Conditional expression of heterozygous or homozygous Jak2V617F from its endogenous promoter induces a polycythemia vera-like disease.
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Megakaryocyte pathology and bone marrow fibrosis: the lysyl oxidase connectionSignal transduction in the chronic leukemias: implications for targeted therapiesSelf-renewal of single mouse hematopoietic stem cells is reduced by JAK2V617F without compromising progenitor cell expansionNovel mutations and their functional and clinical relevance in myeloproliferative neoplasms: JAK2, MPL, TET2, ASXL1, CBL, IDH and IKZF1Efficacy of NS-018, a potent and selective JAK2/Src inhibitor, in primary cells and mouse models of myeloproliferative neoplasmsDifferential biological activity of disease-associated JAK2 mutantsMouse models of myeloproliferative neoplasms: JAK of all gradesTargeting substrate-site in Jak2 kinase prevents emergence of genetic resistanceStem and progenitor cell subsets are affected by JAK2 signaling and can be monitored by flow cytometry.Conditional disruption of interactions between Gαi2 and regulator of G protein signaling (RGS) proteins protects the heart from ischemic injuryDynamin 2-dependent endocytosis is required for normal megakaryocyte development in mice.AKT is a therapeutic target in myeloproliferative neoplasmsIntegrated genomic analysis illustrates the central role of JAK-STAT pathway activation in myeloproliferative neoplasm pathogenesis.Identification of a novel functional JAK1 S646P mutation in acute lymphoblastic leukemia.Generation and characterization of a JAK2V617F-containing erythroleukemia cell line.Co-targeting the PI3K/mTOR and JAK2 signalling pathways produces synergistic activity against myeloproliferative neoplasmsLoss of wild-type Jak2 allele enhances myeloid cell expansion and accelerates myelofibrosis in Jak2V617F knock-in miceA possible contribution of altered cathepsin B expression to the development of skin sclerosis and vasculopathy in systemic sclerosisMyeloproliferative neoplasms can be initiated from a single hematopoietic stem cell expressing JAK2-V617F.Distinct clinical phenotypes associated with JAK2V617F reflect differential STAT1 signalingJAK2 inhibitors do not affect stem cells present in the spleens of patients with myelofibrosis.Relevance of JAK2V617F positivity to hematological diseases--survey of samples from a clinical genetics laboratorymTOR inhibitors alone and in combination with JAK2 inhibitors effectively inhibit cells of myeloproliferative neoplasms.Impact of JAK2 V617F mutation on hemogram variation in patients with non-reactive elevated platelet countsThe thrombopoietin receptor, MPL, is critical for development of a JAK2V617F-induced myeloproliferative neoplasmThe Ph-positive and Ph-negative myeloproliferative neoplasms: some topical pre-clinical and clinical issues.3'UTR-truncated Hmga2 cDNA causes MPN-like hematopoiesis by conferring a clonal growth advantage at the level of HSC in mice.Development of a highly sensitive method for detection of JAK2V617FA truncation mutant of Csf3r cooperates with PML-RARα to induce acute myeloid leukemia in mice.A46, a benzothiophene-derived compound, suppresses Jak2-mediated pathologic cell growthA novel murine model of myeloproliferative disorders generated by overexpression of the transcription factor NF-E2.Critical requirement for Stat5 in a mouse model of polycythemia vera.Efficacy of vorinostat in a murine model of polycythemia veraSafety and efficacy of everolimus, a mTOR inhibitor, as single agent in a phase 1/2 study in patients with myelofibrosis.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 miceErythroid lineage-restricted expression of Jak2V617F is sufficient to induce a myeloproliferative disease in miceMesenchymal Cell Reprogramming in Experimental MPLW515L Mouse Model of Myelofibrosis.Identification of AIM2 as a downstream target of JAK2V617F.
P2860
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P2860
Conditional expression of heterozygous or homozygous Jak2V617F from its endogenous promoter induces a polycythemia vera-like disease.
description
2010 nî lūn-bûn
@nan
2010 թուականի Մարտին հրատարակուած գիտական յօդուած
@hyw
2010 թվականի մարտին հրատարակված գիտական հոդված
@hy
2010年の論文
@ja
2010年論文
@yue
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
name
Conditional expression of hete ...... olycythemia vera-like disease.
@ast
Conditional expression of hete ...... olycythemia vera-like disease.
@en
type
label
Conditional expression of hete ...... olycythemia vera-like disease.
@ast
Conditional expression of hete ...... olycythemia vera-like disease.
@en
prefLabel
Conditional expression of hete ...... olycythemia vera-like disease.
@ast
Conditional expression of hete ...... olycythemia vera-like disease.
@en
P2093
P2860
P1433
P1476
Conditional expression of hete ...... olycythemia vera-like disease.
@en
P2093
Dongqing Yan
Haiying Zou
Hajime Akada
M Golam Mohi
Robert E Hutchison
Steven Fiering
P2860
P304
P356
10.1182/BLOOD-2009-04-215848
P407
P577
2010-03-02T00:00:00Z