P210 Bcr-Abl Interacts with the Interleukin 3 Receptor βc Subunit and Constitutively Induces Its Tyrosine Phosphorylation

作者: Pierre Laneuville , Pierre Laneuville , Ralph B. Arlinghaus , Jeanne Wilson-Rawls , Shanhai Xie

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

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