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- W2791117438 abstract "The nuclear lamina contributes to the regulation of gene expression and to chromatin organization. Mutations in A-type nuclear lamins cause laminopathies, some of which are associated with a loss of heterochromatin at the nuclear periphery. Until recently however, little if any information has been provided on where and how lamin A interacts with the genome and on how disease-causing lamin A mutations may rearrange genome conformation. Here, we review aspects of nuclear lamin association with the genome. We highlight recent evidence of reorganization of lamin A-chromatin interactions in cellular models of laminopathies, and implications on the 3-dimensional rearrangement of chromatin in these models, including patient cells. We discuss how a hot-spot lipodystrophic lamin A mutation alters chromatin conformation and epigenetic patterns at an anti-adipogenic locus, and conclude with remarks on links between lamin A, Polycomb and the pathophysiology of laminopathies. The recent findings presented here collectively argue towards a deregulation of large-scale and local spatial genome organization by a subset of lamin A mutations causing laminopathies." @default.
- W2791117438 created "2018-03-29" @default.
- W2791117438 creator A5047256665 @default.
- W2791117438 creator A5072506531 @default.
- W2791117438 date "2018-04-02" @default.
- W2791117438 modified "2023-10-16" @default.
- W2791117438 title "Laminopathy-causing lamin A mutations reconfigure lamina-associated domains and local spatial chromatin conformation" @default.
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- W2791117438 doi "https://doi.org/10.1080/19491034.2018.1449498" @default.
- W2791117438 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5973257" @default.
- W2791117438 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/29517398" @default.
- W2791117438 hasPublicationYear "2018" @default.
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