Stat5 is indispensable for the maintenance of bcr/abl-positive leukaemia. - Test2 - elhamkhani - TriplyDB

Stat5 is indispensable for the maintenance of bcr/abl-positive leukaemia.

Stat5 is indispensable for the maintenance of bcr/abl-positive leukaemia.

http://www.wikidata.org/entity/Q42089534

about

The Philadelphia chromosome in leukemogenesis New Developments in Chronic Myeloid Leukemia: Implications for Therapy Kinase-independent mechanisms of resistance of leukemia stem cells to tyrosine kinase inhibitors Inhibition of STAT5: a therapeutic option in BCR-ABL1-driven leukemia Signal transduction in the chronic leukemias: implications for targeted therapies STAT5-regulated microRNA-193b controls haematopoietic stem and progenitor cell expansion by modulating cytokine receptor signalling.Targeting the SH2-Kinase Interface in Bcr-Abl Inhibits Leukemogenesis LNK/SH2B3 regulates IL-7 receptor signaling in normal and malignant B-progenitors Co-existence of IL7R high and SH2B3 low expression distinguishes a novel high-risk acute lymphoblastic leukemia with Ikaros dysfunction PAK-dependent STAT5 serine phosphorylation is required for BCR-ABL-induced leukemogenesis Intracellular retention of ABL kinase inhibitors determines commitment to apoptosis in CML cells BCR-ABL affects STAT5A and STAT5B differentially How Intrinsic Molecular Dynamics Control Intramolecular Communication in Signal Transducers and Activators of Transcription Factor STAT5 Novel mechanism of tumor suppression by polarity gene discs large 1 (DLG1) revealed in a murine model of pediatric B-ALL.Mechanistic rationale for targeting the unfolded protein response in pre-B acute lymphoblastic leukemia.Differential signaling networks of Bcr-Abl p210 and p190 kinases in leukemia cells defined by functional proteomics.Overexpression of hepatoma-derived growth factor in melanocytes does not lead to oncogenic transformation.Regulation of the interferon regulatory factor-8 (IRF-8) tumor suppressor gene by the signal transducer and activator of transcription 5 (STAT5) transcription factor in chronic myeloid leukemia Regulation of hTERT by BCR-ABL at multiple levels in K562 cells.JAK2/STAT5 inhibition by nilotinib with ruxolitinib contributes to the elimination of CML CD34+ cells in vitro and in vivo.Transforming and tumorigenic activity of JAK2 by fusion to BCR: molecular mechanisms of action of a novel BCR-JAK2 tyrosine-kinase.PI3Kδ is essential for tumor clearance mediated by cytotoxic T lymphocytes.BCR-JAK2 drives a myeloproliferative neoplasm in transplanted mice.The STAT5 inhibitor pimozide decreases survival of chronic myelogenous leukemia cells resistant to kinase inhibitors.A screening-based approach to circumvent tumor microenvironment-driven intrinsic resistance to BCR-ABL+ inhibitors in Ph+ acute lymphoblastic leukemia Context-Specific Growth Hormone Signaling through the Transcription Factor STAT5: Implications for the Etiology of Hepatosteatosis and Hepatocellular Carcinoma.Loss of STAT3 in Lymphoma Relaxes NK Cell-Mediated Tumor Surveillance The PPARα agonist fenofibrate suppresses B-cell lymphoma in mice by modulating lipid metabolism.FRA2 is a STAT5 target gene regulated by IL-2 in human CD4 T cells.The transcription factors signal transducer and activator of transcription 5A (STAT5A) and STAT5B negatively regulate cell proliferation through the activation of cyclin-dependent kinase inhibitor 2b (Cdkn2b) and Cdkn1a expression LCK over-expression drives STAT5 oncogenic signaling in PAX5 translocated BCP-ALL patients.Ebf1 or Pax5 haploinsufficiency synergizes with STAT5 activation to initiate acute lymphoblastic leukemia.An integrated approach to dissecting oncogene addiction implicates a Myb-coordinated self-renewal program as essential for leukemia maintenance.Structure-Based Screen Identifies a Potent Small Molecule Inhibitor of Stat5a/b with Therapeutic Potential for Prostate Cancer and Chronic Myeloid Leukemia.C/EBPβ promotes BCR-ABL-mediated myeloid expansion and leukemic stem cell exhaustion.Critical requirement for Stat5 in a mouse model of polycythemia vera.Essential role for Stat5a/b in myeloproliferative neoplasms induced by BCR-ABL1 and JAK2(V617F) in mice.Alternative approaches to eradicating the malignant clone in chronic myeloid leukemia: tyrosine-kinase inhibitor combinations and beyond.Diverging fates of cells of origin in acute and chronic leukaemia.Genome-wide analyses reveal the extent of opportunistic STAT5 binding that does not yield transcriptional activation of neighboring genes.

