BCR-ABL binds to IRS-1 and IRS-1 phosphorylation is inhibited by imatinib in K562 cells-Reference-Cited by-同舟云学术

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BCR-ABL binds to IRS-1 and IRS-1 phosphorylation is inhibited by imatinib in K562 cells

Published:2002-12-23 Issue:1-3 Volume:535 Page:17-22
ISSN:0014-5793
Container-title:FEBS Letters
language:en
Short-container-title:

Author:

Traina Fabı́ola,Carvalheira José Barreto C,Saad Mario J.A,Costa Fernando F,Saad Sara T.O

Publisher

Wiley

Subject

Cell Biology,Genetics,Molecular Biology,Biochemistry,Structural Biology,Biophysics

Link

http://onlinelibrary.wiley.com/wol1/doi/10.1016/S0014-5793(02)03845-0/fullpdf

Reference31 articles.

1. Structural and signaling requirements for BCR-ABL-mediated transformation and inhibition of apoptosis

2. The molecular biology of chronic myeloid leukemia

3. Effects of a selective inhibitor of the Abl tyrosine kinase on the growth of Bcr–Abl positive cells

4. Inhibition of the ABL Kinase Activity Blocks the Proliferation of BCR/ABL+Leukemic Cells and Induces Apoptosis

5. The Tyrosine Kinase Inhibitor CGP57148B Selectively Inhibits the Growth of BCR-ABL–Positive Cells

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2. NT157, an IGF1R-IRS1/2 inhibitor, exhibits antineoplastic effects in pre-clinical models of chronic myeloid leukemia;Investigational New Drugs;2021-01-06

3. Insulin Substrate Receptor (IRS) proteins in normal and malignant hematopoiesis;Clinics;2018-10-09

4. De novo AML exhibits greater microenvironment dysregulation compared to AML with myelodysplasia-related changes;Scientific Reports;2017-01-13

5. IRS2 silencing increases apoptosis and potentiates the effects of ruxolitinib in JAK2V617F-positive myeloproliferative neoplasms;Oncotarget;2016-01-09

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