ArticleOncogene2025
Atg16l1 and Xbp1 cooperatively protect from transcription-associated mutagenesis and small intestinal carcinogenesis.
Article in Oncogene, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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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22 authors.
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Abstract
Atg16l1 plays a critical role in autophagy, and Xbp1 is part of the endoplasmic reticulum (ER) homeostasis. Both, Atg16l1 and Xbp1 are known risk genes for inflammatory bowel disease (IBD). Previous studies have shown that dysfunctional Atg16l1 and Xbp1 are epithelial-derived drivers of small intestinal inflammation. Despite a clear link between Crohn's disease and small intestinal adenocarcinoma, the molecular impact of autophagy and ER stress in this malignant transformation is not known. Using a model of impaired ribonucleotide excision repair (RER), a key homeostatic repair mechanism in highly proliferative cells, we investigated the impact of Atg16l1 on epithelial DNA damage responses and small intestinal carcinogenesis with and without functional ER homeostasis. We used conditional mouse models for deficient RER (Rnaseh2b
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