FOXP1 controls mesenchymal stem cell commitment and senescence during skeletal aging. - Wikidata - wikimedia - TriplyDB

FOXP1 controls mesenchymal stem cell commitment and senescence during skeletal aging.

FOXP1 controls mesenchymal stem cell commitment and senescence during skeletal aging.

http://www.wikidata.org/entity/Q37730642

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Senescent cells: an emerging target for diseases of ageing.Autophagy controls mesenchymal stem cell properties and senescence during bone aging.The Differentiation Balance of Bone Marrow Mesenchymal Stem Cells Is Crucial to Hematopoiesis.Osteogenesis and aging: lessons from mesenchymal stem cells prevents bone ageing sensitivity by specifically regulating senescence and differentiation in mesenchymal stem cells Knockdown of FOXA2 enhances the osteogenic differentiation of bone marrow-derived mesenchymal stem cells partly via activation of the ERK signalling pathway H3K36 trimethylation mediated by SETD2 regulates the fate of bone marrow mesenchymal stem cells

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FOXP1 controls mesenchymal stem cell commitment and senescence during skeletal aging.

http://www.wikidata.org/entity/Q37730642

description

article científic

@ca

article scientifique

@fr

articolo scientifico

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artigo científico

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bilimsel makale

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scientific article published on 27 February 2017

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vedecký článok

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vetenskaplig artikel

@sv

videnskabelig artikel

@da

vědecký článek

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name

FOXP1 controls mesenchymal stem cell commitment and senescence during skeletal aging.

@en

FOXP1 controls mesenchymal stem cell commitment and senescence during skeletal aging.

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type

label

FOXP1 controls mesenchymal stem cell commitment and senescence during skeletal aging.

@en

FOXP1 controls mesenchymal stem cell commitment and senescence during skeletal aging.

@nl

prefLabel

FOXP1 controls mesenchymal stem cell commitment and senescence during skeletal aging.

@en

FOXP1 controls mesenchymal stem cell commitment and senescence during skeletal aging.

@nl

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Journal of Clinical Investigation

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FOXP1 controls mesenchymal stem cell commitment and senescence during skeletal aging.

@en

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Baojie Li

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

Gong Yang

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

Haley O Tucker

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

Hanjun Li

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

Joseph D Dekker

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

Pei Liu

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

Shuqin Xu

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

Tingting Tang

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Xizhi Guo

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

Yang Hong

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

P2860

The novel zinc finger-containing transcription factor osterix is required for osteoblast differentiation and bone formation

Foxp1 coordinates cardiomyocyte proliferation through both cell-autonomous and nonautonomous mechanisms

Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a

Hmga2 promotes neural stem cell self-renewal in young but not old mice by reducing p16Ink4a and p19Arf Expression

Fate decision of mesenchymal stem cells: adipocytes or osteoblasts?

DNA methylation and healthy human aging

FoxP1 orchestration of ASD-relevant signaling pathways in the striatum.

Osf2/Cbfa1: a transcriptional activator of osteoblast differentiation

Clearance of p16Ink4a-positive senescent cells delays ageing-associated disorders

p16INK4a induces an age-dependent decline in islet regenerative potential

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1241-1253

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scholarly article

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10.1172/JCI89511

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4

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127

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2017-02-27T00:00:00Z

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28240601

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5373872

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