ArticleFrontiers in cell and developmental biology2019
STAT3 Regulates miR-384 Transcription During Th17 Polarization.
Article in Frontiers in cell and developmental biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 21 citations in OpenAlex.
- Revealing the regulatory role of lncRNAs SNHG1 and CRNDE on Th17/Treg imbalance in diabetic kidney disease.Clinical and experimental medicine · 2025Article
- Insight into the shared pathogenic link between COVID-19 and pterygium: a systematic bioinformatics analysis with experimental validation.Hereditas · 2025Article
- Expression of T cell-related proteins in breast ductal carcinomaHistology and histopathology · 2025Article
- The critical role of Th17 cells and IL-17A in autoimmune and inflammation-associated neurological diseases: mechanisms and therapeutic perspectives.Frontiers in immunology · 2025Review
- Scavenging the hidden impacts of non-coding RNAs in multiple sclerosis.Non-coding RNA research · 2021Article
- Cytokine storm in the pathophysiology of COVID-19: Possible functional disturbances of miRNAs.International immunopharmacology · 2021Review
- The BBX gene family in Moso bamboo (Phyllostachys edulis): identification, characterization and expression profiles.BMC genomics · 2021Article
- miRNAs Alter T Helper 17 Cell Fate in the Pathogenesis of Autoimmune Diseases.Frontiers in immunology · 2021Review
- Brahma Related Gene 1 (Brg1) Regulates Cellular Cholesterol Synthesis by Acting as a Co-factor for SREBP2.Frontiers in cell and developmental biology · 2020Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNAs are powerful regulators of gene expression in physiological and pathological conditions. We previously showed that the dysregulation of miR-384 resulted in a T helper cell 17 (Th17) imbalance and contributed to the pathogenesis of experimental autoimmune encephalomyelitis, an animal model of multiple sclerosis. In this study, we evaluated the molecular mechanisms underlying the abnormal increase in miR-384. We did not detect typical CpG islands in the
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Registered trials
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