Linked Life Data

11369656

Source:http://linkedlifedata.com/resource/pubmed/id/11369656

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
2001-5-22
pubmed:abstractText
Epstein-Barr virus (EBV)-encoded latent membrane protein-1 (LMP1) is highly expressed in Hodgkin and Reed-Sternberg (H-RS) cells from patients with EBV-associated Hodgkin disease. It was previously demonstrated that CD99 can be negatively regulated by LMP1 at the transcriptional level, and the decreased expression of CD99 in a B lymphocyte cell line generates H-RS-like cells. In this study, detailed dissection of the CD99 promoter region was performed to search regulatory factor(s) involved in the expression of the gene. Using various mutant constructs containing deletions in the promoter region, it was revealed that the maximal promoter activity was retained on 5'-deletion to the position -137 from the transcriptional initiation site. Despite the presence of multiple putative Sp1-binding sites in the promoter region, the site located at -95 contributes heavily as a positive cis-acting element to its basal promoter activity. However, on examination of the involvement of the positive-acting Sp1-binding site of the promoter for the repressive activity of LMP1, it appeared to be dispensable. Instead, the repressive effect was mapped to the nuclear factor (NF)-kappaB activation domains in the cytoplasmic carboxyl terminus of LMP1 despite the absence of the NF-kappaB consensus sequences in the CD99 promoter region. Furthermore, the decreased CD99 promoter activity by LMP1 was markedly restored when NF-kappaB activity was inhibited. Taken together, these data suggest that Sp1 activates, whereas LMP1 represses, transcription from the CD99 promoter through the NF-kappaB signaling pathway, and they might aid in the understanding of the molecular mechanisms of viral pathogenesis in EBV-positive Hodgkin disease. (Blood. 2001;97:3596-3604)
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0006-4971
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
97
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3596-604
pubmed:dateRevised
2010-9-1
pubmed:meshHeading
pubmed-meshheading:11369656-Antigens, CD, pubmed-meshheading:11369656-Blotting, Western, pubmed-meshheading:11369656-Cell Adhesion Molecules, pubmed-meshheading:11369656-Cell Line, pubmed-meshheading:11369656-DNA-Binding Proteins, pubmed-meshheading:11369656-Flow Cytometry, pubmed-meshheading:11369656-Gene Deletion, pubmed-meshheading:11369656-Gene Expression, pubmed-meshheading:11369656-Gene Expression Regulation, pubmed-meshheading:11369656-Humans, pubmed-meshheading:11369656-I-kappa B Proteins, pubmed-meshheading:11369656-Mutagenesis, pubmed-meshheading:11369656-NF-kappa B, pubmed-meshheading:11369656-Point Mutation, pubmed-meshheading:11369656-Promoter Regions, Genetic, pubmed-meshheading:11369656-Signal Transduction, pubmed-meshheading:11369656-Sp1 Transcription Factor, pubmed-meshheading:11369656-Transcription, Genetic, pubmed-meshheading:11369656-Transfection, pubmed-meshheading:11369656-Tumor Cells, Cultured, pubmed-meshheading:11369656-Viral Matrix Proteins
pubmed:year
2001
pubmed:articleTitle
CD99 expression is positively regulated by Sp1 and is negatively regulated by Epstein-Barr virus latent membrane protein 1 through nuclear factor-kappaB.
pubmed:affiliation
Department of Pathology, Seoul National University College of Medicine, 28 Yongon-dong Chongno-gu, Seoul 110-799, Korea.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't