Please use this identifier to cite or link to this item:
|Type:||Artigo de periódico|
|Title:||BCR-ABL binds to IRS-1 and IRS-1 phosphorylation is inhibited by imatinib in K562 cells|
|Abstract:||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. (C) 2002 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved.|
chronic myeloid leukemia
|Editor:||Elsevier Science Bv|
|Appears in Collections:||Artigos e Materiais de Revistas Científicas - Unicamp|
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.