ArticlePLoS genetics2013
MicroRNA-17-92, a direct Ap-2α transcriptional target, modulates T-box factor activity in orofacial clefting.
Article in PLoS genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 51 papers, 1 of them a synthesis that pooled it.
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
51 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.
- Genes and microRNAs associated with mouse cleft palate: A systematic review and bioinformatics analysis.Mechanisms of development · 2018Pooled it
- Integrated assessment of differentially expressed plasma microRNAs in subtypes of nonsyndromic orofacial clefts.Medicine · 2018Trial
- Epigenetic Mechanisms in Cleft Lip and Palate: A Comprehensive Review of Current Insights and Future Perspectives.Plastic and reconstructive surgery. Global open · 2026Article
- Multiscale Convergence of Signaling, Epigenetic, and Environmental Networks in Mammalian Palatogenesis and Cleft Palate Pathogenesis.International journal of stem cells · 2026Review
- Article
- Cleft Palate Induced by Mycophenolate Mofetil Is Associated withNon-coding RNA · 2025Article
- Molecular Regulation of Palatogenesis and Clefting: An Integrative Analysis of Genetic, Epigenetic Networks, and Environmental Interactions.International journal of molecular sciences · 2025Review
- The Essential Function of miR-5739 in Embryonic Muscle Development.International journal of stem cells · 2023Article
- GRHL2 and AP2a coordinate early surface ectoderm lineage commitment during development.iScience · 2023Article
- MicroRNAs and Gene Regulatory Networks Related to Cleft Lip and Palate.International journal of molecular sciences · 2023Review
- TCDD induces cleft palate through exosomes derived from mesenchymal cells.Toxicology research · 2022Article
- Craniofacial Phenotypes and Genetics of DiGeorge Syndrome.Journal of developmental biology · 2022Review
- Suppression of microRNA 124-3p and microRNA 340-5p ameliorates retinoic acid-induced cleft palate in mice.Development (Cambridge, England) · 2022Article
- Identification of microRNAs and gene regulatory networks in cleft lip common in humans and mice.Human molecular genetics · 2021Article
- Exosomes-a potential indicator and mediator of cleft lip and palate: a narrative review.Annals of translational medicine · 2021Review
- Differential Spatio-Temporal Regulation of T-Box Gene Expression by microRNAs during Cardiac Development.Journal of cardiovascular development and disease · 2021Article
- Review
- Phenytoin Inhibits Cell Proliferation through microRNA-196a-5p in Mouse Lip Mesenchymal Cells.International journal of molecular sciences · 2021Article
- MicroRNA-124-3p Plays a Crucial Role in Cleft Palate Induced by Retinoic Acid.Frontiers in cell and developmental biology · 2021Article
- Gene-Environment Interplay and MicroRNAs in Cleft Lip and Cleft Palate.Oral science international · 2021Article
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Among the most common human congenital anomalies, cleft lip and palate (CL/P) affects up to 1 in 700 live births. MicroRNA (miR)s are small, non-coding RNAs that repress gene expression post-transcriptionally. The miR-17-92 cluster encodes six miRs that have been implicated in human cancers and heart development. We discovered that miR-17-92 mutant embryos had severe craniofacial phenotypes, including incompletely penetrant CL/P and mandibular hypoplasia. Embryos that were compound mutant for miR-17-92 and the related miR-106b-25 cluster had completely penetrant CL/P. Expression of Tbx1 and Tbx3, the DiGeorge/velo-cardio-facial (DGS) and Ulnar-mammary syndrome (UMS) disease genes, was expanded in miR-17-92 mutant craniofacial structures. Both Tbx1 and Tbx3 had functional miR seed sequences that mediated gene repression. Analysis of miR-17-92 regulatory regions uncovered conserved and functional AP-2α recognition elements that directed miR-17-92 expression. Together, our data indicate that miR-17-92 modulates expression of critical T-box transcriptional regulators during midface development and is itself a target of Bmp-signaling and the craniofacial pioneer factor AP-2α. Our data are the first genetic evidence that an individual miR or miR cluster is functionally important in mammalian CL/P.
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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.