Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
2004-7-5
pubmed:abstractText
In human, three transcriptional enhancers called hs1,2, hs3 and hs4 were identified downstream the 3' Ig heavy (IgH) locus. We previously reported by PCR and Southern blotting the existence of various allelic forms for the hs1,2 enhancer, one allele being associated with a higher efficiency of switching to IgA in IgA nephropathy (IgAN) patients. Since it is strongly suggested in the mouse that the whole 3' regulatory region is broadly involved in the regulation of class switch recombination (CSR), we wondered if the reported hs1,2 polymorphism was the sole difference possibly accounting for the varying ability to produce non-IgM antibodies in the human population. In this study, we report the absence of additional polymorphism of the hs3 and hs4 enhancers either by using a PCR method or by Southern blotting. DNA sequence analysis confirmed the existence of an invariant core sequence for human hs3 and hs4 enhancers, featuring multiple nuclear factor potential binding sites. In conclusion, human hs3 and hs4 enhancers are not polymorphic, a result that markedly contrasts with the hs1,2 enhancer for which the generation of multiple alleles in both rodents and humans has likely been favored by its central position within a large palindromic region.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0165-2478
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
94
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
77-81
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
The polymorphism of the locus control region lying downstream the human IgH locus is restricted to hs1,2 but not to hs3 and hs4 enhancers.
pubmed:affiliation
Laboratoire d'Immunologie, UMR CNRS 6101, Faculté de Médecine, 2 rue Dr. Marcland, 87025 Limoges, France.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't