ArticleExperimental and molecular pathology2019
Comparative analysis of the DYRK1A-SRSF6-TNNT2 pathway in myocardial tissue from individuals with and without Down syndrome.
Article in Experimental and molecular pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 7 citations in OpenAlex.
- Emerging role of DYRK1A as a target in cardiovascular diseases (Review).Molecular medicine reports · 2026Review
- Integrative Insights Into DYRK1A From Molecular Function to Therapeutic Advancement.Chemical biology & drug design · 2026Review
- Targeting DYRKs in Cardiovascular Diseases: From Biological Mechanisms to Therapeutic Translation.International journal of molecular sciences · 2026Review
- Review
- Impact of DYRK1A Expression on TNNT2 Splicing and Daunorubicin Toxicity in Human iPSC-Derived Cardiomyocytes.Cardiovascular toxicology · 2022Article
- Analysis of the intracellular traffic of IgG in the context of Down syndrome (trisomy 21).Scientific reports · 2021Article
- New Molecular and Organelle Alterations Linked to Down Syndrome Heart Disease.Frontiers in genetics · 2021Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Down syndrome (trisomy 21) is characterized by genome-wide imbalances that result in a range of phenotypic manifestations. Altered expression of DYRK1A in the trisomic context has been linked to some Down syndrome phenotypes. DYRK1A regulates the splicing of cardiac troponin (TNNT2) through a pathway mediated by the master splicing factor SRSF6. Here, we documented the expression of the DYRK1A-SRSF6-TNNT2 pathway in a collection of myocardial samples from persons with and without Down syndrome. Results suggest that "gene dosage effect" may drive the expression of DYRK1A mRNA but has no effect on DYRK1A protein levels in trisomic myocardium. The levels of phosphorylated DYRK1A-Tyr321 tended to be higher (~35%) in myocardial samples from donors with Down syndrome. The levels of phosphorylated SRSF6 were 2.6-fold higher in trisomic myocardium. In line, the expression of fetal TNNT2 variants was higher in myocardial tissue with trisomy 21. These data provide a representative picture on the extent of inter-individual variation in myocardial DYRK1A-SRSF6-TNNT2 expression in the context of Down syndrome.
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Registered trials
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