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Characterization of BCR-ABL deletion mutants from patients with chronic myeloid leukemia

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Characterization of BCR-ABL deletion mutants from patients with chronic myeloid leukemia

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Crizotinib acts as ABL1 inhibitor combining ATP-binding with allosteric inhibition and is active against native BCR-ABL1 and its resistance and compound mutants BCR-ABL1(T315I) and BCR-ABL1(T315I-E255K)

Rapid Screen for Tyrosine Kinase Inhibitor Resistance Mutations and Substrate Specificity

γ-Catenin-Dependent Signals Maintain BCR-ABL1+ B Cell Acute Lymphoblastic Leukemia

Allosteric kinase inhibitors

Differential signaling networks of Bcr-Abl p210 and p190 kinases in leukemia cells defined by functional proteomics

Structural and functional dissection of the DH and PH domains of oncogenic Bcr-Abl tyrosine kinase

Unpaired extracellular cysteine mutations of CSF3R mediate gain or loss of function

CRISPR-Cas9-mediated saturated mutagenesis screen predicts clinical drug resistance with improved accuracy

Allosteric regulation and targeting of Abl SH2-kinase interface and other cytoplasmic tyrosine kinases

Normal ABL1 is a tumor suppressor and therapeutic target in human and mouse leukemias expressing oncogenic ABL1 kinases