ArticleMucosal immunology2021
PRKAR2A deficiency protects mice from experimental colitis by increasing IFN-stimulated gene expression and modulating the intestinal microbiota.
Article in Mucosal immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed, 10 citations in OpenAlex.
- Editing regulatory network in non-small cell lung cancer: implications for immunity and metastasis.Human genomics · 2026Article
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- CRFB5a, a Subtype of Japanese Eel (Animals : an open access journal from MDPI · 2023Article
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- Multi-context genetic modeling of transcriptional regulation resolves novel disease loci.Nature communications · 2022Article
- Interleukin-22 Deficiency Contributes to Dextran Sulfate Sodium-Induced Inflammation in Japanese Medaka,Frontiers in immunology · 2021Article
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Authors and funding
8 authors at 3 institutions in 1 country.
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Abstract
Protein kinase A (PKA) plays an important role in regulating inflammation via its catalytic subunits. Recently, PKA regulatory subunits have been reported to directly modulate some signaling pathways and alleviate inflammation. However, the role of PKA regulatory subunits in colonic inflammation remains unclear. Therefore, we conducted this study to investigate the role of the PKA regulatory subunit PRKAR2A in colitis. We observed that PRKAR2A deficiency protected mice from dextran sulfate sodium (DSS)-induced experimental colitis. Our experiments revealed that the intestinal epithelial cell-specific deletion of Prkar2a contributed to this protection. Mechanistically, the loss of PRKAR2A in Prkar2a
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