| Literature DB >> 21076064 |
Robert Berland1, Steven Fiering, Henry H Wortis.
Abstract
We previously identified an enhancer element upstream of the mouse cd5 gene that was required in reporter assays for the induction of cd5 promoter activity by BCR cross-linking. This element is highly conserved in placental mammals. To determine its physiological role, we have now generated mice with a targeted deletion of the enhancer. The result is the loss of CD5 expression in peritoneal and splenic B-1a cells of adult mice and an inability to induce CD5 by cross-linking of the BCR on splenic B-2 cells. Surprisingly, CD5 expression on B-1a cells of neonatal mice was only minimally compromised. Cd5 enhancer deletion also had only a modest effect on CD5 expression in the T lineage. Thus, this enhancer provides age- and tissue-specific regulation of CD5 expression and is an example of the utilization of different modes of regulation of expression in T and B cells.Entities:
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Year: 2010 PMID: 21076064 PMCID: PMC3855468 DOI: 10.4049/jimmunol.1002173
Source DB: PubMed Journal: J Immunol ISSN: 0022-1767 Impact factor: 5.422