ArticleRNA (New York, N.Y.)2020
Human disease-associated single nucleotide polymorphism changes the orientation of DROSHA on pri-mir-146a.
Article in RNA (New York, N.Y.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 14 citations in OpenAlex.
- Association of the miR-146a rs57095329 polymorphism with susceptibility and clinical phenotypes in Parkinson's disease.Neurogenetics · 2026Article
- Physical exercise and miR-146a in type 2 diabetes and obesity: a narrative review.Molecular biology reports · 2026Review
- Therapeutic microRNAs: Mechanisms, Delivery, and Clinical Translation in Oncology.International journal of molecular sciences · 2026Review
- Review
- Multifaceted role of microRNAs in gastric cancer stem cells: Mechanisms and potential biomarkers.World journal of gastrointestinal oncology · 2024Review
- SRSF7 and SRSF3 depend on RNA sequencing motifs and secondary structures to regulate Microprocessor.Life science alliance · 2023Article
- The microRNA Lifecycle in Health and Cancer.Cancers · 2022Review
- Review
- A Mutation in Endogenous saRNA miR-23a Influences Granulosa Cells Response to Oxidative Stress.Antioxidants (Basel, Switzerland) · 2022Article
- Consequences of genetic variants in miRNA genes.Computational and structural biotechnology journal · 2022Review
- The conserved single-cleavage mechanism of animal DROSHA enzymes.Communications biology · 2021Article
- Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Microprocessor complex of DROSHA and DGCR8 initiates the biosynthesis of microRNAs (miRNAs) by processing primary miRNAs (pri-miRNAs). The Microprocessor can be oriented on pri-miRNAs in opposite directions to generate productive and unproductive cleavages at their basal and apical junctions, respectively. However, only the productive cleavage gives rise to miRNAs. A single nucleotide polymorphism (SNP, rs2910164) in pri-mir-146a is associated with various human diseases. Although this SNP was found to reduce the expression of miRNA, it is still not known if it affects the activity of the Microprocessor directly, and how it functions. In this study, we revealed that the SNP creates an unexpected mGHG motif at the apical junction of pri-mir-146a. This mGHG motif interacts with the double-stranded RNA-binding domain (dsRBD) of DROSHA, switching its orientation on pri-mir-146a from the basal to the apical junction. As a result, the SNP facilitates Microprocessor to cleave SNP-pri-mir-146a at its unproductive sites. Our findings help to elucidate the molecular mechanism that explains how the disease-associated SNP modulates the biogenesis of pri-mir-146a and thereby affects its cellular functions.
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