FLT3 mutants recruit PIK3R1 through phosphorylated GAB2

Stable Identifier
R-HSA-9698179
Type
Reaction [binding]
Species
Homo sapiens
Compartment
cytosol, plasma membrane
ReviewStatus
5/5
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FLT3 mutants recruit PIK3R1 through phosphorylated GAB2
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FLT3 ITD mutants signal through the PI3K/AKT pathway in a GRB2-GAB2-dependent manner. As is the case for the wild-type receptor, FLT3 ITD-associated GAB2 is phosphorylated and recruits the p85 regulatory subunit of PI3K to the activated receptor (Masson et al, 2009; Zhang et al, 1999; Zhang et al, 2000). Other FLT3-interacting adaptor proteins have also been shown to bind to p85 and may additionally contribute to PI3K/AKT signaling downstream of FLT3; these alternate mechanisms are not shown in this pathway (reviewed in Kazi and Ronnstrand, 2019).
Literature References
Participants
Input
Output
Participates
as an event of
Normal reaction
Active FLT3:GRB2:p-Y-GAB2 binds PIK3R1 (Homo sapiens)
Functional status

Gain of function of p-6Y FLT3 mutant dimers:GRB2:p-Y GAB2 [plasma membrane]

Normal Entity
Disease Entity
Status
Inferred From
Active Flt3:Grb2:p-Y-Gab2 binds Pik3r1 (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  (2020-08-24)
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