Phosphorylated FLT3 fusions bind GRB2

Stable Identifier
R-HSA-9703442
Type
Reaction [binding]
Species
Homo sapiens
Compartment
cytosol
ReviewStatus
5/5
Locations in the PathwayBrowser
Expand all
General
SVG | 
PNG
Low
Medium
High
 | PPTX  | SBGN
Phosphorylated FLT3 fusions bind GRB2
Click the image above or here to open this reaction in the Pathway Browser
The layout of this reaction may differ from that in the pathway view due to the constraints in pathway layout
FLT3 fusion proteins may signal through the PI3K/AKT and MAP kinase signaling pathway by first recruiting GRB2 to the phosphorylated receptor. This has been directly demonstrated for one of the ETV6-FLT3 fusions, where GRB2 binding was shown to depend on tyrosine residues corresponding to Y314 and Y354 of the ETV6 portion and Y768, Y955 and Y969 of the FLT3 portion. Mutation of these residues to phenylalanies abrogates GRB2 binding and interferes with downstream signaling and the ability of the fusion protein to transform BaF3 cells to IL-3-independent growth (Chonabayashi et al, 2013).
Literature References
PubMed ID Title Journal Year
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
Participants
Input
Output
Participates
as an event of
Inferred From
Active Flt3 dimer binds Grb2 (Mus musculus)
Disease
Name Identifier Synonyms
cancer DOID:162 malignant tumor, malignant neoplasm, primary cancer
Authored
Rothfels, K  (2020-11-06)
Reviewed
Kazi, JU  (2020-11-06)
Created
Rothfels, K  (2020-10-06)
Cite Us!