ArticleCell death and differentiation2016
ΔNp63 regulates IL-33 and IL-31 signaling in atopic dermatitis.
Article in Cell death and differentiation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
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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.
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Who cites it
40 citing papers in PubMed, 51 citations in OpenAlex.
- Review
- Misregulation of T-box transcription factors drives BNP-NPR1 signalling underlying chronic itch.Nature communications · 2026Article
- Keratinocytes: A key player in skin immunity and their emerging roles in secondary lymphedema.JID innovations : skin science from molecules to population health · 2026Review
- Keratinocytes: pleiotropic orchestrators of cutaneous immunity and Inflammation - Emerging therapeutic paradigms in dermatological pathologies.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- p63 in skin homeostasis and disease: molecular mechanisms and therapeutic potentials.Cell death discovery · 2026Review
- Unveiling critical signaling pathways in the murine salivary gland and the role of midkine.iScience · 2026Article
- Extracellular vesicles ofGut microbes · 2025Article
- IL-31/33 Axis in Atopic Dermatitis.International journal of molecular sciences · 2025Review
- Targeting NLRP10 in Atopic Dermatitis: An Emerging Strategy to Modulate Epidermal Cell Death and Barrier Function.International journal of molecular sciences · 2025Review
- Neutrophil swarming is crucial for limiting oral mucosal infection by Candida albicans.Journal of leukocyte biology · 2025Article
- Review
- Molecular mechanisms of thalidomide effectiveness on COVID-19 patients explained: ACE2 is a new ΔNp63α target gene.Journal of molecular medicine (Berlin, Germany) · 2024Article
- Glucocorticoid receptor controls atopic dermatitis inflammation via functional interactions with P63 and autocrine signaling in epidermal keratinocytes.Cell death & disease · 2024Article
- ΔNp63 Regulates Homeostasis, Stemness, and Suppression of Inflammation in the Adult Epidermis.The Journal of investigative dermatology · 2024Article
- Article
- Direct 3D Sampling of the Embryonic Mouse Head: Layer-wise Nanosecond Infrared Laser (NIRL) Ablation from Scalp to Cortex for Spatially Resolved Proteomics.Analytical chemistry · 2023Article
- Neutrophil swarms containing myeloid-derived suppressor cells are crucial for limiting oral mucosal infection by C. albicans.Research square · 2023Article
- Orchestration of Mesenchymal Stem/Stromal Cells and Inflammation During Wound Healing.Stem cells translational medicine · 2023Review
- The Role of Tight Junctions in Atopic Dermatitis: A Systematic Review.Journal of clinical medicine · 2023Review
- Safe and Effective Antioxidant: The Biological Mechanism and Potential Pathways of Ergothioneine in the Skin.Molecules (Basel, Switzerland) · 2023Review
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
Abstract
Atopic dermatitis (AD) is the most common inflammatory skin disease with no well-delineated cause or effective cure. Here we show that the p53 family member p63, specifically the ΔNp63, isoform has a key role in driving keratinocyte activation in AD. We find that overexpression of ΔNp63 in transgenic mouse epidermis results in a severe skin phenotype that shares many of the key clinical, histological and molecular features associated with human AD. This includes pruritus, epidermal hyperplasia, aberrant keratinocyte differentiation, enhanced expression of selected cytokines and chemokines and the infiltration of large numbers of inflammatory cells including type 2 T-helper cells - features that are highly representative of AD dermatopathology. We further demonstrate several of these mediators to be direct transcriptional targets of ΔNp63 in keratinocytes. Of particular significance are two p63 target genes, IL-31 and IL-33, both of which are key players in the signaling pathways implicated in AD. Importantly, we find these observations to be in good agreement with elevated levels of ΔNp63 in skin lesions of human patients with AD. Our studies reveal an important role for ΔNp63 in the pathogenesis of AD and offer new insights into its etiology and possible therapeutic targets.
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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.