The gatekeeper mutation T315I confers resistance against small molecules by increasing or restoring the ABL-kinase activity accompanied by aberrant transphosphorylation of endogenous BCR, even in loss-of-function mutants of BCR/ABL

Leukemia

Volumn 23, Issue 9, 2009, Pages 1614-1621

  Mian, A A ^a   Schull M ^a   Zhao, Z ^a   Oancea, C ^a   Hundertmark, A ^a   Beissert, T ^a   Ottmann, O G ^a   Ruthardt, M ^a  

^a GOETHE UNIVERSITY   (Germany)

Author keywords

'gatekeeper' mutation T315I; BCR ABL; Imatinib resistance; Inhibition of oligomerization; Philadelphia chromosome positive leukemia

Indexed keywords

ABELSON KINASE; BCR ABL PROTEIN; BREAKPOINT CLUSTER REGION PROTEIN;

ANIMAL; ARTICLE; CELL LINE; CHRONIC MYELOID LEUKEMIA; DRUG ANTAGONISM; DRUG RESISTANCE; GENETICS; HUMAN; METABOLISM; MUTATION; PHOSPHORYLATION; RAT;

ANIMALS; CELL LINE; DRUG RESISTANCE, NEOPLASM; FUSION PROTEINS, BCR-ABL; HUMANS; LEUKEMIA, MYELOGENOUS, CHRONIC, BCR-ABL POSITIVE; MUTATION; PHOSPHORYLATION; PROTO-ONCOGENE PROTEINS C-ABL; PROTO-ONCOGENE PROTEINS C-BCR; RATS;

EID: 70349308803     PISSN: 08876924     EISSN: 14765551     Source Type: Journal    
DOI: 10.1038/leu.2009.69     Document Type: Article

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