The SH2 domain of ABL is not required for factor-independent growth induced by BCR-ABL in a murine myeloid cell line

Tsukasa Oda, Shu Tamura, Tetsuya Matsuguchi, James D. Griffin, Brian J. Druker

Research output: Contribution to journalArticlepeer-review

40 Scopus citations

Abstract

Chronic myelogenous leukemia (CML) is characterized by the presence of a specific chromosomal translocation between the long arms of chromosomes 9 and 22 that results in the fusion of BCR encoded sequences upstream of exon 2 of c-ABL. This fusion gene produces a 210-kDa chimeric BCR-ABL protein that has elevated tyrosine kinase activity. Several substrates of this activated tyrosine kinase have been reported. However, their necessity for the transforming functions of BCR-ABL has not been determined. A specific deletion of the SH2 domain of ABL was created to determine whether this mutation would alter the ability of BCR-ABL to induce factor-independent growth of a murine myeloid cell line and to determine whether the SH2 domain mediates the interaction of BCR-ABL with any of its substates. Our results indicate that the SH2 domain of BCR-ABL is not required for the induction of growth factor independence and is not required for the association of BCR-ABL with rasGAP or SHC. However, myeloid cells expressing this mutant lack the tyrosine phosphorylation of a 62-kDa ras-GAP associated protein.

Original languageEnglish (US)
Pages (from-to)295-301
Number of pages7
JournalLeukemia
Volume9
Issue number2
StatePublished - Feb 1995

Keywords

  • BCR-ABL
  • CML
  • Philadelphia chromosome

ASJC Scopus subject areas

  • Hematology
  • Oncology
  • Cancer Research

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