ArticleClinical rheumatology2015
Tespa1 is associated with susceptibility but not severity of rheumatoid arthritis in the Zhejiang Han population in China.
Article in Clinical rheumatology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed, 8 citations in OpenAlex.
- Identification of SLAMF1 as an immune-related key gene associated with rheumatoid arthritis and verified in mice collagen-induced arthritis model.Frontiers in immunology · 2022Article
- Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Observational and experimental studies in animal models have shown that Tespa1 may be associated with B cell function and the onset of rheumatoid arthritis (RA). We hypothesized that Tespa1 may also play an important role in patients with RA. To test this hypothesis, we investigated the expression level, gene polymorphisms, and promoter methylation of the Tespa1 gene in 77 RA patients and 113 matched healthy controls. We found that the expression of Tespa1 is significantly lower in RA patients with both low and moderate-to-high disease activity. Moreover, patients with familial (first-degree siblings) but not sporadic RA have a statistically significant difference at the rs4758993 locus with healthy people. Furthermore, we found seven methylation sites on the Tespa1 promoter, but no evidence of the association between methylation at these sites and RA susceptibility. These data support a potential role for Tespa1 in the pathogenesis of RA.
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