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A. M. Pendergast, L. A. Quillian, L. D. Cripe, C. H. Bassing, Z. Dai, N. Li, A. Batzer, K. M. Rabun, C. J. Der, J. Schlessinger and M. L. Gishizky, “BCR-ABL Induced Oncogenesis Is Mediated by Direct Interaction with the SH2 Domain of the GRB2 Adaptor Protein,” Cell, Vol. 75, 1993, pp. 175-185.

has been cited by the following article:

• 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.