Mechanisms of Autoinhibition and STI-571/Imatinib Resistance Revealed by Mutagenesis of BCR-ABL
Top Cited Papers
- 1 March 2003
- journal article
- research article
- Published by Elsevier BV in Cell
- Vol. 112 (6), 831-843
- https://doi.org/10.1016/s0092-8674(03)00190-9
Abstract
No abstract availableKeywords
This publication has 40 references indexed in Scilit:
- In Vitro Evolution of Recognition Specificity Mediated by SH3 Domains Reveals Target Recognition RulesJournal of Biological Chemistry, 2002
- Autoinhibition of c-AblCell, 2002
- Clinical Resistance to STI-571 Cancer Therapy Caused by BCR-ABL Gene Mutation or AmplificationScience, 2001
- Activity of a Specific Inhibitor of the BCR-ABL Tyrosine Kinase in the Blast Crisis of Chronic Myeloid Leukemia and Acute Lymphoblastic Leukemia with the Philadelphia ChromosomeNew England Journal of Medicine, 2001
- Structural Mechanism for STI-571 Inhibition of Abelson Tyrosine KinaseScience, 2000
- Mutational investigation of the specificity determining region of the src SH2 domainJournal of Molecular Biology, 2000
- The P190, P210, and P230 Forms of the BCR/ABL Oncogene Induce a Similar Chronic Myeloid Leukemia–like Syndrome in Mice but Have Different Lymphoid Leukemogenic ActivityThe Journal of Experimental Medicine, 1999
- An intramolecular SH3-domain interaction regulates c-Abl activityNature Genetics, 1998
- Three-dimensional structure of the tyrosine kinase c-SrcNature, 1997
- BCR sequences essential for transformation by the BCR-ABL oncogene bind to the ABL SH2 regulatory domain in a non-phosphotyrosine-dependent mannerCell, 1991