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Model of ABD/SHP1c-mediated inhibition of BCR/ABL signaling. The ABD of the fusion protein directs binding to BCR/ABL through complementary interactions with the SH2 and SH3 domains of ABL (23). This brings the PTP domain (SHP1c) of the fusion protein into proximity with the ABL kinase domain. The active PTP may inhibit signaling by reversing the autophosphorylation of ABL (A) and/or by releasing phosphate from newly phosphorylated ABL substrates (B).
