ArticleJournal of immunology research2022
lncRNA STAT4-AS1 Inhibited TH17 Cell Differentiation by Targeting ROR
Article in Journal of immunology research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- Whole-genome profiling of age- and sex-associated DNA methylation signatures in human plasma cell-free DNA.Communications medicine · 2025Article
- Th17 cell pathogenicity in autoimmune disease.Experimental & molecular medicine · 2025Review
- miRNAs and T cell-mediated Immune Response in Disease.The Yale journal of biology and medicine · 2025Review
- The Role of Long Non-Coding RNA in the Pathogenesis of Psoriasis.Non-coding RNA · 2025Review
- Mechanisms and therapeutic prospect of the JAK-STAT signaling pathway in liver cancer.Molecular and cellular biochemistry · 2025Review
- Regulation of T cell differentiation and function by long noncoding RNAs in homeostasis and cancer.Frontiers in immunology · 2023Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: From our previous study, we obtained long noncoding RNA (lncRNA) STAT4-AS1, which is related to asthma through high-throughput screening. However, we could not determine the specific mechanism involved and in response to this. We further designed this study. Results: First, we found that lncRNA STAT4-AS1 was downregulated in T cells from patients with asthma when compared to healthy controls. Next, we confirmed that lncRNA STAT4-AS1 was significantly negatively correlated with T helper 17 (TH17) differentiation in vitro experiments. The decreases of STAT4-AS1 promoted TH17 differentiation, while the increases of STAT4-AS1 inhibited TH17 differentiation. Subsequently, through RNA pull-down, RNA-binding protein immunoprecipitation (RIP), and dual luciferase reporter assay, we found that STAT4-AS1 could inhibit the binding of retinoid-related orphan receptor- Conclusion: Overall, STAT4-AS1 directly targets ROR
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Registered trials
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