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

STAT1 modulates tissue wasting or overgrowth downstream from PDGFRβ.

Genes & development - 15 Aug 2017

He Chaoyong, Medley Shayna C, Kim Jang, Sun Chengyi, Kwon Hae Ryong, Sakashita Hiromi, Pincu Yair, Yao Longbiao, Eppard Danielle, Dai Bojie, Berry William L, Griffin Timothy M, Olson Lorin E

Abstract excerpt

Platelet-derived growth factor (PDGF) acts through two conserved receptor tyrosine kinases: PDGFRα and PDGFRβ. Gain-of-function mutations in human PDGFRB have been linked recently to genetic diseases characterized by connective tissue wasting (Penttinen syndrome) or overgrowth (Kosaki overgrowth syndrome), but it is unclear whether PDGFRB mutations alone are responsible. Mice with constitutive PDGFRβ signaling...

Read the complete abstract on PubMed

Topics

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

Share to Aorta
Share to Atrophy

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

Share to Fibrosis

Share to Growth Disorders

Share to Hyperplasia

Share to NIH 3T3 Cells

Share to Receptor, Platelet-Derived Growth Factor beta

Share to STAT1 Transcription Factor

Source

Open in PubMed Open full text

Identifiers

PMID: 28924035
DOI: 10.1101/gad.300384.117
PMCID: PMC5647937

Genes

STAT1
PDGFRB

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

STAT1 modulates tissue wasting or overgrowth downstream from PDGFRβ.PMID 28924035Read ↗

Connective tissue growth in a mouse model of Kosaki overgrowth syndrome is limited by STAT1Semantic proximity Read ↗

Constitutive PDGFRb activation drives connective tissue overgrowth through STAT5-IGF1 signalingSemantic proximity Read ↗

Increased PDGFRalpha activation disrupts connective tissue development and drives systemic fibrosis.Semantic proximity Read ↗

An activating mutation in <i>Pdgfrb</i> causes skeletal stem cell defects with osteopenia and overgrowth in miceSemantic proximity Read ↗

Roles of PDGF/PDGFR signaling in various organsSemantic proximity Read ↗

Dysregulation of the immune response in TGF-β signalopathiesSemantic proximity Read ↗

Insight into the physiological functions of PDGF through genetic studies in mice.Semantic proximity Read ↗

Overactive PDGFRα and PDGFRβ promote distinct phenotypes of skeletal muscle fibrosis and stiffness, with PDGFRβ also driving muscle growth.Semantic proximity Read ↗

PDGFRβ signaling regulates mural cell plasticity and inhibits fat development.Semantic proximity Read ↗

Identification and characterization of PDGFRα+ mesenchymal progenitors in human skeletal muscleSemantic proximity Read ↗

Role of platelet-derived growth factors in physiology and medicine.Semantic proximity Read ↗

Overactive PDGFRα and PDGFRβ promote distinct yet overlapping phenotypes of skeletal muscle fibrosis and stiffness, with PDGFRβ also driving drastic muscle growthSemantic proximity Read ↗

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