor non-responsive TrkA receptor mutant" @default.
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• W1569363665 doi "https://doi.org/10.1046/j.1471-4159.2002.00867.x" @default.
• W1569363665 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/12065641" @default.
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