Recombinant EBV gp350/220 (RBD, a.a. 4-450)[His] (DAGA-3072)

EBV gp350/220 (RBD, a.a. 4-450)[His], Recombinant protein from 293 cell culture for WB, ELISA

Product Overview
C-terminal 6xHis tagged gp350/220 (RBD/(a.a.4-450))(EBV) (a.a.4-450) (Genebank #: AHA36359). The receptor binding region of the gp350 protein.
Nature
Recombinant
Tag/Conjugate
His
Alternative Names
Epstein Barr Virus; EBV; Epstein–Barr virus; human herpesvirus 4; HHV-4; Human herpesvirus 4
Purity
>=95%
Format
Each vial contains 100 µg of purified protein (1 mg/ml) in PBS
Concentration
Batch dependent - please inquire should you have specific requirements.
Size
100ug
Storage
Keep it at 4 centigrade if used within a month. For long term storage, split it into small aliquots and keep at -80 centigrade. Avoid repeated freezing and thawing. The product will be expired one year after receiving if stored properly. Non-hazardous. No MSDS required.

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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.

Hydroa Vacciniforme-Like Lymphoproliferative Disorder With Progression to EBV plus Cytotoxic Peripheral T-Cell Lymphoma

AMERICAN JOURNAL OF DERMATOPATHOLOGY

Authors: Lyapichev, Kirill A.; Sukswai, Narittee; Wang, Xiaohong I.; Khoury, Joseph D.; Medeiros, L. Jeffrey

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