ArticleFrontiers in genetics2022
Overexpression of the Hsa21 Transcription Factor RUNX1 Modulates the Extracellular Matrix in Trisomy 21 Cells.
Article in Frontiers in genetics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 12 citations in OpenAlex.
- Promoting Research Excellence in Down Syndrome: Proceedings of the 5th International Conference of the Trisomy 21 Research Society.Neuromolecular medicine · 2026Article
- The placental effects of trisomy for human chromosome 21 orthologs in four mouse models of Down syndrome.Biology open · 2025Article
- Non-Invasive Prenatal Screening for Down Syndrome: A Review of Mass-Spectrometry-Based Approaches.Life (Basel, Switzerland) · 2025Review
- Analysis of genotype effects and inter-individual variability in iPSC-derived trisomy 21 neural progenitor cells.Human molecular genetics · 2025Article
- Comparison of the amyloid plaque proteome in Down syndrome, early-onset Alzheimer's disease, and late-onset Alzheimer's disease.Acta neuropathologica · 2025Article
- Runt-related transcription factors: from pathogenesis to therapeutic targets in multiple-organ fibrosis.Frontiers in cell and developmental biology · 2025Review
- Comparison of the Amyloid Plaque Proteome in Down Syndrome, Early-Onset Alzheimer's Disease and Late-Onset Alzheimer's Disease.Research square · 2024Article
- Transcriptional consequences of trisomy 21 on neural induction.Frontiers in cellular neuroscience · 2024Article
- Runx1 Deficiency Promotes M2 Macrophage Polarization Through Enhancing STAT6 Phosphorylation.Inflammation · 2023Article
- RUN(X) out of blood: emerging RUNX1 functions beyond hematopoiesis and links to Down syndrome.Human genomics · 2023Review
- Genetics and Molecular Basis of Congenital Heart Defects in Down Syndrome: Role of Extracellular Matrix Regulation.International journal of molecular sciences · 2023Review
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Down syndrome is a neurodevelopmental disorder frequently characterized by other developmental defects, such as congenital heart disease. Analysis of gene expression profiles of hearts from trisomic fetuses have shown upregulation of extracellular matrix (ECM) genes. The aim of this work was to identify genes on chromosome 21 potentially responsible for the upregulation of ECM genes and to pinpoint any functional consequences of this upregulation. By gene set enrichment analysis of public data sets, we identified the transcription factor RUNX1, which maps to chromosome 21, as a possible candidate for regulation of ECM genes. We assessed that approximately 80% of ECM genes overexpressed in trisomic hearts have consensus sequences for RUNX1 in their promoters. We found that in human fetal fibroblasts with chromosome 21 trisomy there is increased expression of both
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