Loss of methylation in CpG sites in the NF-κB enhancer elements of inducible nitric oxide synthase is responsible for gene induction in human articular chondrocytes. - Test2 - elhamkhani - TriplyDB

Loss of methylation in CpG sites in the NF-κB enhancer elements of inducible nitric oxide synthase is responsible for gene induction in human articular chondrocytes.

Loss of methylation in CpG sites in the NF-κB enhancer elements of inducible nitric oxide synthase is responsible for gene induction in human articular chondrocytes.

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Increased DNA Methylation and Reduced Expression of Transcription Factors in Human Osteoarthritis Cartilage.Nitrosative stress and nitrated proteins in trichloroethene-mediated autoimmunity.Pentosan polysulfate inhibits IL-1β-induced iNOS, c-Jun and HIF-1α upregulation in canine articular chondrocytes.Myogenic differential methylation: diverse associations with chromatin structure.Mitochondrial epigenetics in bone remodeling during hyperhomocysteinemia Association of reduced type IX collagen gene expression in human osteoarthritic chondrocytes with epigenetic silencing by DNA hypermethylation Effects of hypoxia on anabolic and catabolic gene expression and DNA methylation in OA chondrocytes.Characterization of the cartilage DNA methylome in knee and hip osteoarthritis Inducible nitric oxide synthase (iNOS) regulatory region variation in non-human primates.Genome-wide DNA methylation study of hip and knee cartilage reveals embryonic organ and skeletal system morphogenesis as major pathways involved in osteoarthritis.Epigenetic regulation of interleukin-8, an inflammatory chemokine, in osteoarthritis.Identification of differentially methylated regions in new genes associated with knee osteoarthritis.Phlpp1 facilitates post-traumatic osteoarthritis and is induced by inflammation and promoter demethylation in human osteoarthritis.Epigenetically mediated spontaneous reduction of NFAT1 expression causes imbalanced metabolic activities of articular chondrocytes in aged mice.Epigenetic and microRNA regulation during osteoarthritis development Inflammation and epigenetic regulation in osteoarthritis.Osteoarthritis year in review 2013: biology.Epigenetics of osteoarticular diseases: recent developments.Chromatin modifiers and histone modifications in bone formation, regeneration, and therapeutic intervention for bone-related disease.Genome-wide DNA methylation study identifies significant epigenomic changes in osteoarthritic cartilage.DNA Methylation in Osteoarthritis.The Epigenomic Landscape in Osteoarthritis.ELF3 modulates type II collagen gene (COL2A1) transcription in chondrocytes by inhibiting SOX9-CBP/p300-driven histone acetyltransferase activity.Genomics and epigenomics in rheumatic diseases: what do they provide in terms of diagnosis and disease management?DNA methylation of the RUNX2 P1 promoter mediates MMP13 transcription in chondrocytes.Size and dielectric properties of skeletal stem cells change critically after enrichment and expansion from human bone marrow: consequences for microfluidic cell sorting.Editorial: More evidence for a role of CpG methylation in the pathogenesis of osteoarthritis.A global increase in 5-hydroxymethylcytosine levels marks osteoarthritic chondrocytes.Hypomethylation of interleukin-6 (IL-6) gene increases the risk of essential hypertension: a matched case-control study.Genome-wide DNA methylation analysis of articular chondrocytes identifies TRAF1, CTGF, and CX3CL1 genes as hypomethylated in osteoarthritis.Interplay of Inflammatory Mediators with Epigenetics and Cartilage Modifications in Osteoarthritis.DNA Methylation in Osteoarthritis: Current Status and Therapeutic Implications.MiR-455-3p inhibits the degenerate process of chondrogenic differentiation through modification of DNA methylation.Use of integrative epigenetic and mRNA expression analyses to identify significantly changed genes and functional pathways in osteoarthritic cartilage.Editorial: Is It Time for Epigenetics in Osteoarthritis?

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Loss of methylation in CpG sites in the NF-κB enhancer elements of inducible nitric oxide synthase is responsible for gene induction in human articular chondrocytes.

http://www.wikidata.org/entity/Q37609036

description

article científic

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article scientifique

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articolo scientifico

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artigo científico

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bilimsel makale

@tr

scientific article published on March 2013

@en

vedecký článok

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vetenskaplig artikel

@sv

videnskabelig artikel

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vědecký článek

@cs

name

Loss of methylation in CpG sit ...... human articular chondrocytes.

@en

Loss of methylation in CpG sit ...... human articular chondrocytes.

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type

label

Loss of methylation in CpG sit ...... human articular chondrocytes.

@en

Loss of methylation in CpG sit ...... human articular chondrocytes.

@nl

prefLabel

Loss of methylation in CpG sit ...... human articular chondrocytes.

@en

Loss of methylation in CpG sit ...... human articular chondrocytes.

@nl

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Arthritis and Rheumatism

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Loss of methylation in CpG sit ...... n human articular chondrocytes

@en

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Helmtrud I Roach

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

Kei Imagawa

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

Ko Hashimoto

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

Mary B Goldring

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

María C de Andrés

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

P2860

The phosphorylation status of nuclear NF-kappa B determines its association with CBP/p300 or HDAC-1

Transcriptional activation of the NF-kappaB p65 subunit by mitogen- and stress-activated protein kinase-1 (MSK1)

Contribution of H3K4 methylation by SET-1A to interleukin-1-induced cyclooxygenase 2 and inducible nitric oxide synthase expression in human osteoarthritis chondrocytes

Cloning, characterization, and expression of a cDNA encoding an inducible nitric oxide synthase from the human chondrocyte

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732-742

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scholarly article

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10.1002/ART.37806

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3

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65

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Antonio Gonzalez

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2013-03-01T00:00:00Z

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