ArticleJournal of molecular histology2022
Knockdown of lncRNA HAGLR promotes Treg cell differentiation through increasing the RUNX3 level in dermatomyositis.
Article in Journal of molecular histology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Review
- A symphony of signals: the intricate role of lncRNAs in dermatological disorders.Clinical and experimental medicine · 2025Review
- The epigenetic hallmarks of immune cells in cancer.Molecular cancer · 2025Review
- CD4+ T-cell subsets in autoimmune hepatitis: A review.Hepatology communications · 2023Review
- LncRNA HAGLR silencing inhibits IL-1β-induced chondrocytes inflammatory injury via miR-130a-3p/JAK1 axis.Journal of orthopaedic surgery and research · 2023Article
- Review
- Idiopathic inflammatory myopathy and non-coding RNA.Frontiers in immunology · 2023Review
- Five genes as diagnostic biomarkers of dermatomyositis and their correlation with immune cell infiltration.Frontiers in immunology · 2023Article
- Nature vs. nurture: FOXP3, genetics, and tissue environment shape Treg function.Frontiers in immunology · 2022Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Dermatomyositis (DM) is a systemic autoimmune disease. It's known that the number of regulatory T (Treg) cells was decreased in DM. Besides, Treg cells were increased after treatment in DM patients. Forkhead box P3 (Foxp3) is specifically expressed in Treg cells and Runt-related transcription factor (RUNX3) could regulate Foxp3 transcription. And our previous experiment showed that Homeobox D gene cluster antisense growth-associated long noncoding RNA (HAGLR) was up-regulated in DM patients. Here, we aimed to explore whether HAGLR regulated the differentiation of Treg cells through RUNX3-mediated transcription of Foxp3, thus affecting the progression of DM. The levels of HAGLR, Foxp3, and RUNX3 were examined by quantitative real-time PCR. The protein levels of Foxp3 and RUNX3 were examined by western blot. The proportions of Treg cells in CD4
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Registered trials
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