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dc.contributor.authorClelland, Allyson K.
dc.contributor.authorKinnear, Nicholas P.
dc.contributor.authorOram, Lisa
dc.contributor.authorBurza, Julie
dc.contributor.authorSleeman, Judith Elizabeth
dc.identifier.citationClelland , A K , Kinnear , N P , Oram , L , Burza , J & Sleeman , J E 2009 , ' The SMN protein is a key regulator of nuclear architecture in differentiating neuroblastoma cells ' , Traffic , vol. 10 , no. 11 , pp. 1585-1598 .
dc.identifier.otherPURE: 3727938
dc.identifier.otherPURE UUID: 3d3e82b4-fc1a-4309-b91b-a4858cb53b1d
dc.identifier.otherWOS: 000270665300004
dc.identifier.otherScopus: 70350635179
dc.identifier.otherORCID: /0000-0003-0345-6508/work/60426889
dc.description.abstractThe cell nucleus contains two closely related structures, Cajal bodies (CBs) and gems. CBs are the first site of accumulation of newly assembled splicing snRNPs (small nuclear ribonucleoproteins) following their import into the nucleus, before they form their steady-state localization in nuclear splicing speckles. Gems are the nuclear site of accumulation of survival motor neurons (SMNs), an insufficiency of which leads to the inherited neurodegenerative condition, spinal muscular atrophy (SMA). SMN is required in the cytoplasm for the addition of core, Sm, proteins to new snRNPs and is believed to accompany snRNPs to the CB. In most cell lines, gems are indistinguishable from CBs, although the structures are often separate in vivo. The relationship between CBs and gems is not fully understood, but there is evidence that symmetrical dimethylation of arginine residues in the CB protein coilin brings them together in HeLa cells. During neuronal differentiation of the human neuroblastoma cell line SH-SY5Y, CBs and gems increase their colocalization, mimicking changes seen during foetal development. This does not result from alterations in the methylation of coilin, but from increased levels of SMN. Expression of exogenous SMN results in an increased efficiency of snRNP transport to nuclear speckles. This suggests different mechanisms are present in different cell types and in vivo that may be significant for the tissue-specific pathology of SMA.
dc.rightsThis is an OnlineOpen article available from http://onlinelibrary.wiley.comen
dc.subjectCajal bodyen
dc.subjectsnRNP maturationen
dc.subjectSpinal muscular atrophyen
dc.subjectSurvival motor neuronen
dc.subjectCajal bodiesen
dc.subjectCoiled bodiesen
dc.subjectSpliceosomal SNRNPSen
dc.subjectFluorescent proteinen
dc.subjectSplicing SNRNPSen
dc.subjectBody formationen
dc.subjectQH301 Biologyen
dc.titleThe SMN protein is a key regulator of nuclear architecture in differentiating neuroblastoma cellsen
dc.typeJournal articleen
dc.description.versionPublisher PDFen
dc.contributor.institutionUniversity of St Andrews. School of Biologyen
dc.contributor.institutionUniversity of St Andrews. Institute of Behavioural and Neural Sciencesen
dc.contributor.institutionUniversity of St Andrews. Biomedical Sciences Research Complexen
dc.description.statusPeer revieweden

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