ArticleCell reports2018
Trisomy of a Down Syndrome Critical Region Globally Amplifies Transcription via HMGN1 Overexpression.
Article in Cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 2 of them syntheses that pooled it.
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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
41 citing papers in PubMed, 2 syntheses or guidelines pooled it, 66 citations in OpenAlex.
- Incidence of urological tumors in Down's syndrome: a systematic review and meta-analysis.International urology and nephrology · 2023Pooled it
- Meta-analysis of transcriptomic data reveals clusters of consistently deregulated gene and disease ontologies in Down syndrome.PLoS computational biology · 2021Pooled it
- The spatial and multi-omic landscape of Down syndrome leukemogenesis: moving beyond cellular heterogeneity.Experimental hematology & oncology · 2026Article
- Biological and pathogenic roles of major genes harbored in intrachromosomal amplification of chromosome 21 in childhood acute lymphoblastic leukemia (Review).Oncology letters · 2026Review
- Single-cell atlas of the developing Down syndrome brain cortex.Nature medicine · 2026Article
- Article
- RNADecayCafe, a uniformly processed atlas of RNA half-life estimates across multiple human cell lines.bioRxiv : the preprint server for biology · 2025Article
- The Hallmarks of Aneuploidy in Cancer and Congenital Syndromes.Annual review of genomics and human genetics · 2025Review
- Single-cell transcriptome analysis upon ECM-remodeling meningioma cells.Neurosurgical review · 2024Article
- A combination of long- and short-read genomics reveals frequent p-arm breakpoints within chromosome 21 complex genomic rearrangements.Genetics in medicine open · 2024Article
- Article
- Transcriptional repression by a secondary DNA binding surface of DNA topoisomerase I safeguards against hypertranscription.Nature communications · 2023Article
- Down syndrome and leukemia: from basic mechanisms to clinical advances.Haematologica · 2023Review
- Identification and Genome-Wide Gene Expression Perturbation of a Trisomy in Chinese Kale (Plants (Basel, Switzerland) · 2023Article
- The growth hormone receptor interacts with transcriptional regulator HMGN1 upon GH-induced nuclear translocation.Journal of cell communication and signaling · 2023Article
- The genomic landscape of acute lymphoblastic leukemia with intrachromosomal amplification of chromosome 21.Blood · 2023Article
- Article
- Overexpression screen of chromosome 21 genes reveals modulators of Sonic hedgehog signaling relevant to Down syndrome.Disease models & mechanisms · 2023Article
- Gain of chromosome 21 increases the propensity forFrontiers in oncology · 2023Article
- Integrating copy number data of 64 iAMP21 BCP-ALL patients narrows the common region of amplification to 1.57 Mb.Frontiers in oncology · 2023Article
Corrections and comments
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Authors and funding
19 authors at 5 institutions in 2 countries.
Funding
Abstract
Down syndrome (DS, trisomy 21) is associated with developmental abnormalities and increased leukemia risk. To reconcile chromatin alterations with transcriptome changes, we performed paired exogenous spike-in normalized RNA and chromatin immunoprecipitation sequencing in DS models. Absolute normalization unmasks global amplification of gene expression associated with trisomy 21. Overexpression of the nucleosome binding protein HMGN1 (encoded on chr21q22) recapitulates transcriptional changes seen with triplication of a Down syndrome critical region on distal chromosome 21, and HMGN1 is necessary for B cell phenotypes in DS models. Absolute exogenous-normalized chromatin immunoprecipitation sequencing (ChIP-Rx) also reveals a global increase in histone H3K27 acetylation caused by HMGN1. Transcriptional amplification downstream of HMGN1 is enriched for stage-specific programs of B cells and B cell acute lymphoblastic leukemia, dependent on the developmental cellular context. These data offer a mechanistic explanation for DS transcriptional patterns and suggest that further study of HMGN1 and RNA amplification in diverse DS phenotypes is warranted.
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