#COL17A1
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acr-journals.bsky.social
In vitro study of cutaneous lupus skin found accumulation of CDKN1A (p21WAF1/CIP1)-positive senescent epidermal cells. Senescent cells may contribute to CLE disease pathology by enabling cytotoxic T cell-mediated responses against normal epidermis

A&R
doi.org/10.1002/art....

#Medsky #Immunosky
Identification of the senescent epidermal basal cell population in the skin of patients with systemic lupus erythematosus (SLE). UMAP of epidermal basal cells from the skin of patients with SLE. Heatmap of differentially expressed genes across five cell clusters of epidermal basal cells. c Violin plots of the median enrichment scores for 7 senescence-associated gene sets. The cellular senescence-associated gene sets Casella UP, Fridman UP, SenMayo, Global Senescence Literature Curated 2020, SASP Literature Curated gene set, Purcell, and Hernandez were used. d Heatmap showing differential pathway activity between COL17A1-high and CDKN1A-high senescence clusters. e–f Bubble plot of the top 10 gene ontology (GO) terms for biological processes in COL17A1-high and CDKN1A-high senescence clusters. g Violin plots of the ssGSEA scores for type I interferon (IFN) production. Data are presented as violin plots. Schematic diagram showing the contribution of senescent epidermal basal cells to systemic lupus erythematosus (SLE) skin pathogenesis. Senescent epidermal basal cells, characterized by increased CDKN1A and decreased COL17A1 expression, accumulate in the epidermis of skin lesions in SLE. These cells secrete senescence-associated secretory phenotype (SASP) factors, including type I interferons (IFN) and epidermal growth factor receptor (EGFR) ligands. The autocrine effect of EGFR ligands in senescent epidermal basal cells results in decreased HLA-I expression. Conversely, non-senescent epidermal basal cells exhibit a type I IFN response-dominant phenotype, leading to increased HLA-I expression, as well as antigen
May 28, 2025 at 8:21 PM
moltherapy.bsky.social
Differential Responses of COL17A1 Nonsense Mutations to Readthrough Drugs and NOG as a Novel Enhancer in Junctional Epidermolysis Bullosa
COL17A1 nonsense mutations generate premature termination codons, reducing collagen XVII through truncated protein production and/or nonsense-mediated decay (NMD), and causing junctional epidermolysis bullosa. Translational readthrough drug offers a potential approach to nonsense mutations suppression. Different COL17A1 nonsense mutations showed distinct responses to readthrough drugs and NMD inhibitors, supporting personalized therapeutic strategies.
dlvr.it
September 3, 2026 at 6:07 PM
prepub-singlecell.bsky.social
scRNA-seq of preeclamptic trophoblasts identifies EBI3, COL17A1, miR-27a-5p, and miR-193b-5p as hypoxia markers: validation of neuradapt as a superior mimetic to cobalt chloride #SingleCell 🧪🧬🖥️
https://arxiv.org/abs/2510.01935
February 11, 2026 at 8:00 AM
prepub-singlecell.bsky.social
Single-cell sequencing of trophoblasts in preeclampsia and chemical hypoxia in BeWo b30 cells reveals EBI3, COL17A1, miR-27a-5p, and miR-193b-5p as hypoxia-response markers #SingleCell 🧪🧬🖥️
https://arxiv.org/abs/2510.01935
October 3, 2025 at 7:00 AM
longtail-news.bsky.social
Feed: "STITCHES"
By: STITCHES Newsletter on Saturday, December 27, 2025
New Prognostic Model for Pancreatic Cancer Outcomes
A novel risk model using stress granule-related gene signatures (sgrgs) shows promise for improving prognostic accuracy in pancreatic ductal adenocarcinoma (PDAC).Four key sgrgs (lama3, itga6, col17a1...
www.stitches.today
December 28, 2025 at 10:46 AM
qbiogn-bot.bsky.social
Evgeny Knyazev, Timur Kulagin, Ivan Antipenko, Alexander Tonevitsky: Single-cell sequencing of trophoblasts in preeclampsia and chemical hypoxia in BeWo b30 cells reveals EBI3, COL17A1, miR-2... https://arxiv.org/abs/2510.01935 https://arxiv.org/pdf/2510.01935 https://arxiv.org/html/2510.01935
October 3, 2025 at 6:50 AM
jax.org
📘 New in PLOS ONE from @plos.bsky.social, "Dystonin modifiers of junctional epidermolysis bullosa and models of epidermolysis bullosa simplex without dystonia musculorum" with T.Sproule, R.Wilpan, J.Wilson, B.Low, M.Wiles, D.Roopenian & J.Sundberg:

#jaxresearch

doi.org/10.1371/jour...
Dystonin modifiers of junctional epidermolysis bullosa and models of epidermolysis bullosa simplex w...
The Lamc2jeb junctional epidermolysis bullosa (EB) mouse model has been used to demonstrate that significant genetic modification of EB symptoms is possible, identifying as modifiers Col17a1 and six o...
doi.org
December 5, 2023 at 2:25 PM
biorxiv-devbio.bsky.social
Single-cell sequencing of trophoblasts in preeclampsia and chemical hypoxia in BeWo b30 cells reveals EBI3, COL17A1, miR-27a-5p, and miR-193b-5p as hypoxia-response markers https://www.biorxiv.org/content/10.1101/2025.09.30.679431v1
October 2, 2025 at 12:30 AM
biorxivpreprint.bsky.social
Single-cell sequencing of trophoblasts in preeclampsia and chemical hypoxia in BeWo b30 cells reveals EBI3, COL17A1, miR-27a-5p, and miR-193b-5p as hypoxia-response markers https://www.biorxiv.org/content/10.1101/2025.09.30.679431v1
October 2, 2025 at 12:30 AM
thejidinnovations.bsky.social
From the March 2026 issue: Association of #immunecheckpointinhibitor induced #bullouspemphigoid with underlying cancer type: a lack of association with cancer tissue #COL17A1 mutations and dysregulation https://ow.ly/zNhA50Yzb4J #dermatology #dermsky
April 17, 2026 at 6:55 PM
thejidinnovations.bsky.social
Association of #immunecheckpointinhibitor induced #bullouspemphigoid with underlying cancer type: a lack of association with cancer tissue #COL17A1 mutations and dysregulation https://www.jidinnovations.org/article/S2667-0267(26)00001-9/fulltext #dermatology #dermsky
January 20, 2026 at 2:50 PM
ipatramanis.bsky.social
How much phylogenetic information is in these proteins?

We saw that these proteins can vary greatly, with collagen and amelogenin (AMELX) being quite conserved, but other proteins (ODAM,COL17A1 and even AMELY!) being far more variable.
April 15, 2025 at 11:06 AM