Physiological Jak2V617F expression causes a lethal myeloproliferative neoplasm with differential effects on hematopoietic stem and progenitor cells. - Wikidata - wikimedia - TriplyDB

Physiological Jak2V617F expression causes a lethal myeloproliferative neoplasm with differential effects on hematopoietic stem and progenitor cells.

Physiological Jak2V617F expression causes a lethal myeloproliferative neoplasm with differential effects on hematopoietic stem and progenitor cells.

http://www.wikidata.org/entity/Q42133453

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JAK2 Inhibition: Reviewing a New Therapeutical Option in Myeloproliferative Neoplasms Megakaryocyte pathology and bone marrow fibrosis: the lysyl oxidase connection The Hen or the Egg: Inflammatory Aspects of Murine MPN Models JAK2 and genomic instability in the myeloproliferative neoplasms: a case of the chicken or the egg?Signal transduction in the chronic leukemias: implications for targeted therapies Self-renewal of single mouse hematopoietic stem cells is reduced by JAK2V617F without compromising progenitor cell expansion Quantitative histological image analyses of reticulin fibers in a myelofibrotic mouse Differential biological activity of disease-associated JAK2 mutants Efficacious intermittent dosing of a novel JAK2 inhibitor in mouse models of polycythemia vera Multifaceted intervention by the Hsp90 inhibitor ganetespib (STA-9090) in cancer cells with activated JAK/STAT signaling Mouse models of myeloproliferative neoplasms: JAK of all grades Targeting substrate-site in Jak2 kinase prevents emergence of genetic resistance Stem and progenitor cell subsets are affected by JAK2 signaling and can be monitored by flow cytometry.Safety and efficacy of TG101348, a selective JAK2 inhibitor, in myelofibrosis.Safety and efficacy of CYT387, a JAK1 and JAK2 inhibitor, in myelofibrosis.Dynamin 2-dependent endocytosis is required for normal megakaryocyte development in mice.AKT is a therapeutic target in myeloproliferative neoplasms Generation and characterization of a JAK2V617F-containing erythroleukemia cell line.Co-targeting the PI3K/mTOR and JAK2 signalling pathways produces synergistic activity against myeloproliferative neoplasms Loss of wild-type Jak2 allele enhances myeloid cell expansion and accelerates myelofibrosis in Jak2V617F knock-in mice Myeloproliferative neoplasms can be initiated from a single hematopoietic stem cell expressing JAK2-V617F.Distinct clinical phenotypes associated with JAK2V617F reflect differential STAT1 signaling Disease burden at the progenitor level is a feature of primary myelofibrosis: a multivariable analysis of 164 JAK2 V617F-positive myeloproliferative neoplasm patients JAK2 inhibitors do not affect stem cells present in the spleens of patients with myelofibrosis.CHZ868, a Type II JAK2 Inhibitor, Reverses Type I JAK Inhibitor Persistence and Demonstrates Efficacy in Myeloproliferative Neoplasms.Relevance of JAK2V617F positivity to hematological diseases--survey of samples from a clinical genetics laboratory mTOR inhibitors alone and in combination with JAK2 inhibitors effectively inhibit cells of myeloproliferative neoplasms.Myeloproliferative neoplasms: from JAK2 mutations discovery to JAK2 inhibitor therapies.The Ph-positive and Ph-negative myeloproliferative neoplasms: some topical pre-clinical and clinical issues.Distinct effects of concomitant Jak2V617F expression and Tet2 loss in mice promote disease progression in myeloproliferative neoplasms.JAK-STAT pathway activation in malignant and nonmalignant cells contributes to MPN pathogenesis and therapeutic response Role of the clathrin adaptor PICALM in normal hematopoiesis and polycythemia vera pathophysiology.Development of a highly sensitive method for detection of JAK2V617F TNFα facilitates clonal expansion of JAK2V617F positive cells in myeloproliferative neoplasms.Small RNA Sequencing Uncovers New miRNAs and moRNAs Differentially Expressed in Normal and Primary Myelofibrosis CD34+ Cells.Critical requirement for Stat5 in a mouse model of polycythemia vera.Distinct roles for long-term hematopoietic stem cells and erythroid precursor cells in a murine model of Jak2V617F-mediated polycythemia vera.Deletion of Stat3 enhances myeloid cell expansion and increases the severity of myeloproliferative neoplasms in Jak2V617F knock-in mice.Tyrosine 201 is required for constitutive activation of JAK2V617F and efficient induction of myeloproliferative disease in mice Erythroid lineage-restricted expression of Jak2V617F is sufficient to induce a myeloproliferative disease in mice

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Physiological Jak2V617F expression causes a lethal myeloproliferative neoplasm with differential effects on hematopoietic stem and progenitor cells.

http://www.wikidata.org/entity/Q42133453

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

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2010年論文

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2010年論文

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2010年論文

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2010年论文

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2010年论文

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2010年论文

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name

Physiological Jak2V617F expres ...... tic stem and progenitor cells.

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Physiological Jak2V617F expres ...... tic stem and progenitor cells.

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type

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Physiological Jak2V617F expres ...... tic stem and progenitor cells.

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Physiological Jak2V617F expres ...... tic stem and progenitor cells.

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prefLabel

Physiological Jak2V617F expres ...... tic stem and progenitor cells.

@en

Physiological Jak2V617F expres ...... tic stem and progenitor cells.

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J.CCR.2010.05.015

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Physiological Jak2V617F expres ...... tic stem and progenitor cells.

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Allegra M Lord

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Ann Mullally

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Benjamin L Ebert

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Brian Ball

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Christine Megerdichian

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D Gary Gilliland

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Elizabeth Housman

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Fatima Al-Shahrour

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Gerlinde Wernig

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J Erika Haydu

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P2860

Jak2 deficiency defines an essential developmental checkpoint in definitive hematopoiesis

Conversion of 5-methylcytosine to 5-hydroxymethylcytosine in mammalian DNA by MLL partner TET1

JAK2 phosphorylates histone H3Y41 and excludes HP1alpha from chromatin

Gene set enrichment analysis: a knowledge-based approach for interpreting genome-wide expression profiles.

The JAK2V617F activating mutation occurs in chronic myelomonocytic leukemia and acute myeloid leukemia, but not in acute lymphoblastic leukemia or chronic lymphocytic leukemia

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

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

Jak2 is essential for signaling through a variety of cytokine receptors

Efficient in vivo manipulation of mouse genomic sequences at the zygote stage

Activating mutation in the tyrosine kinase JAK2 in polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis

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