ArticleFrontiers in neurology2020
Mir106b-25 and Mir17-92 Are Crucially Involved in the Development of Experimental Neuroinflammation.
Article in Frontiers in neurology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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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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
5 citing papers in PubMed, 6 citations in OpenAlex.
- Deregulation of ceRNA Networks in Frontal Cortex and Choroid Plexus of Brain during SARS-CoV-2 Infection Aggravates Neurological Manifestations: An Insight from Bulk and Single-Cell Transcriptomic Analyses.Advanced biology · 2022Article
- The role of non-coding RNAs in neuroinflammatory process in multiple sclerosis.Molecular neurobiology · 2022Review
- Scavenging the hidden impacts of non-coding RNAs in multiple sclerosis.Non-coding RNA research · 2021Article
- Article
- miR-21 sustains CD28 signalling and low-affinity T-cell responses at the expense of self-tolerance.Clinical & translational immunology · 2021Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNAs (miRNAs) are single-stranded RNA that have key roles in the development of the immune system and are involved in the pathogenesis of various autoimmune diseases. We previously demonstrated that two members of the miR106b-25 cluster and the miR17-92 paralog cluster were upregulated in T regulatory cells from multiple sclerosis (MS) patients. The aim of the present work was to clarify the impact of miR106b-25 and miR17-92 clusters in MS pathogenesis. Here, we show that the mice lacking miR17-92 specifically in CD4
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