BREACHing new grounds in fragile X syndrome: Trinucleotide expansion linked to 
genome-wide heterochromatin domains and genome misfolding

Schulz, Edda G.

doi:10.1016/j.molcel.2023.12.042

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BREACHing new grounds in fragile X syndrome: Trinucleotide expansion linked to genome-wide heterochromatin domains and genome misfolding

Schulz, E. G. (2024). BREACHing new grounds in fragile X syndrome: Trinucleotide expansion linked to genome-wide heterochromatin domains and genome misfolding. Molecular Cell, 84(3), 413-414. doi:10.1016/j.molcel.2023.12.042.

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Item Permalink: https://hdl.handle.net/21.11116/0000-000E-57B9-0 Version Permalink: https://hdl.handle.net/21.11116/0000-000E-57BA-F

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Creators:
Schulz, Edda G.¹, Author

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1Systems Epigenetics (Edda G. Schulz), Independent Junior Research Groups (OWL), Max Planck Institute for Molecular Genetics, Max Planck Society, ou_2117286

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Abstract: In a recent study in Cell, Malachowski et al. show that the trinucleotide expansion in the FMR1 gene underlying fragile X syndrome triggers formation of large heterochromatin domains across the genome, resulting in the repression of synaptic genes housed within these domains.

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Language(s): eng - English

Dates: Date issued: 2024-02-01

Publication Status: Issued

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Identifiers: DOI: 10.1016/j.molcel.2023.12.042

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Title: Molecular Cell

Source Genre: Journal

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Publ. Info: Cambridge, Mass. : Cell Press

Pages: - Volume / Issue: 84 (3) Sequence Number: - Start / End Page: 413 - 414 Identifier: ISSN: 1097-2765
CoNE: https://pure.mpg.de/cone/journals/resource/954925610929