Source:http://linkedlifedata.com/resource/pubmed/id/20152818
Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
|
pubmed:dateCreated |
2010-3-22
|
pubmed:abstractText |
The dendritic cell-specific intercellular adhesion molecule-3-grabbing nonintegrin (DC-SIGN) and DC-SIGN-related (DC-SIGNR) molecules on the cell surface are known to enhance human immunodeficiency virus type 1 (HIV-1) infection by capturing the virions and transmitting them to CD4+ T-cell, a process termed trans-infection. The neck region and carbohydrate recognition domain of the two proteins are important for efficient binding to the HIV-1 envelope protein. DC-SIGNR is polymorphic in Exons 4 and 5 that encode the neck region and carbohydrate recognition domain, respectively; the former contains a variable number of tandem repeats, and the latter the SNP (rs2277998). Since it remains unclear whether the DC-SIGNR polymorphism is related to the risk of HIV-1 infection, we tested possible effects of the polymorphism on HIV-1 trans-infection efficiency, by constructing six kinds of cDNAs encoding DC-SIGNR variants with various numbers of repeat units and various SNP. We were able to express the variants on the surface of Raji cells, a human B cell line. Flow cytometry showed that all the tested DC-SIGNR molecules were efficiently expressed on the cell surface at various levels; the assay for HIV trans-infection efficacy showed that all the tested variants had that activity with different efficacy levels. We found a correlation between the HIV trans-infection efficiency and the mean fluorescent intensity of DC-SIGNR expression (R(2)=0.95). Thus, our results suggest that the variation of the tested DC-SIGNR genotypes affects the efficacy of trans-infection by affecting the amounts of the protein expressed on the cell surface.
|
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical | |
pubmed:status |
MEDLINE
|
pubmed:month |
Mar
|
pubmed:issn |
1090-2104
|
pubmed:author | |
pubmed:copyrightInfo |
Copyright 2010 Elsevier Inc. All rights reserved.
|
pubmed:issnType |
Electronic
|
pubmed:day |
19
|
pubmed:volume |
393
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
598-602
|
pubmed:meshHeading |
pubmed-meshheading:20152818-CD4-Positive T-Lymphocytes,
pubmed-meshheading:20152818-Cell Adhesion Molecules,
pubmed-meshheading:20152818-Cell Line,
pubmed-meshheading:20152818-Dendritic Cells,
pubmed-meshheading:20152818-Exons,
pubmed-meshheading:20152818-HIV Infections,
pubmed-meshheading:20152818-HIV-1,
pubmed-meshheading:20152818-Humans,
pubmed-meshheading:20152818-Lectins, C-Type,
pubmed-meshheading:20152818-Polymorphism, Single Nucleotide,
pubmed-meshheading:20152818-Receptors, Cell Surface,
pubmed-meshheading:20152818-Tandem Repeat Sequences
|
pubmed:year |
2010
|
pubmed:articleTitle |
Influence of polymorphism in dendritic cell-specific intercellular adhesion molecule-3-grabbing nonintegrin-related (DC-SIGNR) gene on HIV-1 trans-infection.
|
pubmed:affiliation |
Division of Infectious Diseases, Advanced Clinical Research Center, Institute of Medical Science, University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan. zhu@ims.u-tokyo.ac.jp
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|