Publication year
2002Source
Cell, 108, 2, (2002), pp. 247-59ISSN
Publication type
Article / Letter to editor

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Organization
Cell Biology (UMC)
Journal title
Cell
Volume
vol. 108
Issue
iss. 2
Page start
p. 247
Page end
p. 59
Subject
Study of abnormal differentiation and transformation processes in heritable and acquired disorders with the use of cell and animal models; Bestudering van abnormale differentiatie en transformatieprocessen bij erfelijke of verworven aandoeningen m.b.v. cel- en diermodellenAbstract
Despite years of investigation, the molecular mechanism responsible for regulation of the c-Abl tyrosine kinase has remained elusive. We now report inhibition of the catalytic activity of purified c-Abl in vitro, demonstrating that regulation is an intrinsic property of the molecule. We show that the interaction of the N-terminal 80 residues with the rest of the protein mediates autoregulation. This N-terminal "cap" is required to achieve and maintain inhibition, and its loss turns c-Abl into an oncogenic protein and contributes to deregulation of BCR-Abl.
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