FLT3 fusions phosphorylate GAB2

Stable Identifier
R-HSA-9703438
Type
Reaction [transition]
Species
Homo sapiens
Compartment
ReviewStatus
5/5
Locations in the PathwayBrowser
General
SVG |   | PPTX  | SBGN
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
GAB2 is presumed to be phosphorylated downstream of active FLT3 fusion proteins, but this has not been directly demonstrated. ETV6-FLT3 is unable to transform primary myeloid cells from the bone marrow of Gab2-/- mice, implicating signaling through this pathway (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
Participates
Catalyst Activity

protein tyrosine kinase activity of p-Y FLT3 fusions:GRB2:GAB2 [cytosol]

Disease
Name Identifier Synonyms
cancer DOID:162 malignant tumor, malignant neoplasm, primary cancer
Authored
Reviewed
Created
Cite Us!