Transcriptome remodeling in hypoxic inflammation. - Test2 - elhamkhani - TriplyDB

Transcriptome remodeling in hypoxic inflammation.

Transcriptome remodeling in hypoxic inflammation.

http://www.wikidata.org/entity/Q37720331

about

Acute hypoxia affects P-TEFb through HDAC3 and HEXIM1-dependent mechanism to promote gene-specific transcriptional repression.Central role for MCP-1/CCL2 in injury-induced inflammation revealed by in vitro, in silico, and clinical studies Epigenetic mechanisms in inflammation.Chromatin as an oxygen sensor and active player in the hypoxia response.Modulation of hypoxia-inducible factors (HIF) from an integrative pharmacological perspective.Dietary metabolites derived from gut microbiota: critical modulators of epigenetic changes in mammals.Hypoxia enhances the effect of lipopolysaccharide-stimulated IL-1β expression in human periodontal ligament cells.Hypoxia reduces the response of human adipocytes towards TNFα resulting in reduced NF-κB signaling and MCP-1 secretion.Treponema denticola increases MMP-2 expression and activation in the periodontium via reversible DNA and histone modifications.Acetylation of lysine 9 on histone H3 is associated with increased pro-inflammatory cytokine release in a cigarette smoke-induced rat model through HDAC1 depression.

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Transcriptome remodeling in hypoxic inflammation.

http://www.wikidata.org/entity/Q37720331

description

article científic

@ca

article scientifique

@fr

articolo scientifico

@it

artigo científico

@pt

bilimsel makale

@tr

scientific article published on 26 March 2010

@en

vedecký článok

@sk

vetenskaplig artikel

@sv

videnskabelig artikel

@da

vědecký článek

@cs

name

Transcriptome remodeling in hypoxic inflammation.

@en

Transcriptome remodeling in hypoxic inflammation.

@nl

type

label

Transcriptome remodeling in hypoxic inflammation.

@en

Transcriptome remodeling in hypoxic inflammation.

@nl

prefLabel

Transcriptome remodeling in hypoxic inflammation.

@en

Transcriptome remodeling in hypoxic inflammation.

@nl

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0022034510366813

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Journal of Dental Research

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Transcriptome remodeling in hypoxic inflammation.

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I Morita

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O Safronova

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P2860

Epigenetic regulation of gene expression: how the genome integrates intrinsic and environmental signals

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

Modulation of NF-kappaB-dependent transcription and cell survival by the SIRT1 deacetylase.

A nuclear factor induced by hypoxia via de novo protein synthesis binds to the human erythropoietin gene enhancer at a site required for transcriptional activation

FIH-1 is an asparaginyl hydroxylase enzyme that regulates the transcriptional activity of hypoxia-inducible factor

Posttranslational hydroxylation of ankyrin repeats in IkappaB proteins by the hypoxia-inducible factor (HIF) asparaginyl hydroxylase, factor inhibiting HIF (FIH)

Chromatin-specific remodeling by HMGB1 and linker histone H1 silences proinflammatory genes during endotoxin tolerance

Transcriptional activation of hypoxia-inducible factor-1alpha by HDAC4 and HDAC5 involves differential recruitment of p300 and FIH-1

Dnmt3a binds deacetylases and is recruited by a sequence-specific repressor to silence transcription

Histone deacetylases (HDACs): characterization of the classical HDAC family

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