Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Repression of IP-10 by Interactions between Histone Deacetylation and Hypermethylation in Idiopathic Pulmonary Fibrosis

20 Apr 2010

Abstract excerpt

Targeted repression of a subset of key genes involved in tissue remodeling is a cardinal feature of idiopathic pulmonary fibrosis (IPF). The mechanism is unclear but is potentially important in disease pathogenesis and therapeutic targeting. We have previously reported that defective histone acetylation is responsible for the repression of the antifibrotic cyclooxygenase-2 gene. Here we extended our study to the...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
Share to Lung Cancer Treatments and Mutations
Share to Peptidase Inhibition and Analysis

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 20404089
DOI: 10.1128/mcb.01527-09

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Repression of IP-10 by Interactions between Histone Deacetylation and Hypermethylation in Idiopathic Pulmonary FibrosisPMID 20404089Read ↗

Interplay between EZH2 and G9a Regulates CXCL10 Gene Repression in Idiopathic Pulmonary FibrosisSemantic proximity Read ↗

IL-10 Targets IRFs to Suppress IFN and Inflammatory Response Genes by Epigenetic MechanismsSemantic proximity Read ↗

Targeting Histone Deacetylases in Idiopathic Pulmonary Fibrosis: A Future Therapeutic OptionSemantic proximity Read ↗

A central role for G9a and EZH2 in the epigenetic silencing of cyclooxygenase‐2 in idiopathic pulmonary fibrosisSemantic proximity Read ↗

Histone deacetylases: potential therapeutic targets for idiopathic pulmonary fibrosisSemantic proximity Read ↗

Absence of HDAC3 by Matrix Stiffness Promotes Chromatin Remodeling and Fibroblast Activation in Idiopathic Pulmonary FibrosisSemantic proximity Read ↗

TGFβ-induced fibroblast activation requires persistent and targeted HDAC-mediated gene repressionSemantic proximity Read ↗

Lung resident mesenchymal cells isolated from patients with the Bronchiolitis Obliterans Syndrome display a deregulated epigenetic profileSemantic proximity Read ↗

Epigenetic Histone Methylation Modulates Fibrotic Gene ExpressionSemantic proximity Read ↗

Histone acetylation and deacetylation: importance in inflammatory lung diseasesSemantic proximity Read ↗

Targeting Transcription Factor Lysine Acetylation in Inflammatory Airway DiseasesSemantic proximity Read ↗

CIITA mediates interferon-gamma repression of collagen transcription through phosphorylation-dependent interactions with co-repressor molecules.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.