The c-KIT mutation causing human mastocytosis is resistant to STI571 and other KIT kinase inhibitors; kinases with enzymatic site mutations show different inhibitor sensitivity profiles than wild-type kinases and those with regulatory-type mutations.

@article{Ma2002TheCM,
  title={The c-KIT mutation causing human mastocytosis is resistant to STI571 and other KIT kinase inhibitors; kinases with enzymatic site mutations show different inhibitor sensitivity profiles than wild-type kinases and those with regulatory-type mutations.},
  author={Yongsheng Ma and Shan Zeng and Dean D Metcalfe and Cem Akin and Sa{\vs}a Dimitrijevi{\'c} and Joseph Butterfield and Gerald McMahon and B. Jack Longley},
  journal={Blood},
  year={2002},
  volume={99 5},
  pages={1741-4}
}
Mutations of c-KIT causing spontaneous activation of the KIT receptor kinase are associated with sporadic adult human mastocytosis (SAHM) and with human gastrointestinal stromal tumors. We have classified KIT-activating mutations as either "enzymatic site" type (EST) mutations, affecting the structure of the catalytic portion of the kinase, or as "regulatory" type (RT) mutations, affecting regulation of an otherwise normal catalytic site. Using COS cells expressing wild-type or mutant KIT, 2… CONTINUE READING

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