ArticleImmunologic research2021
AKAP12/Gravin is over-expressed in patients with ulcerative colitis.
Article in Immunologic research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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7 citing papers in PubMed, 6 citations in OpenAlex.
- Deletion of Circadian Rhythms Gene BMAL1 Impairs the Intestinal Epithelial Barrier and Exacerbates Intestinal Inflammation by Inducing Pyroptosis.Mediators of inflammation · 2026Article
- Protective role of ABCC drug subfamily resistance transporters (ABCC1-7) in intestinal inflammation.Immunologic research · 2025Article
- AKAP12, mediated by transcription factor 21, inhibits cell proliferation, metastasis, and glycolysis in lung squamous cell carcinoma.Open life sciences · 2025Article
- Participation of Semaphorin Family and Plexins in the Clinical Course of Patients with Inflammatory Bowel Disease.International journal of molecular sciences · 2024Article
- Differential expression of TOB/BTG family members in patients with plaque psoriasis: cross-sectional study.Immunologic research · 2024Observational
- Increased synthesis and intestinal expression of IL-39 in patients with inflammatory bowel disease.Immunologic research · 2024Article
- Physiologic and pathophysiologic roles of AKAP12.Science progressArticle
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6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The gene of A-kinase anchor protein 12 (AKAP12) regulates cell cycle progression, cell motility, and morphology through its multiple scaffolding domains. However, the role of AKAP12 expression in ulcerative colitis (UC) patients has not been yet described. The aim of the study was to describe the gene and protein of AKAP12 expression in patients with UC and its association regarding the disease severity. We included a total of 40 patients with confirmed diagnosis of UC and 25 controls without endoscopic evidence of colitis or neoplasia. The relative quantification of the gene expression was performed by real-time PCR for AKAP12. Kruskal-Wallis was used to test differences among groups, and Spearman correlation to assess the relationship between AKAP12 gene and clinical outcomes. The extent of disease was evaluated using total colonoscopy, and biopsies were taken from rectum segments. The AKAP12 gene expression was increased in colonic mucosa from patients with active UC when compared with UC remission and control group. The overexpression of AKAP12 in patients with UC was associated with the presence of extensive colitis (p = 0.04, RM = 12, IC = 1.29-186.37). AKAP12/CD16 double positive cells were higher in submucosa (p = 0.04), muscular (p < 0.001), and cells from serosa (p < 0.001) in patients affected by UC in comparison to controls. The overexpression of AKAP12 was associated with the extent of disease. This is the first report about the role of AKAP12 in patients with UC suggesting that this gene and its protein could be involved in the modulation of the disease.
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