Csf3r mutations in mice confer a strong clonal HSC advantage via activation of Stat5. - Wikidata - awgldk - TriplyDB

Csf3r mutations in mice confer a strong clonal HSC advantage via activation of Stat5.

Csf3r mutations in mice confer a strong clonal HSC advantage via activation of Stat5.

http://www.wikidata.org/entity/Q36470463

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Engineering mouse models with myelodysplastic syndrome human candidate genes; how relevant are they?STAT5 in hematopoietic stem cell biology and transplantation STAT5-regulated microRNA-193b controls haematopoietic stem and progenitor cell expansion by modulating cytokine receptor signalling.Development of mammary luminal progenitor cells is controlled by the transcription factor STAT5A Dynamic ligand modulation of EPO receptor pools, and dysregulation by polycythemia-associated EPOR alleles Disruption of Notch signaling aggravates irradiation-induced bone marrow injury, which is ameliorated by a soluble Dll1 ligand through Csf2rb2 upregulation G-CSFR ubiquitination critically regulates myeloid cell survival and proliferation.Calcineurin/Nfatc1 signaling links skin stem cell quiescence to hormonal signaling during pregnancy and lactation CSF3R T618I is a highly prevalent and specific mutation in chronic neutrophilic leukemia.Oncogenic Nras has bimodal effects on stem cells that sustainably increase competitiveness.Sequencing a mouse acute promyelocytic leukemia genome reveals genetic events relevant for disease progression A truncation mutant of Csf3r cooperates with PML-RARα to induce acute myeloid leukemia in mice.Signal transducer and activator of transcription 5 as a key signaling pathway in normal mammary gland developmental biology and breast cancer.ELANE mutations in cyclic and severe congenital neutropenia: genetics and pathophysiology Interpretation of cytokine signaling through the transcription factors STAT5A and STAT5B Genetic and molecular diagnosis of severe congenital neutropenia.Arteriolar niches maintain haematopoietic stem cell quiescence.An activating mutation in the CSF3R gene induces a hereditary chronic neutrophilia.Hematopoietic stem cell transplantation for severe congenital neutropenia.Regulation of hematopoietic stem cell activity by inflammation.Granulocyte colony-stimulating factor receptor mutations in myeloid malignancy.A Truncated Granulocyte Colony-stimulating Factor Receptor (G-CSFR) Inhibits Apoptosis Induced by Neutrophil Elastase G185R Mutant: IMPLICATION FOR UNDERSTANDING CSF3R GENE MUTATIONS IN SEVERE CONGENITAL NEUTROPENIA.Granulocyte colony-stimulating factor receptor signaling in severe congenital neutropenia, chronic neutrophilic leukemia, and related malignancies.Severe congenital neutropenias.Unpaired Extracellular Cysteine Mutations of CSF3R Mediate Gain or Loss of Function.Bortezomib inhibits STAT5-dependent degradation of LEF-1, inducing granulocytic differentiation in congenital neutropenia CD34(+) cells Severe congenital neutropenia and chronic neutrophilic leukemia: an intriguing molecular connection unveiled by oncogenic mutations in CSF3R.Discovering early molecular determinants of leukemogenesis.Chronic neutrophilic leukemia: new science and new diagnostic criteria.Gain-of-function mutations in granulocyte colony-stimulating factor receptor (CSF3R) reveal distinct mechanisms of CSF3R activation.

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P2860

Csf3r mutations in mice confer a strong clonal HSC advantage via activation of Stat5.

http://www.wikidata.org/entity/Q36470463

description

2008 nî lūn-bûn

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2008年の論文

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2008年学术文章

@wuu

2008年学术文章

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2008年学术文章

@zh-hans

2008年学术文章

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2008年学术文章

@zh-sg

2008年學術文章

@yue

2008年學術文章

@zh

2008年學術文章

@zh-hant

name

Csf3r mutations in mice confer a strong clonal HSC advantage via activation of Stat5.

@ast

Csf3r mutations in mice confer a strong clonal HSC advantage via activation of Stat5.

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type

label

Csf3r mutations in mice confer a strong clonal HSC advantage via activation of Stat5.

@ast

Csf3r mutations in mice confer a strong clonal HSC advantage via activation of Stat5.

@en

prefLabel

Csf3r mutations in mice confer a strong clonal HSC advantage via activation of Stat5.

@ast

Csf3r mutations in mice confer a strong clonal HSC advantage via activation of Stat5.

@en

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P1433

Journal of Clinical Investigation

P1476

Csf3r mutations in mice confer a strong clonal HSC advantage via activation of Stat5

@en

P2093

Daniel C Link

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

Fulu Liu

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

Ghada Kunter

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

Jennifer A Cain

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Maxwell M Krem

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

Michael H Tomasson

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

William C Eades

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P2860

Mutations in the gene for the granulocyte colony-stimulating-factor receptor in patients with acute myeloid leukemia preceded by severe congenital neutropenia

Human acute myeloid leukemia is organized as a hierarchy that originates from a primitive hematopoietic cell

Infantile genetic agranulocytosis; agranulocytosis infantilis hereditaria

SOCS proteins: negative regulators of cytokine signaling

Tie2/angiopoietin-1 signaling regulates hematopoietic stem cell quiescence in the bone marrow niche

Enhancement of hematopoietic stem cell repopulating capacity and self-renewal in the absence of the transcription factor C/EBP alpha

A role for Wnt signalling in self-renewal of haematopoietic stem cells

Granulocyte-macrophage progenitors as candidate leukemic stem cells in blast-crisis CML

SLAM family receptors distinguish hematopoietic stem and progenitor cells and reveal endothelial niches for stem cells

Pten dependence distinguishes haematopoietic stem cells from leukaemia-initiating cells

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946-955

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10.1172/JCI32704

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3

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118

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Lothar Hennighausen

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2008-03-01T00:00:00Z

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18292815

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2248325

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