ArticleCell genomics2022
Genome-wide functional perturbation of human microsatellite repeats using engineered zinc finger transcription factors.
Article in Cell genomics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Ancient and animal-specific regulatory modes of EWS::FLI1 revealed by a minimal yeast model.PNAS nexus · 2026Article
- Epigenetic collapse establishes transcriptional bottlenecks in malignant rhabdoid tumor.Clinical epigenetics · 2026Review
- Fulfilling multiple roles in PROTAC design: The emerging potential of oligonucleotides.European journal of medicinal chemistry · 2026Review
- Satellite DNA Genomics: The Ongoing Story.International journal of molecular sciences · 2025Review
- Subcellular localization of pro-gastrin releasing peptide in human Ewing sarcoma cell lines.Medical molecular morphology · 2025Article
- TFE3 fusion oncoprotein condensates drive transcriptional reprogramming and cancer progression in translocation renal cell carcinoma.Cell reports · 2025Article
- Highly connected 3D chromatin networks established by an oncogenic fusion protein shape tumor cell identity.Science advances · 2023Article
- Oncogenic inspiration for programmable activators.Cell genomics · 2022Article
Corrections and comments
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Authors and funding
17 authors.
Funding
Abstract
Repeat elements can be dysregulated at a genome-wide scale in human diseases. For example, in Ewing sarcoma, hundreds of inert GGAA repeats can be converted into active enhancers when bound by EWS-FLI1. Here we show that fusions between EWS and GGAA-repeat-targeted engineered zinc finger arrays (ZFAs) can function at least as efficiently as EWS-FLI1 for converting hundreds of GGAA repeats into active enhancers in a Ewing sarcoma precursor cell model. Furthermore, a fusion of a KRAB domain to a ZFA can silence GGAA microsatellite enhancers genome wide in Ewing sarcoma cells, thereby reducing expression of EWS-FLI1-activated genes. Remarkably, this KRAB-ZFA fusion showed selective toxicity against Ewing sarcoma cells compared with non-Ewing cancer cells, consistent with its Ewing sarcoma-specific impact on the transcriptome. These findings demonstrate the value of ZFAs for functional annotation of repeats and illustrate how aberrant microsatellite activities might be regulated for potential therapeutic applications.
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Registered trials
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