EBV p23 protein [His] (DAG1584)

EBV [His], recombinant protein from E. coli

Product Overview
Recombinant EBV p23 protein was expressed in E. coli and purified by proprietary chromatographic technique, 17.7kDa.
Nature
Recombinant
Tag/Conjugate
His
Procedure
None
Purity
> 95% pure as determined by 10% PAGE (coomassie staining).
Buffer
1xPBS pH-8 and 300mM Imidazole.
Preservative
None
Storage
2-8°C short term, -20°C long term
Introduction
The Epstein-Barr virus (EBV), also called Human herpes virus 4 (HHV-4), is a virusof the herpes family(which includes Herpes simplex virusand Cytomegalovirus. On infecting the B-lymphocyte, the linear virus genome circularizes and the virus subsequently persists within the cell as an episome. The virus can execute several distinct programs of gene expressionwhich can be broadly categorized as being lytic cycle or latent cycle. The lytic cycleor productive infection results in staged expression of a host of viral proteinswith the ultimate objective of producing infectious virions. Formally, this phase of infection does not inevitably lead to lysis of the host cellas EBV virions are produced by budding from the infected cell. The latent cycle(lysogenic) programs are those that do not result in production of virions. A very limited, distinct set of viral proteins are produced during latent cycle infection. These include Epstein-Barr nuclear antigen(EBNA)-1, EBNA-2, EBNA-3A, EBNA-3B, EBNA-3C, EBNA-leader protein (EBNA-LP) and latent membrane proteins(LMP)-1, LMP-2A and LMP-2B and the Epstein-Barr encoded RNAs(EBERs).
Antigen Description
p23 is one of the two small viral capsid antigens (VCA). EBV p23 is a viral late complex associated with virion particles and consists of two gene products, BFRF3 and BLRF2
Keywords
Epstein–Barr virus; Herpesviridae; Gammaherpesvirinae; Lymphocryptovirus; Human herpesvirus 4; HHV-4; EBV; p18 protein; Epstein-Barr Virus (EBV) p18 (VP26); Recombinant EBV (HHV-4) p18 virus capsid antigen (VP26, BFRF3); VP26; BFRF3; EBV p18; Epstein–Barr

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References


EBV-induced gene 3 augments IL-23R alpha protein expression through a chaperone calnexin

JOURNAL OF CLINICAL INVESTIGATION

Authors: Mizoguchi, Izuru; Ohashi, Mio; Hasegawa, Hideaki; Chiba, Yukino; Orii, Naoko; Inoue, Shinya; Kawana, Chiaki; Xu, Mingli; Sudo, Katsuko; Fujita, Koji; Kuroda, Masahiko; Hashimoto, Shin-Ichi; Matsushima, Kouji; Yoshimoto, Takayuki

Epstein-Barr virus-induced gene 3 (EBI3) is a subunit common to IL-27, IL-35, and IL-39. Here, we explore an intracellular role of EBI3 that is independent of its function in cytokines. EBI3-deficient naive CD4+ T cells had reduced IFN-gamma production and failed to induce T cell-dependent colitis in mice. Similarly reduced IFN-gamma production was observed in vitro in EBI3-deficient CD4+ T cells differentiated under pathogenic Th17 polarizing conditions with IL-23. This is because the induction of expression of one of the IL-23 receptor (IL-23R) subunits, IL-23R alpha, but not another IL-23R subunit, IL-12R beta 1, was selectively decreased at the protein level, but not the mRNA level. EBI3 augmented IL-23R alpha expression via binding to the chaperone molecule calnexin and to IL-23R alpha in a peptide-dependent manner, but not a glycan-dependent manner. Indeed, EBI3 failed to augment IL-23R alpha expression in the absence of endogenous calnexin. Moreover, EBI3 poorly augmented the expression of G149R, an IL-23R alpha variant that protects against the development of human colitis, because binding of EBI3 to the variant was reduced. Taken together with the result that EBI3 expression is inducible in T cells, the present results suggest that EBI3 plays a critical role in augmenting IL-23R alpha protein expression via calnexin under inflammatory conditions.

Magnesium: The overlooked electrolyte in blood cancers?

BLOOD REVIEWS

Authors: Gile, Jennifer; Ruan, Gordon; Abeykoon, Jithma; McMahon, M. Molly; Witzig, Thomas

Magnesium is an important element that has essential roles in the regulation of cell growth, division, and differentiation. Mounting evidence in the literature suggests an association between hypomagnesemia and all-cause mortality. In addition, epidemiologic studies have demonstrated that a diet poor in magnesium increases the risk of developing cancer, highlighting its importance in the field of hematology and oncology. In solid malignancies, hypomagnesemia at diagnosis portends a worse prognosis. However, little is known about prognosis in patients with hypomagnesemia and blood cancers in general; lymphoma more specifically. Hypomagnesemia has been associated with a higher viral load of the Epstein Barr virus, a virus associated with a multitude of hematologic malignancies. The role of magnesium in the immune system has been further elucidated in studies of patients with a rare primary immunodeficiency known as XMEN disease (X-linked immunodeficiency with Magnesium defect, Epstein-Barr virus (EBV) infection, and Neoplasia disease). These patients have a mutation in the MAGT1 gene, which codes for a magnesium transporter. The mutation leads to impaired T cell activation and an increased risk of developing hematologic malignancies. In this review we discuss the relevance of magnesium as an electrolyte, current measurement techniques, and the known data related to cause and prognosis of blood cancers. The goal is to use these data to stimulate additional high-quality and well powered studies to further investigate the role of magnesium in preventing cancer and improving outcomes of patients with malignancy and concomitant magnesium deficiency.

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