FLT3 mutants recruit PIK3CA through PIK3R1

The 110 kDa catalytic subunit of PI3K is recruited to the mutant FLT3 receptor through interaction with the p85 regulatory subunit, as is the case for the wild-type receptor. GAB2-mediated conformational changes in the p85 regulatory subunit stimulate interaction with p110, and promote PI3K/AKT signaling downstream of activated FLT3 (Zhang et al, 1999; Zhang et al, 2000; Masson et al, 2009; Mandelker et al, 2009; Burke et al, 2011; reviewed in Kazi and Ronnstrand, 2019).

PI3K的110 kDa催化亚基通过与p85调控亚基的相互作用而被募集至突变型FLT3受体，此现象与野生型受体相似。GAB2介导的p85调控亚基构象变化刺激其与p110的相互作用，并促进激活的FLT3下游的PI3K/AKT信号传导（参见Zhang等，1999；Zhang等，2000；Masson等，2009；Mandelker等，2009；Burke等，2011；Kazi和Ronnstrand，2019年综述）。