FLT3 mutant dimers:GRB2 bind SOS1

Stable Identifier
Reaction [binding]
Homo sapiens
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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).
Literature References
PubMed ID Title Journal Year
31066629 FMS-like Tyrosine Kinase 3/FLT3: From Basic Science to Clinical Implications

Kazi, JU, Rönnstrand, L

Physiol. Rev. 2019
11090077 Flt3 mutations from patients with acute myeloid leukemia induce transformation of 32D cells mediated by the Ras and STAT5 pathways

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

Blood 2000
10698507 Tandem-duplicated Flt3 constitutively activates STAT5 and MAP kinase and introduces autonomous cell growth in IL-3-dependent cell lines

Hayakawa, F, Saito, H, Towatari, M, Tanimoto, M, Naoe, T, Kitamura, T, Kiyoi, H

Oncogene 2000
21262971 Protein-tyrosine phosphatase DEP-1 controls receptor tyrosine kinase FLT3 signaling

Bauer, R, Godfrey, R, Masson, K, Müller, JP, Schons, J, Böhmer, SA, Tänzer, S, Razumovskaya, E, Böhmer, FD, Arora, D, Stopp, S, Rönnstrand, L

J. Biol. Chem. 2011
10080542 Flt3 signaling involves tyrosyl-phosphorylation of SHP-2 and SHIP and their association with Grb2 and Shc in Baf3/Flt3 cells

Mantel, C, Zhang, S, Broxmeyer, HE

J. Leukoc. Biol. 1999
Normal reaction
Functional status

Gain of function of p-6Y FLT3 mutant dimers:GRB2 [plasma membrane]

Name Identifier Synonyms
cancer DOID:162 malignant tumor, malignant neoplasm, primary cancer
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