FLT3 fusions:GRB2 bind SOS1

Stable Identifier
R-HSA-9703430
Type
Reaction [binding]
Species
Homo sapiens
Compartment
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Activated FTL3 fusion mutants have been shown to signal through the MAP kinase pathway as assessed through increased levels of phosphorylated ERK/MAPK proteins (Grand et al, 2007; Vu et al, 2009; Troadec et al, 2017; Chonabayashi et al, 2013; reviewed in Kazi and Roonstrand, 2019). The RAS guanine nucleotide exchange factor (GEF) SOS1 is presumed to be recruited downstream of GRB2 binding to FLT3 fusion protein, but this has not been directly demonstrated.

Literature References
PubMed ID Title Journal Year
19345670 The juxtamembrane domain in ETV6/FLT3 is critical for PIM-1 up-regulation and cell proliferation

Xinh, PT, Vu, HA, Kano, Y, Tokunaga, K, Sato, Y

2009
23168613 Direct binding of Grb2 has an important role in the development of myeloproliferative disease induced by ETV6/FLT3

Ishikawa, T, Kawamata, S, Ohno, T, Chonabayashi, K, Hishizawa, M, Uchiyama, T, Nagai, Y, Takaori-Kondo, A

Leukemia 2013
31066629 FMS-like Tyrosine Kinase 3/FLT3: From Basic Science to Clinical Implications

Kazi, JU, Rönnstrand, L

Physiol. Rev. 2019
27795560 A novel t(3;13)(q13;q12) translocation fusing FLT3 with GOLGB1: toward myeloid/lymphoid neoplasms with eosinophilia and rearrangement of FLT3?

Petit, B, Dobbelstein, S, Chauzeix, J, Touati, M, Gachard, N, Faumont, N, Bertrand, P, Troadec, E, Trimoreau, F, Bordessoule, D, Bastard, C, Feuillard, J

2017
17764812 A constitutively active SPTBN1-FLT3 fusion in atypical chronic myeloid leukemia is sensitive to tyrosine kinase inhibitors and immunotherapy

Grand, FH, Zhang, L, Russell, NH, Cross, NC, Chase, A, Iqbal, S

2007
Participants
Participates
Disease
Name Identifier Synonyms
cancer DOID:162 malignant tumor, malignant neoplasm, primary cancer
Authored
Reviewed
Created
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