P210 Bcr-Abl interacts with the interleukin 3 receptor β(c) subunit and constitutively induces its tyrosine phosphorylation

Jeanne Wilson-Rawls, Shanhai Xie, Jiaxin Liu, Pierre Laneuville, Ralph B. Arlinghaus

Research output: Contribution to journalArticle

58 Scopus citations

Abstract

Chronic myelogenous leukemia is a neoplasm of pluripotent hematopoietic cells. The P210 Bcr-Abl oncoprotein is a deregulated cytoplasmic tyrosine kinase that has been shown to cause chronic myelogenous leukemia-like neoplasms in mice. Cytokines such as interleukin 3 and granulocyte/macrophage-colony-stimulating factor regulate the growth and differentiation of hematopoietic precursors. These cytokines activate two distinct signals to the nucleus. One signal is through the Ras pathway, and the second involves activation of Jak2. We demonstrated that Bcr-Abl co- immunoprecipitates with, and constitutively phosphorylates, the common β(c) subunit of the interleukin 3 and granulocyte/macrophage-colony-stimulating factor receptors. Our data show that formation of this complex leads to the constitutive tyrosine phosphorylation of Jak2. It has been demonstrated that Bcr-Abl interacts with Grb2 and Shc, which in turn activates the Ras pathway. Our new findings raise the possibility that Bcr-Abl activates signaling through both pathways in a factor-independent fashion.

Original languageEnglish (US)
Pages (from-to)3426-3430
Number of pages5
JournalCancer Research
Volume56
Issue number15
StatePublished - Aug 1 1996

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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