FGFR1- and PTPN11- associated PI3K phosphorylates PIP2 to PIP3
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Once recruited to the activated receptor, PI3K phosphorylates PIP2 to PIP3, leading to activation of AKT signaling. PI3K signaling has been demonstrated in ZMYM2-, FOP- and BCR-FGFR1 fusions (Chen, 2004; Demiroglu, 2001; Guasch, 2001), as well as downstream of a number of other FGFR mutants (see for instance, Byron, 2008; Kunii, 2008; Agazie, 2003; Takeda, 2007).
一旦被激活的受体招募,PI3K将PIP2磷酸化为PIP3,进而激活AKT信号通路。PI3K信号通路已在ZMYM2、FOP以及BCR-FGFR1融合(Chen,2004;Demiroglu,2001;Guasch,2001)中得以证实,同时也在众多FGFR突变体下游得到验证(例如,参见Byron,2008;Kunii,2008;Agazie,2003;Takeda,2007)。
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