EBV P18 [Biotin] (DAG2699)

Product Overview
The EBV antigen p18 has been prepared as a recombinant antigen from the complete ORF of BFRF3
Specificity
Immunoreactive with sera of IgM VCA positive infected individuals
Nature
Recombinant
Tag/Conjugate
Biotin
Procedure
None
Purity
> 98% in a 15% SDS-PAGE
Preservative
None
Storage
2-8°C short term, -20°C long term
Introduction
Epstein-Barr virus is a member of the herpesvirus family and one of the most common human viruses. The envelope glycoprotein Gp340/Gp220 is the most abundant vomponent of the viral envelope and is believed to be responsible for EBV binding to CR2 receptor on human B-Cells.
Keywords
EBV p18; HHV-4 p18; HHV4 p18 protein; EBV p18 protein; EBV; Epstein Barr virus p18 protein; HHV4 p18; Human Herpesvirus 4; Probable capsid protein VP18; Protein BFRF3; VP18; Herpesviridae; Lymphocryptovirus

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Related Products


EBV P18 [GST] (DAG3927)
EBV P18 (DAG-T1132)

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References


GENE-MAPPING AND EXPRESSION OF 2 IMMUNODOMINANT EPSTEIN-BARR-VIRUS CAPSID PROTEINS

JOURNAL OF VIROLOGY

Authors: VANGRUNSVEN, WMJ; VANHEERDE, EC; DEHAARD, HJW; SPAAN, WJM; MIDDELDORP, JM

The genomic localization of two immunodominant genes encoding two proteins of the Epstein-Barr virus capsid antigen (VCA) complex, VCA-p18 and VCA-p40, has been identified. For that purpose, lambda gt11-based cDNA libraries were constructed from HH514.c16 cells induced for virus production. The libraries were screened with a monoclonal antibody, EBV.OT41A, directed against VCA-p40 or with affinity-purified human antibodies against VCA-p18. Sequencing of the inserts of positive plaques showed that VCA-p18 and VCA-p40 are encoded within open reading frames (ORFs) BFRF3 and BdRF1, respectively. Peptide scanning analysis of the predicted protein of ORF BdRF1 resulted in defining the epitope of monoclonal antibody EBV.OT41A at the C-terminal region. The dominant VCA-p18 reactivity of human sera can be completely inhibited by preadsorption with Escherichia coli-expressed BFRF3-beta-galactosidase. Serum of a rabbit immunized with BFRF3-betagalactosidase reacts with a VCA-specific protein of 18 kDa. In addition, BFRF3-beta-galactosidase affinity-purified antibodies react with VCA-p18 of virus-producing cells (HH514.c16). Complete inhibition of viral DNA polymerase activity by phosphonoacetic acid is associated with the absence of RNAs and protein products of both ORFs, indicating that VCA-p18 and VCA-p40 are true late antigens.

Proliferation and differentiation in isogenic populations of peripheral B cells activated by Epstein-Barr virus or T cell-derived mitogens

JOURNAL OF GENERAL VIROLOGY

Authors: O'Nions, J; Aday, MJ

Human B cells isolated from peripheral blood were activated and induced to proliferate by either Epstein-Barr virus (EBV) or the T cell-derived mitogens CD40 ligand (CD40L) plus interleukin (IL)-4. Although both populations initially proliferated as B-blasts, significant differences were revealed over a longer period. EBV infection resulted in continuously proliferating lymphoblastoid cell lines (LCLs), whereas most of the CD40L/IL-4-stimulated B cells had a finite proliferative lifespan of 3-4 weeks. Cell cycle analysis, trypan blue staining and Western blot analysis for cleavage of poly(ADP-ribose) polymerase (PARP) all demonstrated that the decrease in proliferation in CD40L/IL-4-stimulated B cells is not due to cell death. Instead, these cells arrest, accumulate in G(0)/G(1) and undergo alterations in cell surface marker expression, cellular morphology and immunoglobulin production, all consistent with plasmacytoid differentiation. In contrast, B cells infected with EBV continued to proliferate and retained a blast-like phenotype. Differences in both cytokine production and the expression of cell cycle regulators were identified between the two B-cell populations, which might contribute to the differentiation of the CD40L/IL-4-stimulated B cells and suggest potential mechanisms by which EBV may overcome this. The study has also identified a window of opportunity during which a comparison of isogenic populations of EBV- and mitogen-driven B blasts can be made.

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