When TADs go bad: chromatin structure and nuclear organisation in human disease [version 1; referees: 2 approved]

Chromatin in the interphase nucleus is organised as a hierarchical series of structural domains, including self-interacting domains called topologically associating domains (TADs). This arrangement is thought to bring enhancers into closer physical proximity with their target genes, which often are...
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Gespeichert in:

Autor*in:	Vera B Kaiser [verfasserIn] Colin A Semple [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2017

Schlagwörter:	Control of Gene Expression Genomics Medical Genetics Nuclear Structure & Function

Übergeordnetes Werk:	In: F1000Research - F1000 Research Ltd, 2013, 6(2017)
Übergeordnetes Werk:	volume:6 ; year:2017

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.12688/f1000research.10792.1

Katalog-ID:	DOAJ069227942

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author	Vera B Kaiser
spellingShingle	Vera B Kaiser misc Control of Gene Expression misc Genomics misc Medical Genetics misc Nuclear Structure & Function misc Medicine misc R misc Science misc Q When TADs go bad: chromatin structure and nuclear organisation in human disease [version 1; referees: 2 approved]
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topic_title	When TADs go bad: chromatin structure and nuclear organisation in human disease [version 1; referees: 2 approved] Control of Gene Expression Genomics Medical Genetics Nuclear Structure & Function
topic	misc Control of Gene Expression misc Genomics misc Medical Genetics misc Nuclear Structure & Function misc Medicine misc R misc Science misc Q
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title	When TADs go bad: chromatin structure and nuclear organisation in human disease [version 1; referees: 2 approved]
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title_full	When TADs go bad: chromatin structure and nuclear organisation in human disease [version 1; referees: 2 approved]
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title_sort	when tads go bad: chromatin structure and nuclear organisation in human disease [version 1; referees: 2 approved]
title_auth	When TADs go bad: chromatin structure and nuclear organisation in human disease [version 1; referees: 2 approved]
abstract	Chromatin in the interphase nucleus is organised as a hierarchical series of structural domains, including self-interacting domains called topologically associating domains (TADs). This arrangement is thought to bring enhancers into closer physical proximity with their target genes, which often are located hundreds of kilobases away in linear genomic distance. TADs are demarcated by boundary regions bound by architectural proteins, such as CTCF and cohesin, although much remains to be discovered about the structure and function of these domains. Recent studies of TAD boundaries disrupted in engineered mouse models show that boundary mutations can recapitulate human developmental disorders as a result of aberrant promoter-enhancer interactions in the affected TADs. Similar boundary disruptions in certain cancers can result in oncogene overexpression, and CTCF binding sites at boundaries appear to be hyper-mutated across cancers. Further insights into chromatin organisation, in parallel with accumulating whole genome sequence data for disease cohorts, are likely to yield additional valuable insights into the roles of noncoding sequence variation in human disease.
abstractGer	Chromatin in the interphase nucleus is organised as a hierarchical series of structural domains, including self-interacting domains called topologically associating domains (TADs). This arrangement is thought to bring enhancers into closer physical proximity with their target genes, which often are located hundreds of kilobases away in linear genomic distance. TADs are demarcated by boundary regions bound by architectural proteins, such as CTCF and cohesin, although much remains to be discovered about the structure and function of these domains. Recent studies of TAD boundaries disrupted in engineered mouse models show that boundary mutations can recapitulate human developmental disorders as a result of aberrant promoter-enhancer interactions in the affected TADs. Similar boundary disruptions in certain cancers can result in oncogene overexpression, and CTCF binding sites at boundaries appear to be hyper-mutated across cancers. Further insights into chromatin organisation, in parallel with accumulating whole genome sequence data for disease cohorts, are likely to yield additional valuable insights into the roles of noncoding sequence variation in human disease.
abstract_unstemmed	Chromatin in the interphase nucleus is organised as a hierarchical series of structural domains, including self-interacting domains called topologically associating domains (TADs). This arrangement is thought to bring enhancers into closer physical proximity with their target genes, which often are located hundreds of kilobases away in linear genomic distance. TADs are demarcated by boundary regions bound by architectural proteins, such as CTCF and cohesin, although much remains to be discovered about the structure and function of these domains. Recent studies of TAD boundaries disrupted in engineered mouse models show that boundary mutations can recapitulate human developmental disorders as a result of aberrant promoter-enhancer interactions in the affected TADs. Similar boundary disruptions in certain cancers can result in oncogene overexpression, and CTCF binding sites at boundaries appear to be hyper-mutated across cancers. Further insights into chromatin organisation, in parallel with accumulating whole genome sequence data for disease cohorts, are likely to yield additional valuable insights into the roles of noncoding sequence variation in human disease.
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title_short	When TADs go bad: chromatin structure and nuclear organisation in human disease [version 1; referees: 2 approved]
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