Please use this identifier to cite or link to this item: http://buratest.brunel.ac.uk/handle/2438/2959
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dc.contributor.authorMeaburn, KJ-
dc.contributor.authorLevy, N-
dc.contributor.authorToniolo, D-
dc.contributor.authorBridger, JM-
dc.coverage.spatial3en
dc.date.accessioned2009-01-15T17:48:24Z-
dc.date.available2009-01-15T17:48:24Z-
dc.date.issued2005-
dc.identifier.citationBiochemical Society Transactions. 33 ( 6) 1438-1440en
dc.identifier.issn0300-5127-
dc.identifier.urihttp://bura.brunel.ac.uk/handle/2438/2959-
dc.description.abstractGene-poor human chromosomes are reproducibly found at the nuclear periphery in proliferating cells. There are a number of inner nuclear envelope proteins that may have roles in chromosome location and anchorage, e.g. emerin and A-type lamins. In the last decade, a number of diseases associated with tissue degeneration and premature aging have been linked with mutations in lamin A or emerin. These are termed laminopathies, withmutations in emerin causing Emery–Dreifuss muscular dystrophy. Despite highly aberrant nuclear distributions of A-type lamins and emerin in lymphoblastoid cell lines derived from patients with emerin or lamin A mutations, little or no change in chromosome location was detected.en
dc.format.extent265568 bytes-
dc.format.mimetypeapplication/pdf-
dc.language.isoen-
dc.publisherPortland Pressen
dc.titleChromosome positioning is largely unaffected in lymphoblastoid cell lines containing emerin or A-type lamin mutationsen
dc.typeResearch Paperen
Appears in Collections:Biological Sciences
Dept of Life Sciences Research Papers

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