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Table 1 Oncogenic events in human and murine leukemias involving Gab2

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
[185, 187]
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
[36, 81]
Amplification of MLL locus AML/MDS Gab2 is frequently co-amplified with the mixed lineage leukaemia (MLL) gene [210]