ArticleRNA biology
Trisomy-21 gene dosage over-expression of miRNAs results in the haploinsufficiency of specific target proteins.
Article in RNA biology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 83 citations in OpenAlex.
- Dysregulated miR-155 and miR-125b Are Related to Impaired B-cell Responses in Down Syndrome.Frontiers in immunology · 2018Trial
- Long-Term Non-Congenital Cardiac and Renal Complications in Down Syndrome: A Study of 32,936 Patients.Children (Basel, Switzerland) · 2023Article
- Mir125b-2 imprinted in human but not mouse brain regulates hippocampal function and circuit in mice.Communications biology · 2023Article
- A message passing framework with multiple data integration for miRNA-disease association prediction.Scientific reports · 2022Article
- Profiling of circulating chromosome 21-encoded microRNAs, miR-155, and let-7c, in down syndrome.Molecular genetics & genomic medicine · 2022Article
- Advances in molecular characterization of myeloid proliferations associated with Down syndrome.Frontiers in genetics · 2022Review
- Functional Role of miR-155 in the Pathogenesis of Diabetes Mellitus and Its Complications.Non-coding RNA · 2021Review
- The Potential Role of miRNAs as Predictive Biomarkers in Neurodevelopmental Disorders.Journal of molecular neuroscience : MN · 2021Review
- Fetal sex modulates placental microRNA expression, potential microRNA-mRNA interactions, and levels of amino acid transporter expression and substrates: INFAT study subpopulation analysis of n-3 LCPUFA intervention during pregnancy and associations with offspring body composition.BMC molecular and cell biology · 2021Article
- Interpreting the impact of noncoding structural variation in neurodevelopmental disorders.Genetics in medicine : official journal of the American College of Medical Genetics · 2021Review
- Inborn Errors of Adaptive Immunity in Down Syndrome.Journal of clinical immunology · 2020Review
- Mature miR-99a Upregulation in the Amniotic Fluid Samples from Female Fetus Down Syndrome Pregnancies: A Pilot Study.Medicina (Kaunas, Lithuania) · 2019Article
- Expression of miR-132 in Down syndrome subjects.Human cell · 2018Article
- Lifespan analysis of brain development, gene expression and behavioral phenotypes in the Ts1Cje, Ts65Dn and Dp(16)1/Yey mouse models of Down syndrome.Disease models & mechanisms · 2018Article
- MicroRNA Expression Profile in the Prenatal Amniotic Fluid Samples of Pregnant Women with Down Syndrome.Balkan medical journal · 2018Article
- Down syndrome and microRNAs.Biomedical reports · 2018Article
- Expression patterns of the chromosome 21 MicroRNA cluster (miR-99a, miR-125b and let-7c) in chorioamniotic membranes.Placenta · 2017Article
- Overexpression of Chromosome 21 miRNAs May Affect Mitochondrial Function in the Hearts of Down Syndrome Fetuses.International journal of genomics · 2017Article
- Integrated microRNA and protein expression analysis reveals novel microRNA regulation of targets in fetal down syndrome.Molecular medicine reports · 2016Article
- DYRK1A, a Dosage-Sensitive Gene Involved in Neurodevelopmental Disorders, Is a Target for Drug Development in Down Syndrome.Frontiers in behavioral neuroscience · 2016Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Down syndrome (DS) or Trisomy 21 (Ts21) is caused by the presence of an extra copy of all or part of human chromosome 21 (Hsa21) and is the most frequent survivable congenital chromosomal abnormality. Bioinformatic annotation has established that Hsa21 harbors more than 400 genes, including five microRNA (miRNA) genes (miR-99a, let-7c, miR-125b-2, miR-155, and miR-802). MiRNAs are endogenous, single-stranded, small non-coding RNA molecules that regulate gene expression by interacting with specific recognition elements harbored within the 3'-untranslated region (3'-UTR) of mRNAs and subsequently target these mRNAs for translational repression or destabilization. MiRNA expression profiling, miRNA RT-PCR, and miRNA in situ hybridization experiments have demonstrated that Hsa21-derived miRNAs were over-expressed in fetal brain and heart specimens isolated from individuals with DS. We now propose that Ts21 gene dosage over-expression of Hsa21-derived miRNAs in DS individuals result in the decreased expression of specific target proteins (i.e. haploinsufficiency) that contribute, in part, to the DS phenotype.
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Registered trials
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