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BCR‐ABL binds to IRS‐1 and IRS‐1 phosphorylation is inhibited by imatinib in K562 cells
Author(s) -
Traina Fabı́ola,
Carvalheira José Barreto C,
Saad Mario J.A,
Costa Fernando F,
Saad Sara T.O
Publication year - 2003
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(02)03845-0
Subject(s) - k562 cells , tyrosine kinase , cancer research , imatinib , abl , breakpoint cluster region , chemistry , imatinib mesylate , kinase , microbiology and biotechnology , biology , signal transduction , receptor , biochemistry , cell , myeloid leukemia
In the present study we used K562 cells to demonstrate that insulin receptor substrate 1 (IRS‐1) is expressed and constitutively phosphorylated in BCR‐ABL + cells. We observed association between BCR‐ABL/IRS‐1, IRS‐1/phosphoinositide 3′‐kinase (PI3‐kinase), and IRS‐1/Grb2 in the K562 cell line. Our findings demonstrate that imatinib treatment resulted in marked attenuation of BCR‐ABL/IRS‐1 association and of IRS‐1‐stimulated PI3‐kinase activity in K562 cells. We concluded that the IRS‐1 protein is involved in the signalling pathway of the BCR‐ABL tyrosine kinase.