| pubmed-article:11322942 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11322942 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:11322942 | lifeskim:mentions | umls-concept:C0027882 | lld:lifeskim |
| pubmed-article:11322942 | lifeskim:mentions | umls-concept:C0521449 | lld:lifeskim |
| pubmed-article:11322942 | lifeskim:mentions | umls-concept:C0751972 | lld:lifeskim |
| pubmed-article:11322942 | lifeskim:mentions | umls-concept:C0597298 | lld:lifeskim |
| pubmed-article:11322942 | lifeskim:mentions | umls-concept:C0038952 | lld:lifeskim |
| pubmed-article:11322942 | lifeskim:mentions | umls-concept:C1420295 | lld:lifeskim |
| pubmed-article:11322942 | lifeskim:mentions | umls-concept:C1416797 | lld:lifeskim |
| pubmed-article:11322942 | lifeskim:mentions | umls-concept:C0376315 | lld:lifeskim |
| pubmed-article:11322942 | lifeskim:mentions | umls-concept:C1704711 | lld:lifeskim |
| pubmed-article:11322942 | lifeskim:mentions | umls-concept:C1705994 | lld:lifeskim |
| pubmed-article:11322942 | lifeskim:mentions | umls-concept:C1513492 | lld:lifeskim |
| pubmed-article:11322942 | pubmed:issue | 1-2 | lld:pubmed |
| pubmed-article:11322942 | pubmed:dateCreated | 2001-4-27 | lld:pubmed |
| pubmed-article:11322942 | pubmed:abstractText | Homozygous mutations of the telomeric survival motor neurone gene (SMN1) cause spinal muscular atrophy (SMA). The centromeric copy gene (SMN2) generally skips exon 7 during splicing and fails to compensate for SMN1 deficits, so SMA cells have reduced SMN protein and few nuclear gems. To investigate the role of exon 7 in SMN localisation, cDNAs for full-length SMN and SMNDeltaexon 7 were overexpressed in COS cells, neurones and SMA fibroblasts. Both constructs formed discrete intranuclear bodies colocalising with p80-coilin, but produced more cytoplasmic aggregates in cells overexpressing exon 7. Hence, the exon 7 domain enhances SMN aggregation but is not critical for gem formation. | lld:pubmed |
| pubmed-article:11322942 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11322942 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11322942 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:11322942 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11322942 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11322942 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11322942 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11322942 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11322942 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11322942 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11322942 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11322942 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11322942 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11322942 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11322942 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11322942 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11322942 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11322942 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11322942 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:11322942 | pubmed:issn | 0014-5793 | lld:pubmed |
| pubmed-article:11322942 | pubmed:author | pubmed-author:RobertsR GRG | lld:pubmed |
| pubmed-article:11322942 | pubmed:author | pubmed-author:ShawC ECE | lld:pubmed |
| pubmed-article:11322942 | pubmed:author | pubmed-author:DunckleyM GMG | lld:pubmed |
| pubmed-article:11322942 | pubmed:author | pubmed-author:MuntoniFF | lld:pubmed |
| pubmed-article:11322942 | pubmed:author | pubmed-author:DoddsEE | lld:pubmed |
| pubmed-article:11322942 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11322942 | pubmed:day | 20 | lld:pubmed |
| pubmed-article:11322942 | pubmed:volume | 495 | lld:pubmed |
| pubmed-article:11322942 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11322942 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11322942 | pubmed:pagination | 31-8 | lld:pubmed |
| pubmed-article:11322942 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:11322942 | pubmed:meshHeading | pubmed-meshheading:11322942... | lld:pubmed |
| pubmed-article:11322942 | pubmed:year | 2001 | lld:pubmed |
| pubmed-article:11322942 | pubmed:articleTitle | Overexpressed human survival motor neurone isoforms, SMNDeltaexon7 and SMN+exon7, both form intranuclear gems but differ in cytoplasmic distribution. | lld:pubmed |
| pubmed-article:11322942 | pubmed:affiliation | Division of Medical and Molecular Genetics, GKT School of Medicine, Guy's Hospital, London SE1 9RT, UK. | lld:pubmed |
| pubmed-article:11322942 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11322942 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
