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

TNFalpha shedding and epidermal inflammation are controlled by Jun proteins.

Genes & development - 15 Nov 2009

Guinea-Viniegra Juan, Zenz Rainer, Scheuch Harald, Hnisz Denes, Holcmann Martin, Bakiri Latifa, Schonthaler Helia B, Sibilia Maria, Wagner Erwin F

Abstract excerpt

Inducible epidermal deletion of JunB and c-Jun in adult mice causes a psoriasis-like inflammatory skin disease. Increased levels of the proinflammatory cytokine TNFalpha play a major role in this phenotype. Here we define the underlying molecular mechanism using genetic mouse models. We show that Jun proteins control TNFalpha shedding in the epidermis by direct transcriptional activation of tissue inhibitor of...

Topics

Join the communities discussing this publication.

Cachexia
Epidermis
Keratinocytes
Mice, Inbred C3H
Proto-Oncogene Proteins c-jun

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Tissue Inhibitor of Metalloproteinase-3

Tumor Necrosis Factor-alpha

Source

Open in PubMed Open full text

Identifiers

PMID: 19933155
DOI: 10.1101/gad.543109
PMCID: PMC2779759

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 1 Sept 2026.

Community interpretation

Discuss the evidence

Ask a question, add context or challenge an interpretation. Community activity is separate from scientific evidence strength.

0

discussions

0

replies

Citations encouraged

Claims remain attributable.

No discussion yet

Be the first to add a careful, cited interpretation.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

TNFalpha shedding and epidermal inflammation are controlled by Jun proteins.PMID 19933155Read ↗

Signalling in inflammatory skin disease by AP-1 (Fos/Jun).Semantic proximity Read ↗

Psoriasis-like skin disease and arthritis caused by inducible epidermal deletion of Jun proteins.Semantic proximity Read ↗

JunB defines functional and structural integrity of the epidermo-pilosebaceous unit in the skinSemantic proximity Read ↗

Role of IL-17A signalling in psoriasis and associated bone loss.Semantic proximity Read ↗

The transcription factors c-rel and RelA control epidermal development and homeostasis in embryonic and adult skin via distinct mechanisms.Semantic proximity Read ↗

c-Jun and JunB antagonistically control cytokine-regulated mesenchymal-epidermal interaction in skin.Semantic proximity Read ↗

TNF-mediated inflammatory skin disease in mice with epidermis-specific deletion of IKK2Semantic proximity Read ↗

NF-kappaB and inflammation in genetic disease.Semantic proximity Read ↗

RNA-Seq and ChIP-Seq reveal SQSTM1/p62 as a key mediator of JunB suppression of NF-κB-dependent inflammation.Semantic proximity Read ↗

Keratinocyte-specific ablation of the NF-κB regulatory protein A20 (TNFAIP3) reveals a role in the control of epidermal homeostasis.Semantic proximity Read ↗

Tumor necrosis factor-alpha converting enzyme (TACE) regulates epidermal growth factor receptor ligand availability.Semantic proximity Read ↗

An essential role for ectodomain shedding in mammalian development.Semantic proximity Read ↗

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