SOS1 is presumed to be recruited to FLT3 receptors through interaction with GRB2, as is the case for the wild-type receptor (reviewed in Kazi and Ronnstrand, 2019). SOS is a nucleotide exchange factor for RAS and activates signaling through the RAS-RAF-MAPK pathway downstream of oncogenic FLT3 mutants (Zhang et al, 1999; Mizuki et al, 2000; Hayakawa et al, 2000; Voisset et al, 2010; Arora et al, 2011; reviewed in Kazi and Ronnstrand, 2019).
Kazi, JU, Rönnstrand, L
Büchner, T, Kratz-Albers, K, Serve, H, Matsumura, I, Müller, C, Serve, S, Steur, C, Kanakura, Y, Berdel, WE, Schmidt, R, Halfter, H, Fenski, R, Grüning, W, Kienast, J, Mizuki, M
Hayakawa, F, Saito, H, Towatari, M, Tanimoto, M, Naoe, T, Kitamura, T, Kiyoi, H
Bauer, R, Godfrey, R, Masson, K, Müller, JP, Schons, J, Böhmer, SA, Tänzer, S, Razumovskaya, E, Böhmer, FD, Arora, D, Stopp, S, Rönnstrand, L
Mantel, C, Zhang, S, Broxmeyer, HE
Gain of function of p-6Y FLT3 mutant dimers:GRB2 [plasma membrane]
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