A unique clonal JAK2 mutation leading to constitutive signalling causes polycythaemia vera - Wikidata - awgldk - TriplyDB

A unique clonal JAK2 mutation leading to constitutive signalling causes polycythaemia vera

A unique clonal JAK2 mutation leading to constitutive signalling causes polycythaemia vera

http://www.wikidata.org/entity/Q28241887

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Conditional deletion of Jak2 reveals an essential role in hematopoiesis throughout mouse ontogeny: implications for Jak2 inhibition in humans Essential thrombocythemia JAK2 Inhibition: Reviewing a New Therapeutical Option in Myeloproliferative Neoplasms Phosphorylation of p27Kip1 by JAK2 directly links cytokine receptor signaling to cell cycle control Mpl traffics to the cell surface through conventional and unconventional routes JAK2 phosphorylates histone H3Y41 and excludes HP1alpha from chromatin Janus kinases in immune cell signaling The molecular mechanisms that control thrombopoiesis Platelet genomics and proteomics in human health and disease.Somatic CALR mutations in myeloproliferative neoplasms with nonmutated JAK2 JAK2 exon 12 mutations in polycythemia vera and idiopathic erythrocytosis Venous thromboembolic disease Reticulin accumulation in essential thrombocythemia: prognostic significance and relationship to therapy Mast cell homeostasis and the JAK-STAT pathway Genetic characterization of TET1, TET2, and TET3 alterations in myeloid malignancies Molecular allelokaryotyping of pediatric acute lymphoblastic leukemias by high-resolution single nucleotide polymorphism oligonucleotide genomic microarray Selectivity and therapeutic inhibition of kinases: to be or not to be?Lestaurtinib (CEP701) is a JAK2 inhibitor that suppresses JAK2/STAT5 signaling and the proliferation of primary erythroid cells from patients with myeloproliferative disorders Therapeutic targeting of Janus kinases Abnormalities of GATA-1 in megakaryocytes from patients with idiopathic myelofibrosis Transformation of hematopoietic cells and activation of JAK2-V617F by IL-27R, a component of a heterodimeric type I cytokine receptor Highly sensitive method for genomewide detection of allelic composition in nonpaired, primary tumor specimens by use of affymetrix single-nucleotide-polymorphism genotyping microarrays Erythropoietin stimulates phosphorylation and activation of GATA-1 via the PI3-kinase/AKT signaling pathway Erlotinib effectively inhibits JAK2V617F activity and polycythemia vera cell growth Suppression of Fas-FasL coexpression by erythropoietin mediates erythroblast expansion during the erythropoietic stress response in vivo Recent advances in understanding myelofibrosis and essential thrombocythemia Therapeutic approaches in myelofibrosis and myelodysplastic/myeloproliferative overlap syndromes Potential Role of JAK-STAT Signaling Pathway in the Neurogenic-to-Gliogenic Shift in Down Syndrome Brain Integration of Signaling Pathways with the Epigenetic Machinery in the Maintenance of Stem Cells Genomic diversity in myeloproliferative neoplasms: focus on myelofibrosis Genomic landscape of megakaryopoiesis and platelet function defects Rationale for revision and proposed changes of the WHO diagnostic criteria for polycythemia vera, essential thrombocythemia and primary myelofibrosis Inflammation as a Keystone of Bone Marrow Stroma Alterations in Primary Myelofibrosis Budd-Chiari syndrome Blast transformation and fibrotic progression in polycythemia vera and essential thrombocythemia: a literature review of incidence and risk factors Circulating Cytokine Levels as Markers of Inflammation in Philadelphia Negative Myeloproliferative Neoplasms: Diagnostic and Prognostic Interest HSP90 and HSP70: Implication in Inflammation Processes and Therapeutic Approaches for Myeloproliferative Neoplasms Cytokine Regulation of Microenvironmental Cells in Myeloproliferative Neoplasms The Role of Reactive Oxygen Species in Myelofibrosis and Related Neoplasms Pathogenesis of Myeloproliferative Neoplasms: Role and Mechanisms of Chronic Inflammation

P2860

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P2860

A unique clonal JAK2 mutation leading to constitutive signalling causes polycythaemia vera

http://www.wikidata.org/entity/Q28241887

description

2005 nî lūn-bûn

@nan

2005 թուականի Ապրիլին հրատարակուած գիտական յօդուած

@hyw

2005 թվականի ապրիլին հրատարակված գիտական հոդված

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2005年の論文

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2005年論文

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2005年論文

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2005年論文

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2005年論文

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2005年論文

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2005年论文

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name

A unique clonal JAK2 mutation ...... ling causes polycythaemia vera

@ast

A unique clonal JAK2 mutation ...... ling causes polycythaemia vera

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A unique clonal JAK2 mutation ...... ling causes polycythaemia vera

@nl

type

label

A unique clonal JAK2 mutation ...... ling causes polycythaemia vera

@ast

A unique clonal JAK2 mutation ...... ling causes polycythaemia vera

@en

A unique clonal JAK2 mutation ...... ling causes polycythaemia vera

@nl

prefLabel

A unique clonal JAK2 mutation ...... ling causes polycythaemia vera

@ast

A unique clonal JAK2 mutation ...... ling causes polycythaemia vera

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A unique clonal JAK2 mutation ...... ling causes polycythaemia vera

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A unique clonal JAK2 mutation ...... ling causes polycythaemia vera

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Catherine Lacout

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Chloé James

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Jean-Pierre Le Couédic

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Judith Staerk

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Loïc Garçon

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Nicole Casadevall

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Roland Berger

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Valérie Ugo

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P2860

Human interleukin-10-related T cell-derived inducible factor: molecular cloning and functional characterization as an hepatocyte-stimulating factor

Autophosphorylation of JAK2 on tyrosines 221 and 570 regulates its activity

The N-terminal domain of Janus kinase 2 is required for Golgi processing and cell surface expression of erythropoietin receptor

A TEL-JAK2 fusion protein with constitutive kinase activity in human leukemia

JAK2 associates with the erythropoietin receptor and is tyrosine phosphorylated and activated following stimulation with erythropoietin

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10.1038/NATURE03546

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7037

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William Vainchenker

Stefan N Constantinescu

Jean-Luc Villeval

Annelise Bennaceur Griscelli

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2005-04-01T00:00:00Z

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1041406511

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15793561

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