ArticleNucleic acids research2015
Cooperation meets competition in microRNA-mediated DMPK transcript regulation.
Article in Nucleic acids research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
28 citing papers in PubMed, 34 citations in OpenAlex.
- Technologies for engineering repetitive DNA.Quantitative biology (Beijing, China) · 2026Review
- Emerging roles of microRNAs and other non-coding transcriptome in muscular dystrophies.Inflammation and regeneration · 2026Review
- Local Non-Coding Regulatory Elements in Muscular Dystrophies.International journal of molecular sciences · 2025Review
- miR-107 repressesMolecular therapy. Nucleic acids · 2025Article
- Oncoprotein LAMTOR5-mediated CHOP silence via DNA hypermethylation and miR-182/miR-769 in promotion of liver cancer growth.Acta pharmacologica Sinica · 2024Article
- AntimiR treatment corrects myotonic dystrophy primary cell defects across several CTG repeat expansions with a dual mechanism of action.Science advances · 2024Article
- BlockmiR AONs as Site-Specific Therapeutic MBNL Modulation in Myotonic Dystrophy 2D and 3D Muscle Cells and HSAPharmaceutics · 2023Article
- TNF Signaling Acts Downstream of MiR-322/-503 in Regulating DM1 Myogenesis.Frontiers in endocrinology · 2022Article
- Emergent correlations in gene expression dynamics as footprints of resource competition.The European physical journal. E, Soft matter · 2021Article
- Regulatory Potential of Competing Endogenous RNAs in Myotonic Dystrophies.International journal of molecular sciences · 2021Review
- Overlapping mechanisms of lncRNA and expanded microsatellite RNA.Wiley interdisciplinary reviews. RNA · 2021Review
- miR-322/-503 rescues myoblast defects in myotonic dystrophy type 1 cell model by targeting CUG repeats.Cell death & disease · 2020Article
- Quantitative and time-resolved miRNA pattern of early human T cell activation.Nucleic acids research · 2020Article
- AON-induced splice-switching and DMPK pre-mRNA degradation as potential therapeutic approaches for Myotonic Dystrophy type 1.Nucleic acids research · 2020Article
- MicroRNA-Based Therapeutic Perspectives in Myotonic Dystrophy.International journal of molecular sciences · 2019Review
- MicroRNA (miRNA)-to-miRNA Regulation of Programmed Cell Death 4 (PDCD4).Molecular and cellular biology · 2019Article
- Systems biology-based investigation of cooperating microRNAs as monotherapy or adjuvant therapy in cancer.Nucleic acids research · 2019Review
- Combination Treatment of Erythromycin and Furamidine Provides Additive and Synergistic Rescue of Mis-Splicing in Myotonic Dystrophy Type 1 Models.ACS pharmacology & translational science · 2019Article
- A mathematical model as a tool to identify microRNAs with highest impact on transcriptome changes.BMC genomics · 2019Article
- Ciphers and Executioners: How 3'-Untranslated Regions Determine the Fate of Messenger RNAs.Frontiers in genetics · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The fundamental role of microRNAs (miRNAs) in the regulation of gene expression has been well-established, but many miRNA-driven regulatory mechanisms remain elusive. In the present study, we demonstrate that miRNAs regulate the expression of DMPK, the gene mutated in myotonic dystrophy type 1 (DM1), and we provide insight regarding the concerted effect of the miRNAs on the DMPK target. Specifically, we examined the binding of several miRNAs to the DMPK 3' UTR using luciferase assays. We validated the interactions between the DMPK transcript and the conserved miR-206 and miR-148a. We suggest a possible cooperativity between these two miRNAs and discuss gene targeting by miRNA pairs that vary in distance between their binding sites and expression profiles. In the same luciferase reporter system, we showed miR-15b/16 binding to the non-conserved CUG repeat tract present in the DMPK transcript and that the CUG-repeat-binding miRNAs might also act cooperatively. Moreover, we detected miR-16 in cytoplasmic foci formed by exogenously expressed RNAs with expanded CUG repeats. Therefore, we propose that the expanded CUGs may serve as a target for concerted regulation by miRNAs and may also act as molecular sponges for natural miRNAs with CAG repeats in their seed regions, thereby affecting their physiological functions.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.