ArticleeLife2016
Epidermal RAF prevents allergic skin disease.
Article in eLife, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- Article
- Better understanding the phenotypic effects of drugs through shared targets in genetic disease networks.Frontiers in pharmacology · 2024Article
- Ex-Vivo Skin Explant Culture Is a Model for TSLP-Mediated Skin Barrier Immunity.Life (Basel, Switzerland) · 2021Article
- Costello syndrome model mice with a HrasCell death & disease · 2020Article
- EMSY expression affects multiple components of the skin barrier with relevance to atopic dermatitis.The Journal of allergy and clinical immunology · 2019Article
- RAF dimers control vascular permeability and cytoskeletal rearrangements at endothelial cell-cell junctions.The FEBS journal · 2019Article
- GDF11 Antagonizes Psoriasis-like Skin Inflammation via Suppression of NF-κB Signaling Pathway.Inflammation · 2019Article
- Outstanding animal studies in allergy II. From atopic barrier and microbiome to allergen-specific immunotherapy.Current opinion in allergy and clinical immunology · 2017Review
- A cell-autonomous tumour suppressor role of RAF1 in hepatocarcinogenesis.Nature communications · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The RAS pathway is central to epidermal homeostasis, and its activation in tumors or in Rasopathies correlates with hyperproliferation. Downstream of RAS, RAF kinases are actionable targets regulating keratinocyte turnover; however, chemical RAF inhibitors paradoxically activate the pathway, promoting epidermal proliferation. We generated mice with compound epidermis-restricted BRAF/RAF1 ablation. In these animals, transient barrier defects and production of chemokines and Th2-type cytokines by keratinocytes cause a disease akin to human atopic dermatitis, characterized by IgE responses and local and systemic inflammation. Mechanistically, BRAF and RAF1 operate independently to balance MAPK signaling: BRAF promotes ERK activation, while RAF1 dims stress kinase activation. In vivo, JNK inhibition prevents disease onset, while MEK/ERK inhibition in mice lacking epidermal RAF1 phenocopies it. These results support a primary role of keratinocytes in the pathogenesis of atopic dermatitis, and the animals lacking BRAF and RAF1 in the epidermis represent a useful model for this disease.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.