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Medline ® Abstract for Reference 47

of '慢性髓系白血病的细胞和分子生物学'

47
TI
Autoinhibition of c-Abl.
AU
Pluk H, Dorey K, Superti-Furga G
SO
Cell. 2002;108(2):247.
 
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.
AD
Developmental Biology Programme, European Molecular Biology Laboratory, 69117 Heidelberg, Germany.
PMID