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Recruitment of GAB2 to the BCR-FGFR1 fusion protein results in GAB2 phosphorylation (Roumiatnetsev, 2004). As in the case of BCR-ABL (Sattler, 2002), recruitment and phosphorylation of GAB2 is dependent on BCR residue Y177. Deletion of Y177 abolishes GRB2 recruitment and converts the more aggressive MPD disorder induced by BCR-FGFR1 to the EMS characteristic of other FGFR1 fusions (Demiroglu, 2001; Roumianetsev, 2004)
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