Article citationsMore>>
F. E. Nicolini, M. J. Mauro, G. Martinelli, D. W. Kim, S. Soverini, M. C. Muller, A. Hochhaus, J. Cortes, C. Chuah, I. H. Dufva, J. F. Apperley, F. Yagasaki, J. D. Pearson, S. Peter, C. S. Rodriguez, C. Preudhomme, F. Giles, J. M. Goldman and W. Zhou, “Epidemiologic Study on Survival of Chronic Myeloid Leukemia and Ph(+) Acute Lymphoblastic Leukemia Patients with BCR-ABL T315I Mutation,” Blood, Vol. 114, No. 26, 2009, pp. 5271-5278.
http://dx.doi.org/10.1182/blood-2009-04-219410
has been cited by the following article:
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TITLE:
Distinct Transforming Activity of ABL Family Tyrosine Kinase Oncogenes Is Induced by Their C-Terminal Domain*
AUTHORS:
Keiko Okuda, Hideyo Hirai
KEYWORDS:
Leukemia; Chimeric Oncogene; ABL Family Tyrosine Kinase; Signal Transduction
JOURNAL NAME:
Open Journal of Blood Diseases,
Vol.3 No.3A,
November
4,
2013
ABSTRACT: The TEL/ARG oncogene is similar in structure to the TEL/ABL fusion found in human leukemia, however, we have demonstrated previously that the expression of TEL/ARG in Ba/F3 cells does not sustain strong activity of proliferation, whereas, that of TEL/ABL appeared to induce immediate cell proliferation. To study the molecular basis of the difference in the transforming activity of TEL/ARG and TEL/ABL, TEL/ARG mutants that swapped the kinase domain or C-terminus of ARG with the corresponding domain in ABL were generated, and each mutant was expressed in Ba/F3 cells. A TEL/ARG mutant containing the ABL kinase domain was similar to TEL/ARG in this study, but replacing the ARG C-terminal domain with that of ABL resulted in accelerated proliferation that was similar to that of TEL/ABL. When expressed in primary mouse bone marrow cells by retroviral transduction, spontaneous colony formation in methylcellulose culture was observed, in a fashion dependent on the C-terminal portion of ABL. These results indicate that distinct bio-phenotypes associated with these oncogenes are likely to be regulated by their C-termini, and the C-terminus of ARG contains a functional subdomain that impairs the growth signal induced by ABL family tyrosine kinase.