ArticleScientific reports2019
Neutrophil GM-CSF signaling in inflammatory bowel disease patients is influenced by non-coding genetic variants.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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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Who cites it
3 citing papers in PubMed, 4 citations in OpenAlex.
- Review
- Serum cytokines MCP-1 and GCS-F as potential biomarkers in pediatric inflammatory bowel disease.PloS one · 2023Article
- Rcl1 suppresses tumor progression of hepatocellular carcinoma: a comprehensive analysis of bioinformatics and in vitro experiments.Cancer cell international · 2022Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Neutrophil dysfunction and GM-CSF auto-antibodies are observed in pediatric and adult patients with Crohn's disease (CD). We associated damaging coding variants with low GM-CSF induced STAT5 stimulation index (GMSI) in pediatric CD patients and implicated variation of neutrophil GM-CSF signaling in cell function and disease complications. Because many CD patients with low GMSI do not carry damaging coding mutations, we sought to test the hypothesis that non-coding variants contribute to this phenotype. We enrolled, performed whole genome sequencing, and measured the GMSI in 77 CD and ulcerative colitis (UC) patients (24 low and 53 normal GMSI). We identified 4 non-coding variants (rs3808851, rs10974787, rs10974788 and rs10974789) in RCL1 significantly associated with variation of GMSI level (p < 0.011). They were validated in two independent cohorts with: RNAseq data (n = 50) and blood eQTL dataset (n = 31,684). These variants are in LD and affect expression of JAK2 (p 0.005 to 0.013), RCL1 (p 8.17E-13 to 2.98E-11) and AK3 (p 2.00E-68 to 3.03E-55) genes. Additionally, they influence proteins involved in differentiation of gut epithelium, inflammation, and immune system regulation. In summary, our study outlines the contribution of non-coding variants in neutrophil GM-CSF signaling and the potential importance of RCL1 and AK3 in CD pathogenesis.
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Registered trials
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