ArticleThe Journal of investigative dermatology2025
Crosstalk in Skin: Loss of Desmoglein 1 in Keratinocytes Inhibits BRAF
Article in The Journal of investigative dermatology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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.
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
7 citing papers in PubMed.
- Spatial and Single-Cell Transcriptomics Reveal Keratinocytes as Key Players in Vulvar Lichen Sclerosus Pathogenesis.The Journal of investigative dermatology · 2026Article
- Article
- Chromosome 3p deletion leads to extensive genomic alterations in diverse cancers and confers synthetic lethality in uveal melanoma.bioRxiv : the preprint server for biology · 2026Article
- Evaluation of netrin 1 as a new biomarker in the differentiation of psoriatic arthritis from psoriasis.Scientific reports · 2025Article
- Desmosome mutations in keratinocytes fuel melanoma development.Nature genetics · 2025Article
- Dangerous liaisons: Loss of keratinocyte control over melanocytes in melanomagenesis.BioEssays : news and reviews in molecular, cellular and developmental biology · 2024Review
- The Cross Talk between Cellular Senescence and Melanoma: From Molecular Pathogenesis to Target Therapies.Cancers · 2023Review
Corrections and comments
- Update of
Authors and funding
6 authors.
Funding
Abstract
Melanoma arises from transformation of melanocytes in the basal layer of epidermis where they are surrounded by keratinocytes, with which they interact through cell contact and paracrine communication. Although research focuses on how the accumulation of oncogene and tumor suppressor gene mutations in melanocytes drive melanomagenesis, how alterations in keratinocytes serve as extrinsic drivers of melanoma initiation and progression is poorly understood. We recently identified keratinocyte desmoglein 1 (DSG1) as an mediator of keratinocyte:melanoma crosstalk. In this study, we address the extent to which DSG1 loss, which occurs in response to environmental stress such as UVR, affects early steps in melanomagenesis. RNA-sequencing analysis revealed that paracrine signals from DSG1-deficient keratinocytes mediate a transcriptional switch from a differentiated to undifferentiated cell state in melanocytes expressing BRAF
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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 Socratic graph.