A Direct Binding Site for Grb2 Contributes to Transformation and Leukemogenesis by the Tel-Abl (ETV6-Abl) Tyrosine Kinase
Author:
Affiliation:
1. The Center for Blood Research and Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115
2. Department of Biomedical Research, St. Elizabeths Hospital and Tufts University School of Medicine, Boston, Massachusetts 02135
Abstract
Publisher
American Society for Microbiology
Subject
Cell Biology,Molecular Biology
Link
https://journals.asm.org/doi/pdf/10.1128/MCB.24.11.4685-4695.2004
Reference63 articles.
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2. Brasher, B. B., S. Roumiantsev, and R. A. Van Etten. 2001. Mutational analysis of the regulatory function of the c-Abl Src homology 3 domain. Oncogene 20 : 7744-7752.
3. Brunel, V., D. Sainty, N. Carbuccia, M. Mozzicolacci, F. Fernandez, J. Simonetti, J. Gabert, P. Dubreuil, M. Lafage-Pochitaloff, and F. Birg. 1996. A TEL/ABL fusion gene on chromosome 12p13 in a case of Ph−, BCR− atypical CML. Leukemia 10 : 2003.
4. Carroll, M., S. Ohno-Jones, S. Tamura, E. Buchdunger, J. Zimmermann, N. B. Lydon, D. G. Gilliland, and B. J. Druker. 1997. CGP 57148, a tyrosine kinase inhibitor, inhibits the growth of cells expressing BCR-ABL, TEL-ABL, and TEL-PDGFR fusion proteins. Blood 90 : 4947-4952.
5. Structural and signaling requirements for BCR-ABL-mediated transformation and inhibition of apoptosis
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