Title : BCR-ABL tyrosine kinase inhibition induces metabolic vulnerability by preventing the integrated stress response in K562 cells.

Pub. Date : 2018 Oct 12

PMID : 30217442






1 Functional Relationships(s)
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1 Treatment of CML-derived K562 cells with BCR-ABL tyrosine kinase inhibitors, including imatinib, dasatinib, nilotinib and ponatinib, prevented activation of eIF2alpha kinases, protein kinase-like endoplasmic reticulum kinase (PERK) and general control nonderepressible 2, and downstream ATF4 induction during metabolic stress. ponatinib ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens