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

Association between enhanced type I collagen expression and epigenetic repression of the FLI1 gene in scleroderma fibroblasts.

Arthritis and rheumatism - 1 Jul 2006

Wang Youngqing, Fan Pan-Sheng, Kahaleh Bashar

Abstract excerpt

OBJECTIVE: Scleroderma (systemic sclerosis; SSc) is an autoimmune disease characterized by vasculopathy and widespread organ fibrosis. Altered fibroblast function, both in vivo and in vitro, is well documented and illustrated by augmented synthesis and deposition of extracellular matrix proteins. We undertook this study to investigate the possibility that epigenetic mechanisms mediate the emergence and...

Read the complete abstract on PubMed

Topics

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

Share to Azacitidine
Share to DNA Modification Methylases
Share to Genes, Suppressor

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Histone Deacetylase Inhibitors

Share to Histone Deacetylases

Share to Hydroxamic Acids

Share to Proto-Oncogene Protein c-fli-1

Share to Scleroderma, Systemic

Source

Identifiers

PMID: 16802366
DOI: 10.1002/art.21948

Genes

FLI1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Association between enhanced type I collagen expression and epigenetic repression of the FLI1 gene in scleroderma fibroblasts.PMID 16802366Read ↗

Epigenetic suppression of Fli1, a potential predisposing factor in the pathogenesis of systemic sclerosis.Semantic proximity Read ↗

Epigenetic Factors as Drivers of Fibrosis in Systemic SclerosisSemantic proximity Read ↗

Persistent Down-Regulation of Fli1, a Suppressor of Collagen Transcription, in Fibrotic Scleroderma SkinSemantic proximity Read ↗

Epigenetic modifications: novel therapeutic strategies for systemic sclerosis?Semantic proximity Read ↗

Bosentan reverses the pro-fibrotic phenotype of systemic sclerosis dermal fibroblasts via increasing DNA binding ability of transcription factor Fli1.Semantic proximity Read ↗

Oxidative DNA damage induces the ATM-mediated transcriptional suppression of the Wnt inhibitor WIF-1 in systemic sclerosis and fibrosisSemantic proximity Read ↗

[A Uuifying hypothesis for the pathogenesis of systemic sclerosis based on the deficiency of transcription factor Fli1 - the development of a new animal model of systemic sclerosis -].Semantic proximity Read ↗

TGF-β–induced epigenetic deregulation of SOCS3 facilitates STAT3 signaling to promote fibrosisSemantic proximity Read ↗

Autoantibodies to Fibrillin-1 Activate Normal Human Fibroblasts in Culture through the TGF-β Pathway to Recapitulate the “Scleroderma Phenotype”Semantic proximity Read ↗

Hypomethylation and overexpression of ITGAL (CD11a) in CD4+ T cells in systemic sclerosisSemantic proximity Read ↗

Autocrine activation by interleukin 1alpha induces the fibrogenic phenotype of systemic sclerosis fibroblasts.Semantic proximity Read ↗

Methyl-CpG-binding protein 2 mediates antifibrotic effects in scleroderma fibroblasts.Semantic proximity Read ↗

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