From: Function, regulation and pathological roles of the Gab/DOS docking proteins
Genetic aberration | Leukemic disease | Involvement of Gab2 | References |
---|---|---|---|
Bcr-Abl translocation t(9;22) | CML, B-ALL | Recruitment of Grb2/Gab2 complex to Y177 of Bcr-Abl Y177 and Gab2 are essential for Bcr Abl-mediated transformation and leukemogenesis | |
Bcr-FGFR1 t(8;22) | CML-like disease | Recruitment of Grb2 and presumably Gab2 to Y177 of Bcr-Abl. Increased Gab2 tyrosine phosphorylation | [186] |
Tel-Abl translocation t(9;12) | B-ALL, T-ALL, CML | Recrutiment of Grb2/Gab2 complex to Y314 of Tel-Abl Y314 is essential for Tel Abl-mediated transformation and leukemogenesis | [191] |
Tel-Jak2 translocation t(9,12) | ALL | Some isoforms of Tel-JAK2 recruit the Grb2/Gab2 complex via Y314 | [190] |
Npm-Alk translocation t(2;5) | Anaplastic large cell lymphomas | Gab2, SHP2 and Grb2 form a complex with Npm-Alk | [242] |
SHP2 E76K point mutation | JMML | E76K mutation confers enhanced catalytic activity to SHP2 and requires Gab2 for transformation | [200] |
Sf-Stk | Friend's virus-induced erythroleukemia in mice | Recruitment of the Grb2/Gab2 complex to Sf-Stk is essential for erythroid transformation by Friend virus, this involves the direct binding of STAT3 to Gab2 | |
Amplification of MLL locus | AML/MDS | Gab2 is frequently co-amplified with the mixed lineage leukaemia (MLL) gene | [210] |