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P2860

Stat5 is indispensable for the maintenance of bcr/abl-positive leukaemia.

http://www.wikidata.org/entity/Q42089534

description

2010 nî lūn-bûn

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2010年の論文

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2010年論文

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2010年論文

@zh-hant

2010年論文

@zh-hk

2010年論文

@zh-mo

2010年論文

@zh-tw

2010年论文

@wuu

2010年论文

@zh

2010年论文

@zh-cn

name

Stat5 is indispensable for the maintenance of bcr/abl-positive leukaemia.

@en

Stat5 is indispensable for the maintenance of bcr/abl-positive leukaemia.

@nl

type

label

Stat5 is indispensable for the maintenance of bcr/abl-positive leukaemia.

@en

Stat5 is indispensable for the maintenance of bcr/abl-positive leukaemia.

@nl

prefLabel

Stat5 is indispensable for the maintenance of bcr/abl-positive leukaemia.

@en

Stat5 is indispensable for the maintenance of bcr/abl-positive leukaemia.

@nl

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EMBO Molecular Medicine

P1476

Stat5 is indispensable for the maintenance of bcr/abl-positive leukaemia.

@en

P2093

Andrea Hoelbl

http://www.w3.org/2001/XMLSchema#string

Bingmei Zhu

http://www.w3.org/2001/XMLSchema#string

Christian Schuster

http://www.w3.org/2001/XMLSchema#string

Gabriele Stengl

http://www.w3.org/2001/XMLSchema#string

Hartmut Beug

http://www.w3.org/2001/XMLSchema#string

Maria A Hoelzl

http://www.w3.org/2001/XMLSchema#string

Mark Wickre

http://www.w3.org/2001/XMLSchema#string

Sabine Fajmann

http://www.w3.org/2001/XMLSchema#string

Veronika Sexl

http://www.w3.org/2001/XMLSchema#string

Wolfgang Warsch

http://www.w3.org/2001/XMLSchema#string

P2860

Antiapoptotic activity of Stat5 required during terminal stages of myeloid differentiation

The Hallmarks of Cancer

Lestaurtinib (CEP701) is a JAK2 inhibitor that suppresses JAK2/STAT5 signaling and the proliferation of primary erythroid cells from patients with myeloproliferative disorders

Targeted disruption of the mouse Stat3 gene leads to early embryonic lethality

Efficacy of TG101348, a selective JAK2 inhibitor, in treatment of a murine model of JAK2V617F-induced polycythemia vera.

Principles of tumor suppression

Constitutive activation of STAT5 by the BCR-ABL oncogene in chronic myelogenous leukemia

Stat5a/b contribute to interleukin 7-induced B-cell precursor expansion, but abl- and bcr/abl-induced transformation are independent of stat5

Sox17 dependence distinguishes the transcriptional regulation of fetal from adult hematopoietic stem cells

Reaching for high-hanging fruit in drug discovery at protein-protein interfaces

P304

98-110

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scholarly article

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10.1002/EMMM.201000062

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3

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2

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Florian Grebien

Richard Moriggl

Lothar Hennighausen

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2010-03-01T00:00:00Z

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41722840

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20201032

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2906698

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