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rdf:type |
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lifeskim:mentions |
umls-concept:C0004083,
umls-concept:C0015576,
umls-concept:C0024141,
umls-concept:C0030705,
umls-concept:C0183683,
umls-concept:C0240339,
umls-concept:C0344211,
umls-concept:C0376515,
umls-concept:C0752046,
umls-concept:C0936012,
umls-concept:C1171411,
umls-concept:C1314939,
umls-concept:C1317973,
umls-concept:C1519302,
umls-concept:C1521721,
umls-concept:C1710263,
umls-concept:C2745888
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pubmed:issue |
6
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pubmed:dateCreated |
2001-1-24
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pubmed:abstractText |
We have described suggestive linkage between microsatellite markers within the cytogenetic region 18q21-23 and SLE, a region where linkage with other autoimmune diseases has also been detected. The Bcl-2 gene located within this region, is a candidate gene because of its role in apoptosis, a physiological mechanism that could be deregulated in autoimmune disease. Furthermore, several studies have found abnormalities of Bcl-2 expression in SLE patients. We therefore sought to determine if the Bcl-2 gene is involved in SLE by studying members of a large cohort of Mexican SLE patients (n = 378) and 112 Swedish simplex families. Using a microsatellite marker and two single nucleotide polymorphisms located within the gene, we were unable to detect association between Bcl-2 and SLE in either population. We also tested whether combinations of alleles of the Bcl-2 and IL-10.G microsatellites would increase the risk for SLE. Our results do not support such hypothesis. Our findings suggest that linkage between SLE and the 18q21-23 region is due to a gene other than Bcl-2.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
1466-4879
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pubmed:author |
pubmed-author:Alarcón-RiquelmeM EME,
pubmed-author:Alarcón-SegoviaDD,
pubmed-author:Alcocer-VarelaJJ,
pubmed-author:Castillejo-LópezCC,
pubmed-author:FrostegårdJJ,
pubmed-author:GunnarssonII,
pubmed-author:GyllenstenU BUB,
pubmed-author:JohannesonBB,
pubmed-author:JohanssonCC,
pubmed-author:LöfströmBB,
pubmed-author:LundbergII,
pubmed-author:SturfeltGG,
pubmed-author:SvenungssonEE,
pubmed-author:TruedssonLL
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pubmed:issnType |
Print
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pubmed:volume |
1
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
380-5
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:11196685-Alleles,
pubmed-meshheading:11196685-Base Sequence,
pubmed-meshheading:11196685-Case-Control Studies,
pubmed-meshheading:11196685-Cohort Studies,
pubmed-meshheading:11196685-DNA Primers,
pubmed-meshheading:11196685-Female,
pubmed-meshheading:11196685-Gene Frequency,
pubmed-meshheading:11196685-Genes, bcl-2,
pubmed-meshheading:11196685-Genetic Linkage,
pubmed-meshheading:11196685-Genotype,
pubmed-meshheading:11196685-Humans,
pubmed-meshheading:11196685-Interleukin-10,
pubmed-meshheading:11196685-Lupus Erythematosus, Systemic,
pubmed-meshheading:11196685-Male,
pubmed-meshheading:11196685-Mexico,
pubmed-meshheading:11196685-Microsatellite Repeats,
pubmed-meshheading:11196685-Polymorphism, Single Nucleotide,
pubmed-meshheading:11196685-Sweden
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pubmed:year |
2000
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pubmed:articleTitle |
Association analysis with microsatellite and SNP markers does not support the involvement of BCL-2 in systemic lupus erythematosus in Mexican and Swedish patients and their families.
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pubmed:affiliation |
Department of Genetics & Pathology, Section for Medical Genetics, Rudbeck Laboratory, Uppsala University, S-751 85 Uppsala, Sweden.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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