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

Contribution of activin receptor-like kinase 5 (transforming growth factor beta receptor type I) signaling to the fibrotic phenotype of scleroderma fibroblasts.

Arthritis and rheumatism - 1 Apr 2006

Chen Yunliang, Shi-wen Xu, Eastwood Mark, Black Carol M, Denton Christopher P, Leask Andrew, Abraham David J

Abstract excerpt

OBJECTIVE: To use a specific transforming growth factor beta receptor type I (TGFbetaRI; activin receptor-like kinase 5 [ALK-5]) kinase inhibitor (SD208) to determine the role of activation of the TGFbetaRI kinase (ALK-5) in maintaining the profibrotic phenotype of dermal fibroblasts in systemic sclerosis (SSc). METHODS: The effect of SD208 on the expression of key biochemical markers of the fibrotic phenotype...

Read the complete abstract on PubMed

Topics

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

Share to Activin Receptors, Type I
Share to Cells, Cultured

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Fibroblasts

Share to Phenotype

Share to Protein Serine-Threonine Kinases

Share to Receptor, Transforming Growth Factor-beta Type I

Share to Receptors, Transforming Growth Factor beta

Share to Signal Transduction

Source

Identifiers

PMID: 16575856
DOI: 10.1002/art.21725

Genes

ALK

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. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Contribution of activin receptor-like kinase 5 (transforming growth factor beta receptor type I) signaling to the fibrotic phenotype of scleroderma fibroblasts.PMID 16575856Read ↗

An increased transforming growth factor beta receptor type I:type II ratio contributes to elevated collagen protein synthesis that is resistant to inhibition via a kinase-deficient transforming growth factor beta receptor type II in scleroderma.Semantic proximity Read ↗

Wnt/β‐catenin signaling is hyperactivated in systemic sclerosis and induces Smad‐dependent fibrotic responses in mesenchymal cellsSemantic proximity Read ↗

Transforming growth factor-beta receptor type I-dependent fibrogenic gene program is mediated via activation of Smad1 and ERK1/2 pathways.Semantic proximity Read ↗

Identification of regulators of the myofibroblast phenotype of primary dermal fibroblasts from early diffuse systemic sclerosis patientsSemantic proximity Read ↗

Transforming growth factor-beta in systemic sclerosis sclerodermaSemantic proximity Read ↗

Recent advances in fibroblast signaling and biology in sclerodermaSemantic proximity Read ↗

The fibrotic phenotype of systemic sclerosis fibroblasts varies with disease duration and severity of skin involvement: reconstitution of skin fibrosis development using a tissue engineering approach.Semantic proximity Read ↗

Rac inhibition reverses the phenotype of fibrotic fibroblasts.Semantic 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 ↗

Heparan sulfate-dependent ERK activation contributes to the overexpression of fibrotic proteins and enhanced contraction by scleroderma fibroblasts.Semantic proximity Read ↗

Decreased interleukin-20 expression in scleroderma skin contributes to cutaneous fibrosis.Semantic proximity Read ↗

TGF‐β signaling regulates fibrotic expression and activity in carpal tunnel syndromeSemantic proximity Read ↗

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