JAK2T875N is a novel activating mutation that results in myeloproliferative disease with features of megakaryoblastic leukemia in a murine bone marrow transplantation model.
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Megakaryocyte pathology and bone marrow fibrosis: the lysyl oxidase connectionThe homeobox gene CDX2 is aberrantly expressed in most cases of acute myeloid leukemia and promotes leukemogenesisA novel fusion of RBM6 to CSF1R in acute megakaryoblastic leukemiaA germline JAK2 SNP is associated with predisposition to the development of JAK2(V617F)-positive myeloproliferative neoplasmsTyrosines 868, 966, and 972 in the kinase domain of JAK2 are autophosphorylated and required for maximal JAK2 kinase activityDifferential biological activity of disease-associated JAK2 mutantsJAK and MPL mutations in myeloid malignancies.The OTT-MAL fusion oncogene activates RBPJ-mediated transcription and induces acute megakaryoblastic leukemia in a knockin mouse model.Jak2 inhibitors: rationale and role as therapeutic agents in hematologic malignancies.JAK2 V617F constitutive activation requires JH2 residue F595: a pseudokinase domain target for specific inhibitorsSTAT5 requires the N-domain for suppression of miR15/16, induction of bcl-2, and survival signaling in myeloproliferative diseasePathological interactions between hematopoietic stem cells and their niche revealed by mouse models of primary myelofibrosis.Apoptosis induced by JAK2 inhibition is mediated by Bim and enhanced by the BH3 mimetic ABT-737 in JAK2 mutant human erythroid cells.c-Abl activates janus kinase 2 in normal hematopoietic cells.Investigation and analysis of single nucleotide polymorphisms in Janus kinase/signal transducer and activator of transcription genes with leukemia.Myeloid blastic transformation of myeloproliferative neoplasms--a review of 112 cases.Coordinate loss of a microRNA and protein-coding gene cooperate in the pathogenesis of 5q- syndrome.Characterization of novel genomic alterations and therapeutic approaches using acute megakaryoblastic leukemia xenograft models.Comparison of mutated ABL1 and JAK2 as oncogenes and drug targets in myeloproliferative disordersThe Jak2V617F oncogene associated with myeloproliferative diseases requires a functional FERM domain for transformation and for expression of the Myc and Pim proto-oncogenesIdentification of somatic JAK1 mutations in patients with acute myeloid leukemia.Update on JAK2 Inhibitors in Myeloproliferative NeoplasmDepletion of Jak2V617F myeloproliferative neoplasm-propagating stem cells by interferon-α in a murine model of polycythemia veraUncoupling JAK2 V617F activation from cytokine-induced signalling by modulation of JH2 αC helix.Constitutive JAK3 activation induces lymphoproliferative syndromes in murine bone marrow transplantation models.JAK2-V617F-induced MAPK activity is regulated by PI3K and acts synergistically with PI3K on the proliferation of JAK2-V617F-positive cellsJAK2 and MPL mutations in myeloproliferative neoplasms: discovery and science.Cooperative effects of Janus and Aurora kinase inhibition by CEP701 in cells expressing Jak2V617F.Molecular drug targets in myeloproliferative neoplasms: mutant ABL1, JAK2, MPL, KIT, PDGFRA, PDGFRB and FGFR1.Redox regulation of Janus kinase: The elephant in the room.Notch signaling specifies megakaryocyte development from hematopoietic stem cells.Perspectives for the use of structural information and chemical genetics to develop inhibitors of Janus kinasesMolecular pathways: molecular basis for sensitivity and resistance to JAK kinase inhibitors.A structure-function perspective of Jak2 mutations and implications for alternate drug design strategies: the road not taken.JAK2 inhibition for the treatment of hematologic and solid malignancies.The implication of identifying JAK2 ( V617F ) in myeloproliferative neoplasms and myelodysplastic syndromes with bone marrow fibrosis.The SKI proto-oncogene enhances the in vivo repopulation of hematopoietic stem cells and causes myeloproliferative disease.Effects of Jak2 type 1 inhibitors NVP-BSK805 and NVP-BVB808 on Jak2 mutation-positive and Bcr-Abl-positive cell lines.SOCS-mediated downregulation of mutant Jak2 (V617F, T875N and K539L) counteracts cytokine-independent signaling.The JAK kinase inhibitor CP-690,550 suppresses the growth of human polycythemia vera cells carrying the JAK2V617F mutation.
P2860
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P2860
JAK2T875N is a novel activating mutation that results in myeloproliferative disease with features of megakaryoblastic leukemia in a murine bone marrow transplantation model.
description
2006 nî lūn-bûn
@nan
2006年の論文
@ja
2006年論文
@yue
2006年論文
@zh-hant
2006年論文
@zh-hk
2006年論文
@zh-mo
2006年論文
@zh-tw
2006年论文
@wuu
2006年论文
@zh
2006年论文
@zh-cn
name
JAK2T875N is a novel activatin ...... marrow transplantation model.
@ast
JAK2T875N is a novel activatin ...... marrow transplantation model.
@en
type
label
JAK2T875N is a novel activatin ...... marrow transplantation model.
@ast
JAK2T875N is a novel activatin ...... marrow transplantation model.
@en
prefLabel
JAK2T875N is a novel activatin ...... marrow transplantation model.
@ast
JAK2T875N is a novel activatin ...... marrow transplantation model.
@en
P2093
P2860
P1433
P1476
JAK2T875N is a novel activatin ...... marrow transplantation model.
@en
P2093
Benjamin H Lee
D Gary Gilliland
Dana Cullen
Gerlinde Wernig
Olivier A Bernard
Roberto D Polakiewicz
Ross L Levine
Sandra A Moore
Stefan Fröhling
Ting-Lei Gu
P2860
P304
P356
10.1182/BLOOD-2006-04-014712
P407
P577
2006-06-27T00:00:00Z