| Predicate | Object |
|---|---|
| rdf:type | |
| biopax3:comment |
Overexpressed FGFR2 in gastric and breast cancer cells has been shown to undergo ligand-independent dimerization (Takeda, 2007; Kunii, 2008; Moffa, 2004; Turner, 2010). Full-length FGFR2 is weakly transforming in NIH 3T3 cells, and is thought to possess a transformation-inhibiting domain in the C-terminus (Itoh, 1994). Interestingly, many cancers with amplifications of FGFR2 show preferrential expression of C-terminally truncated FGFR2 variants, designated C2 and C3, with 788 or 769 residues instead of the wild-type 822 (Hattori, 1990; Itoh, 1994; Ueda, 1999). These variants, which lack a number of carboxy-terminal tyrosine residues, show increased transforming potency compared to the full-length receptor (Cha, 2008; Cha, 2009), and have been shown to be constitutively active and to dimerize spontaneously (Takeda, 2007).
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| biopax3:xref |
http://identifiers.org/pubmed/10626794,
http://identifiers.org/pubmed/15561780,
http://identifiers.org/pubmed/17505008,
http://identifiers.org/pubmed/18337450,
http://identifiers.org/pubmed/18381441,
http://identifiers.org/pubmed/19103595,
http://identifiers.org/pubmed/20101236,
http://identifiers.org/pubmed/2377625,
http://identifiers.org/pubmed/8205545
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| biopax3:evidenceCode |