BCR-ABL uncouples canonical JAK2-STAT5 signaling in chronic myeloid leukemia.
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c-Abl phosphorylates α-synuclein and regulates its degradation: implication for α-synuclein clearance and contribution to the pathogenesis of Parkinson's diseaseInhibition of STAT5: a therapeutic option in BCR-ABL1-driven leukemiaSignal transduction in the chronic leukemias: implications for targeted therapiesExpression of the TEL-Syk fusion protein in hematopoietic stem cells leads to rapidly fatal myelofibrosis in micePAK-dependent STAT5 serine phosphorylation is required for BCR-ABL-induced leukemogenesisBCR-ABL affects STAT5A and STAT5B differentiallyCM363, a novel naphthoquinone derivative which acts as multikinase modulator and overcomes imatinib resistance in chronic myelogenous leukemiaMYC Deregulation in Primary Human Cancers.Differential signaling networks of Bcr-Abl p210 and p190 kinases in leukemia cells defined by functional proteomics.JAK2/STAT5 inhibition by nilotinib with ruxolitinib contributes to the elimination of CML CD34+ cells in vitro and in vivo.MEK-dependent negative feedback underlies BCR-ABL-mediated oncogene addictionCombination of bortezomib and mitotic inhibitors down-modulate Bcr-Abl and efficiently eliminates tyrosine-kinase inhibitor sensitive and resistant Bcr-Abl-positive leukemic cells.Combined STAT3 and BCR-ABL1 inhibition induces synthetic lethality in therapy-resistant chronic myeloid leukemiaKINATEST-ID: a pipeline to develop phosphorylation-dependent terbium sensitizing kinase assays.Emerging therapeutic paradigms to target the dysregulated Janus kinase/signal transducer and activator of transcription pathway in hematological malignanciesStructure-Based Screen Identifies a Potent Small Molecule Inhibitor of Stat5a/b with Therapeutic Potential for Prostate Cancer and Chronic Myeloid Leukemia.JAK2-V617F-mediated signalling is dependent on lipid rafts and statins inhibit JAK2-V617F-dependent cell growthAlternative approaches to eradicating the malignant clone in chronic myeloid leukemia: tyrosine-kinase inhibitor combinations and beyond.Design of substrate-based BCR-ABL kinase inhibitors using the cyclotide scaffold.Diverging fates of cells of origin in acute and chronic leukaemia.The PERK-eIF2α phosphorylation arm is a pro-survival pathway of BCR-ABL signaling and confers resistance to imatinib treatment in chronic myeloid leukemia cells.Structure, regulation, signaling, and targeting of abl kinases in cancer.Heterogeneity of leukemia-initiating capacity of chronic myelogenous leukemia stem cells.Time-resolved luminescence detection of spleen tyrosine kinase activity through terbium sensitizationProteome-wide profiling of activated transcription factors with a concatenated tandem array of transcription factor response elementsUltrasensitive proteomic quantitation of cellular signaling by digitized nanoparticle-protein counting.Emerging therapeutic strategies for targeting chronic myeloid leukemia stem cellsDynamic trafficking of STAT5 depends on an unconventional nuclear localization signalTargeting survival pathways in chronic myeloid leukaemia stem cellsLuminal STAT5 mediates H2AX promoter activity in distinct population of basal mammary epithelial cellsA novel signalling screen demonstrates that CALR mutations activate essential MAPK signalling and facilitate megakaryocyte differentiation.Hematopoietic stem cells, progenitor cells and leukemic stem cells in adult myeloproliferative neoplasms.Advances in the biology and therapy of chronic myeloid leukemia: proceedings from the 6th Post-ASH International Chronic Myeloid Leukemia and Myeloproliferative Neoplasms Workshop.Co-operating STAT5 and AKT signaling pathways in chronic myeloid leukemia and mastocytosis: possible new targets of therapy.Do we need more drugs for chronic myeloid leukemia?Natural course and biology of CML.Discontinuation of tyrosine kinase therapy in CML.Novel drug therapies in myeloid leukemia.Indole-3-carbinol induces apoptosis of chronic myelogenous leukemia cells through suppression of STAT5 and Akt signaling pathways.Effective Concentration of a Multikinase Inhibitor within Bone Marrow Correlates with In Vitro Cell Killing in Therapy-Resistant Chronic Myeloid Leukemia.
P2860
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P2860
BCR-ABL uncouples canonical JAK2-STAT5 signaling in chronic myeloid leukemia.
description
2012 nî lūn-bûn
@nan
2012年の論文
@ja
2012年論文
@yue
2012年論文
@zh-hant
2012年論文
@zh-hk
2012年論文
@zh-mo
2012年論文
@zh-tw
2012年论文
@wuu
2012年论文
@zh
2012年论文
@zh-cn
name
BCR-ABL uncouples canonical JAK2-STAT5 signaling in chronic myeloid leukemia.
@en
BCR-ABL uncouples canonical JAK2-STAT5 signaling in chronic myeloid leukemia.
@nl
type
label
BCR-ABL uncouples canonical JAK2-STAT5 signaling in chronic myeloid leukemia.
@en
BCR-ABL uncouples canonical JAK2-STAT5 signaling in chronic myeloid leukemia.
@nl
prefLabel
BCR-ABL uncouples canonical JAK2-STAT5 signaling in chronic myeloid leukemia.
@en
BCR-ABL uncouples canonical JAK2-STAT5 signaling in chronic myeloid leukemia.
@nl
P2093
P2860
P50
P356
P1476
BCR-ABL uncouples canonical JAK2-STAT5 signaling in chronic myeloid leukemia.
@en
P2093
Eva Eckelhart
Ines Kaupe
Kay-Uwe Wagner
Veronika Sexl
Wolfgang Warsch
P2860
P2888
P304
P356
10.1038/NCHEMBIO.775
P577
2012-01-29T00:00:00Z