ArticleNature communications2017
Systematic proteome and proteostasis profiling in human Trisomy 21 fibroblast cells.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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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.
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Who cites it
91 citing papers in PubMed, 1 synthesis or guideline pooled it, 152 citations in OpenAlex.
- Meta-analysis of metabolites involved in bioenergetic pathways reveals a pseudohypoxic state in Down syndrome.Molecular medicine (Cambridge, Mass.) · 2020Pooled it
- Gene dosage imbalance disrupts systemic metabolism in the Dp16 Down syndrome mouse model.eLife · 2026Article
- A mathematical model of folate-mediated one-carbon metabolism in Down syndrome.NPJ systems biology and applications · 2026Article
- The proteomics and phosphoproteomics landscape of melanoma under T cell attack.Cell reports. Medicine · 2026Article
- Loss of Proteostasis and Early-Onset Neurodegeneration in Down Syndrome: From Mechanisms to Interventions.Antioxidants (Basel, Switzerland) · 2026Review
- Protein buffering of aneuploidy is driven by coordinated factors identified through machine learning.Molecular systems biology · 2026Article
- Impact of Chromosomal Instability and Aneuploidy in Cancer Development.Annual review of cancer biology · 2026Article
- Gene dosage imbalance disrupts systemic metabolism in the Dp16 Down syndrome mouse model.bioRxiv : the preprint server for biology · 2026Article
- Proteome Signature of Alzheimer-Like Phenotypes in Frontal Cortices From Young and Old Individuals With Down Syndrome.Molecular neurobiology · 2025Article
- Divergent proteome tolerance against gain and loss of chromosome arms.Molecular cell · 2025Article
- Energetics of whole genome doubling and genomic instability.Cancer letters · 2025Review
- Role of cystathionine-β-synthase and hydrogen sulfide in down syndrome.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- Molecular cartography of the human down syndrome and trisomic mouse brain.Nature communications · 2025Article
- A robust multiplex-DIA workflow profiles protein turnover regulations associated with cisplatin resistance and aneuploidy.Nature communications · 2025Article
- Proteomics-based characterization of ribosome heterogeneity in adult mouse organs.Cellular and molecular life sciences : CMLS · 2025Article
- Article
- Mitochondrial Imbalance in Down Syndrome: A Driver of Accelerated Brain Aging?Aging and disease · 2025Review
- Analysis of genotype effects and inter-individual variability in iPSC-derived trisomy 21 neural progenitor cells.Human molecular genetics · 2025Article
- An Extensive Atlas of Proteome and Phosphoproteome Turnover Across Mouse Tissues and Brain Regions.bioRxiv : the preprint server for biology · 2024Article
- Comparative modeling reveals the molecular determinants of aneuploidy fitness cost in a wild yeast model.Cell genomics · 2024Article
31 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 7 institutions in 4 countries.
Funding
Abstract
Down syndrome (DS) is mostly caused by a trisomy of the entire Chromosome 21 (Trisomy 21, T21). Here, we use SWATH mass spectrometry to quantify protein abundance and protein turnover in fibroblasts from a monozygotic twin pair discordant for T21, and to profile protein expression in 11 unrelated DS individuals and matched controls. The integration of the steady-state and turnover proteomic data indicates that protein-specific degradation of members of stoichiometric complexes is a major determinant of T21 gene dosage outcome, both within and between individuals. This effect is not apparent from genomic and transcriptomic data. The data also reveal that T21 results in extensive proteome remodeling, affecting proteins encoded by all chromosomes. Finally, we find broad, organelle-specific post-transcriptional effects such as significant downregulation of the mitochondrial proteome contributing to T21 hallmarks. Overall, we provide a valuable proteomic resource to understand the origin of DS phenotypic manifestations.
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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.