Histone deacetylase 3 is required for maintenance of bone mass during aging - Wikidata - thesis-toulmin - TriplyDB

Histone deacetylase 3 is required for maintenance of bone mass during aging

Histone deacetylase 3 is required for maintenance of bone mass during aging

http://www.wikidata.org/entity/Q36442972

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Histone deacetylase 7 (Hdac7) suppresses chondrocyte proliferation and β-catenin activity during endochondral ossification Histone deacetylase 3 supports endochondral bone formation by controlling cytokine signaling and matrix remodeling.The histone deacetylase HDAC3 is essential for Purkinje cell function, potentially complicating the use of HDAC inhibitors in SCA1 Biological regulation of bone quality.Genetic determinants of phosphate response in Drosophila.Aberrant bone density in aging mice lacking the adenosine transporter ENT1.Conditional deletion of Hdac3 in osteoprogenitor cells attenuates diet-induced systemic metabolic dysfunction.The effect of laser therapy on the expression of osteocalcin and osteopontin after tooth extraction in rats treated with zoledronate and dexamethasone.Histone Deacetylases in Bone Development and Skeletal Disorders.Hdac3 Deficiency Increases Marrow Adiposity and Induces Lipid Storage and Glucocorticoid Metabolism in Osteochondroprogenitor Cells Deletion of the intestinal plasma membrane calcium pump, isoform 1, Atp2b1, in mice is associated with decreased bone mineral density and impaired responsiveness to 1, 25-dihydroxyvitamin D3.Runx2 protein represses Axin2 expression in osteoblasts and is required for craniosynostosis in Axin2-deficient mice Histone deacetylase 3 suppression increases PH domain and leucine-rich repeat phosphatase (Phlpp)1 expression in chondrocytes to suppress Akt signaling and matrix secretion Sclerostin alters serum vitamin D metabolite and fibroblast growth factor 23 concentrations and the urinary excretion of calcium Silencing of RUNX2 enhances gemcitabine sensitivity of p53-deficient human pancreatic cancer AsPC-1 cells through the stimulation of TAp63-mediated cell death.Sclerostin deficient mice rapidly heal bone defects by activating β-catenin and increasing intramembranous ossification.Bone cell senescence: mechanisms and perspectives.Towards selective inhibition of histone deacetylase isoforms: what has been achieved, where we are and what will be next.Chromatin modifiers and histone modifications in bone formation, regeneration, and therapeutic intervention for bone-related disease.Targeting cellular senescence prevents age-related bone loss in mice.Epigenetics and Bone Remodeling.Kynurenine, a Tryptophan Metabolite That Accumulates With Age, Induces Bone Loss.Deletion of protein kinase D1 in osteoprogenitor cells results in decreased osteogenesis in vitro and reduced bone mineral density in vivo.Histone deacetylases and their roles in mineralized tissue regeneration Loss of Hdac3 in osteoprogenitors increases bone expression of osteoprotegerin, improving systemic insulin sensitivity.Histone deacetylase 3 suppresses Erk phosphorylation and matrix metalloproteinase (Mmp)-13 activity in chondrocytes.Histone Deacetylase 3 Deletion in Mesenchymal Progenitor Cells Hinders Long Bone Development.

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Histone deacetylase 3 is required for maintenance of bone mass during aging

http://www.wikidata.org/entity/Q36442972

description

2012 nî lūn-bûn

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2012年の論文

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2012年学术文章

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2012年学术文章

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2012年学术文章

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2012年学术文章

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2012年学术文章

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2012年學術文章

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2012年學術文章

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2012年學術文章

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name

Histone deacetylase 3 is required for maintenance of bone mass during aging

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Histone deacetylase 3 is required for maintenance of bone mass during aging

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type

label

Histone deacetylase 3 is required for maintenance of bone mass during aging

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Histone deacetylase 3 is required for maintenance of bone mass during aging

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prefLabel

Histone deacetylase 3 is required for maintenance of bone mass during aging

@ast

Histone deacetylase 3 is required for maintenance of bone mass during aging

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J.BONE.2012.10.015

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P1476

Histone deacetylase 3 is required for maintenance of bone mass during aging

@en

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Amel Dudakovic

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

Jennifer J Westendorf

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Kai-Nan An

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Mahrokh Dadsetan

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

Michael J Yaszemski

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Qingshan Chen

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

Rajiv Kumar

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

Samuel W Carlson

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Zachary C Ryan

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P2860

Histone deacetylases specifically down-regulate p53-dependent gene activation

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

Runx2 (Cbfa1, AML-3) interacts with histone deacetylase 6 and represses the p21(CIP1/WAF1) promoter

Epigenetic control of skull morphogenesis by histone deacetylase 8

Histone deacetylase 3 depletion in osteo/chondroprogenitor cells decreases bone density and increases marrow fat

Mice lacking histone deacetylase 6 have hyperacetylated tubulin but are viable and develop normally.

Deacetylation of p53 modulates its effect on cell growth and apoptosis

Spatial distribution of Bax and Bcl-2 in osteocytes after bone fatigue: complementary roles in bone remodeling regulation?

Matrix-embedded cells control osteoclast formation

Histone deacetylase 3 interacts with runx2 to repress the osteocalcin promoter and regulate osteoblast differentiation

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296-307

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scholarly article

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10.1016/J.BONE.2012.10.015

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1

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52

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Meghan E McGee-Lawrence

Elizabeth W Bradley

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2012-10-18T00:00:00Z

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23085085

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3513670

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