ArticleFrontiers in cell death2025
C/EBPβ Deficiency Enhances Keratinocyte Apoptosis after UVB-Induced DNA Damage via Regulation of the Type I IFN and TNF Responses.
Article in Frontiers in cell death, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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Who cites it
1 citing paper in PubMed.
- Kilobase-scale compartments enabled by CRUSH reveal regulatory programs across cell types, single-cells, and ancient mammoths.bioRxiv : the preprint server for biology · 2026Article
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Authors and funding
6 authors.
Funding
Abstract
The epidermis is routinely subjected to DNA damage induced by ultraviolet B (UVB) solar radiation. In addition to activating canonical DNA damage responses such as cycle cell checkpoints and DNA repair, UVB-induced DNA damage can also activate additional signaling pathways including inflammatory responses. The pathways activated downstream of UVB-induced DNA damage have a critical role in determining cellular survival to UVB radiation. Here we report that loss of CCAAT/enhancer binding protein β (C/EBPβ) in mouse keratinocytes results in enhanced UVB-induced apoptosis through activation of extrinsic apoptosis genes cleaved caspase-8 and truncated BH3 interacting-domain death agonist (tBid). RNAseq and Ingenuity Pathway Analysis of UVB-treated C/EBPβ
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Registered trials
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