Sole BCR-ABL inhibition is insufficient to eliminate all myeloproliferative disorder cell populations.
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Selective regulation of lymphopoiesis and leukemogenesis by individual zinc fingers of IkarosKinase-independent mechanisms of resistance of leukemia stem cells to tyrosine kinase inhibitorsA conserved water-mediated hydrogen bond network defines bosutinib's kinase selectivityIdentification of host-targeted small molecules that restrict intracellular Mycobacterium tuberculosis growthHIV-1 Nef interaction influences the ATP-binding site of the Src-family kinase, HckTarget discovery in small-molecule cell-based screens by in situ proteome reactivity profiling.Clinical targeting of mutated and wild-type protein tyrosine kinases in cancer.BUB3 that dissociates from BUB1 activates caspase-independent mitotic death (CIMD).Chemical genomic profiling to identify intracellular targets of a multiplex kinase inhibitor.Expression of a Src family kinase in chronic myelogenous leukemia cells induces resistance to imatinib in a kinase-dependent manner.Deoxycytidine kinase augments ATM-Mediated DNA repair and contributes to radiation resistanceEnhanced paracrine FGF10 expression promotes formation of multifocal prostate adenocarcinoma and an increase in epithelial androgen receptorAssignment of protein function in the postgenomic era.Subfamily-specific adaptations in the structures of two penicillin-binding proteins from Mycobacterium tuberculosis.The PI-3 kinase-Akt-MDM2-survivin signaling axis in high-risk neuroblastoma: a target for PI-3 kinase inhibitor intervention.Phosphorylation of the ATP-binding loop directs oncogenicity of drug-resistant BCR-ABL mutantsStem cell and kinase activity-independent pathway in resistance of leukaemia to BCR-ABL kinase inhibitorsSmall-molecule kinase-inhibitor target assessment.Sustained suppression of Bcr-Abl-driven lymphoid leukemia by microRNA mimics.Treatment for chronic myelogenous leukemia: the long road to imatinibInhibition of polysome assembly enhances imatinib activity against chronic myelogenous leukemia and overcomes imatinib resistanceCyclin-dependent kinase 1 inhibitor RO-3306 enhances p53-mediated Bax activation and mitochondrial apoptosis in AMLN-myristoylated c-Abl tyrosine kinase localizes to the endoplasmic reticulum upon binding to an allosteric inhibitor.Perspectives for the use of structural information and chemical genetics to develop inhibitors of Janus kinasesValidating cancer drug targets through chemical geneticsSirtuin inhibitors as anticancer agents.Gö6976 is a potent inhibitor of the JAK 2 and FLT3 tyrosine kinases with significant activity in primary acute myeloid leukaemia cells.A dual PI3 kinase/mTOR inhibitor reveals emergent efficacy in glioma.KIT signaling governs differential sensitivity of mature and primitive CML progenitors to tyrosine kinase inhibitors.Identification of target genes using gene expression profile of granulocytes from patients with chronic myeloid leukemia treated with tyrosine kinase inhibitors.A pulse at the heart of targeted therapy.Exploiting Atropisomerism to Increase the Target Selectivity of Kinase Inhibitors.The dual PI3 kinase/mTOR inhibitor PI-103 prevents p53 induction by Mdm2 inhibition but enhances p53-mediated mitochondrial apoptosis in p53 wild-type AML.Enhanced BCR-ABL kinase inhibition does not result in increased inhibition of downstream signaling pathways or increased growth suppression in CML progenitors.Engineering and Functional Analysis of Mitotic Kinases Through Chemical Genetics.Chemical Modification and Organelle-Specific Localization of Orlistat-Like Natural-Product-Based Probes
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P2860
Sole BCR-ABL inhibition is insufficient to eliminate all myeloproliferative disorder cell populations.
description
article científic
@ca
article scientifique
@fr
articolo scientifico
@it
artigo científico
@pt
bilimsel makale
@tr
scientific article published on 25 October 2004
@en
vedecký článok
@sk
vetenskaplig artikel
@sv
videnskabelig artikel
@da
vědecký článek
@cs
name
Sole BCR-ABL inhibition is ins ...... ive disorder cell populations.
@en
Sole BCR-ABL inhibition is ins ...... ive disorder cell populations.
@nl
type
label
Sole BCR-ABL inhibition is ins ...... ive disorder cell populations.
@en
Sole BCR-ABL inhibition is ins ...... ive disorder cell populations.
@nl
prefLabel
Sole BCR-ABL inhibition is ins ...... ive disorder cell populations.
@en
Sole BCR-ABL inhibition is ins ...... ive disorder cell populations.
@nl
P2093
P2860
P356
P1476
Sole BCR-ABL inhibition is ins ...... ive disorder cell populations.
@en
P2093
P2860
P304
17456-17461
P356
10.1073/PNAS.0407061101
P407
P577
2004-10-25T00:00:00Z