Isolation and characterization of the human DC-SIGN and DC-SIGNR promoters

Liu, Hongbing; Yu, Wendong; Liou, Li Ying; Rice, Andrew P.

doi:10.1016/s0378-1119(03)00674-7

Cited by 36 publications

(21 citation statements)

References 20 publications

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“…1, A and B). To analyze the DNA elements and transcription factors that direct the expression of DC-SIGN, we amplified by PCR a genomic region of the DC-SIGN gene (Ϫ1656/Ϫ19) where, in agreement with a previous report (36), preliminary 5Ј-rapid amplification of cDNA ends experiments mapped the DC-SIGN transcriptional start sites (data not shown). Sequencing the amplified region revealed its complete identity to the genomic region upstream of the structural region of the DC-SIGN gene that had been determined previously in the contig sequence AC008812.7.1.143619 within the Ensembl data base.…”

Section: Resultssupporting

confidence: 61%

PU.1 Regulates the Tissue-specific Expression of Dendritic Cell-specific Intercellular Adhesion Molecule (ICAM)-3-grabbing Nonintegrin

Domínguez-Soto¹,

Puig‐Kröger²,

Vega

et al. 2005

Journal of Biological Chemistry

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Dendritic cell-specific intercellular adhesion molecule-3-grabbing nonintegrin (DC-SIGN) is a cell surface C-type lectin expressed on myeloid dendritic cells and certain tissue macrophages, which mediates antigen capture for processing and presentation and participates in intercellular interactions with naive T lymphocytes or endothelial cells. In their strategy to evade immunosurveillance, numerous pathogenic microorganisms, including human immunodeficiency virus and Mycobacterium, bind to DC-SIGN in order to gain access to dendritic cells. We present evidence that PU.1 dictates the basal and cell-specific activity of DC-SIGN gene-regulatory region through in vivo occupancy of two functional Ets elements, whose integrity is required for PU.1 responsiveness and for the cooperative actions of PU.1 and other transcription factors (Myb, RUNX) on the DC-SIGN gene proximal regulatory region. In addition, protein analysis and gene profiling experiments indicate that DC-SIGN and PU.1 are coordinately expressed upon classical and alternative macrophage activation and during dendritic cell maturation. Moreover, small interfering RNA-mediated reduction of PU.1 expression results in diminished DC-SIGN cellular levels. Altogether, these results indicate that PU.1 is involved in the myeloid-specific expression of DC-SIGN in myeloid cells, a contribution that can be framed within the role that PU.1 has on the acquisition of the antigen uptake molecular repertoire by dendritic cells and macrophages.

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Section: Resultssupporting

confidence: 61%

PU.1 Regulates the Tissue-specific Expression of Dendritic Cell-specific Intercellular Adhesion Molecule (ICAM)-3-grabbing Nonintegrin

Domínguez-Soto¹,

Puig‐Kröger²,

Vega

et al. 2005

Journal of Biological Chemistry

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“…level, influencing the amount of expressed protein [20]. An increase of DC-SIGN receptors on DCs and macrophages may enhance the interaction between HIV-1 gp120 and the CRD of DC-SIGN receptor, allowing high affinity binding between virus and receptor, as well as interaction between virus and T-cells, promoting transmission in trans.…”

Section: Tablementioning

confidence: 99%

Polymorphisms in DC-SIGN and L-SIGN genes are associated with HIV-1 vertical transmission in a Northeastern Brazilian population

et al. 2012

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“…A potential mechanism for this may involve differential constitutive or inducible expression of DC-SIGN on blood DCs as a result of this polymorphism, but this remains to be demonstrated. Ϫ336C is located 214 bp upstream of the major transcription start site (11) and is therefore likely to be in a region containing potential binding sites for transcriptional factors. Indeed, a database search (TRANSFAC database) (8) identified a potential Sp1 binding site in the presence of Ϫ336C, which is lost when Ϫ336T is present.…”

Section: Fig 1 Dc-signmentioning

confidence: 99%

“…on April 30, 2019 by guest single-nucleotide polymorphisms (SNPs) were identified in the region 2 kb upstream of the ATG start codon, which includes the promoter region (11). The region was amplified in four overlapping segments of 200 to 300 bp, and analysis of the products was performed using single-strand conformation polymorphism (SSCP), as previously described (3).…”

mentioning

confidence: 99%

Association of DC-SIGN Promoter Polymorphism with Increased Risk for Parenteral, but Not Mucosal, Acquisition of Human Immunodeficiency Virus Type 1 Infection

Martin

Lederman

Hutcheson

et al. 2004

J Virol

105

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There is considerable debate about the fundamental mechanisms that underlie and restrict acquisition of human immunodeficiency virus type 1 (HIV-1) infection. In light of recent studies demonstrating the ability of C type lectins to facilitate infection with HIV-1, we explored the potential relationship between polymorphisms in the DC-SIGN promoter and risk for acquisition of HIV-1 according to route of infection. Using samples obtained from 1,611 European-American participants at risk for parenteral (n ‫؍‬ 713) or mucosal (n ‫؍‬ 898) infection, we identified single-nucleotide polymorphisms in the DC-SIGN promoter using single-strand conformation polymorphism. Individuals at risk for parenterally acquired infection who had ؊336C were more susceptible to infection than were persons with ؊336T (odds ratio ‫؍‬ 1.87, P ‫؍‬ 0.001). This association was not observed in those at risk for mucosally acquired infection. A potential role for DC-SIGN specific to systemic acquisition and dissemination of infection is suggested.

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Isolation and characterization of the human DC-SIGN and DC-SIGNR promoters

Cited by 36 publications

References 20 publications

PU.1 Regulates the Tissue-specific Expression of Dendritic Cell-specific Intercellular Adhesion Molecule (ICAM)-3-grabbing Nonintegrin

PU.1 Regulates the Tissue-specific Expression of Dendritic Cell-specific Intercellular Adhesion Molecule (ICAM)-3-grabbing Nonintegrin

Polymorphisms in DC-SIGN and L-SIGN genes are associated with HIV-1 vertical transmission in a Northeastern Brazilian population

Association of DC-SIGN Promoter Polymorphism with Increased Risk for Parenteral, but Not Mucosal, Acquisition of Human Immunodeficiency Virus Type 1 Infection

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