Human cytomegalovirus (HCMV) (strain AD169) glycoprotein H gH Protein (His & SUMO) is expressed in E. coli expression system with N-6xHis-SUMO tag. The predicted molecular weight is 35.8 kDa and the accession number is P12824.
Human cytomegalovirus (HCMV) Glycoprotein B gB Protein (aa 1-700, hFc) is expressed in HEK293 mammalian cells with Fc tag. The predicted molecular weight is 104 kDa and the accession number is P13201.
Macaca fascicularis Cytomegalovirus (CyCMV) (strain OT-1) glycoprotein B gB Protein (hFc) is expressed in HEK293 mammalian cells with Fc tag. The predicted molecular weight is 102.5 kDa and the accession number is E7DB34.
Plays a role in viral entry into host cells. Forms a pentameric complex at the surface of the viral envelope together with gH, gL, UL130 and UL131. This complex is required for entry in epithelial, endothelial and myeloid host cells. Mechanistically, engages host receptor(s) including neurophilin 2 NRP2 to mediate infection. Human cytomegalovirus (HCMV) (strain AD169) UL130 Protein (His & SUMO) is expressed in E. coli expression system with N-6xHis-SUMO tag. The predicted molecular weight is 37.7 kDa and the accession number is P16772.
Rhesus cytomegalovirus (RhCMV) (strain 68-1) Glycoprotein B gB Protein (His & Myc) is expressed in E. coli expression system with N-10xHis and C-Myc tag. The predicted molecular weight is 18.0 kDa and the accession number is P89053.
Human cytomegalovirus (HCMV) Glycoprotein B gB Protein is expressed in HEK293 mammalian cells. The predicted molecular weight is 92 kDa and the accession number is P13201.
Human cytomegalovirus (HCMV) Glycoprotein B gB Protein (His) is expressed in HEK293 mammalian cells with His tag. The predicted molecular weight is 93.2 kDa and the accession number is P13201.
Human cytomegalovirus (HCMV) Glycoprotein B gB Protein (hFc) is expressed in HEK293 mammalian cells with Fc tag. The predicted molecular weight is 118 kDa and the accession number is P13201.
Functional viral IL-10 homolog. Can bind to the human IL-10 receptor and compete with human IL-10 for binding sites. Requires both subunits of the human IL-10 receptor complex to induce signal transduction events and biological activities. IL-10 signaling pathway has several immunosuppressive activities that are exploited by the virus. Inhibits TLR-induced type I interferon production in host plasmacytoid dendritic cells. Human cytomegalovirus (HCMV) (strain Merlin) Viral interleukin-10 homolog is expressed in E. coli expression system. The predicted molecular weight is 17.5 kDa and the accession number is F5HC71.
NKG2D ligand 1, also called ULBP1, is a member of UL16-binding protein (ULBP) family which has also been termed the retinoic acid early transcript 1 (RAET1) family. Unlike the classical MHC class I molecules and the MIC molecules possess α1, α2 and α3 domains, ULBP RAET1 family members lack α3 domain. ULBP1 is recognized by the activating receptor NKG2D on the surface of cytotoxic natural killer (NK) and T cells, and then promotes the lysis of cells expressing ULBP1 which is important for the immune surveillance. ULBP1 and several other family members, ULBP2 and ULBP5, own the ability to bind the human cytomegalovirus (CMV) UL16 glycoprotein. The human CMV glycoprotein UL16 binds to intracellular ULBP1 and so inhibits its expression at the cell surface, which reduces the susceptibility of the virus-infected cell to cytotoxic destruction by NK cells. The expression of ULBP1 has been found on some tumor cells and is implicated in tumor surveillance.
Functions in nuclear protein import as an adapter protein for nuclear receptor KPNB1. Binds specifically and directly to substrates containing either a simple or bipartite NLS motif. Docking of the importin substrate complex to the nuclear pore complex (NPC) is mediated by KPNB1 through binding to nucleoporin FxFG repeats and the complex is subsequently translocated through the pore by an energy requiring, Ran-dependent mechanism. At the nucleoplasmic side of the NPC, Ran binds to importin-beta and the three components separate and importin-alpha and -beta are re-exported from the nucleus to the cytoplasm where GTP hydrolysis releases Ran from importin. The directionality of nuclear import is thought to be conferred by an asymmetric distribution of the GTP- and GDP-bound forms of Ran between the cytoplasm and nucleus. In vitro, mediates the nuclear import of human cytomegalovirus UL84 by recognizing a non-classical NLS.
C-C motif chemokine 5(CCL5) is a β-chemokine that plays a primary role in the inflammatory immune response by means of its ability to attract and activate leukocytes. CCL5 is secreted by many cell types at inflammatory sites, and it exerts a wide range of activities through the receptors CCR1, CCR3, CCR4, and CCR5. Inflammatory responses can be impaired by the sequestration of CCL5 by the cytomegalovirus protein US28. Oligomerization of CCL5 on glycosaminoglycans is required for CCR1mediated leukocyte adhesion and activation as well as CCL5’s interaction with the chemokine CXCL4 PF4.The deposition of CCL5 on activated vascular endothelial cells is crucial for monocyte adhesion to damaged vasculature, but CCL5 oligomerization is not required for the extravasation of adherent leukocytes.CCL5 is upregulated in breast cancer and promotes tumor progression through the attraction of proinflammatory macrophages in addition to its actions on tumor cells, stromal cells, and the vasculature.
SerpinB9, also known as Cytoplasmic antiproteinase 3, CAP-3, Peptidase inhibitor 9, SERPINB9 and PI-9, is a cytoplasm protein that belongs to the serpin family and Ov-serpin subfamily. Serpin-B9 ( CAP-3 PI-9 ) is the only known human intracellular inhibitor of granzyme B (GrB), the effector molecule in immunity against cytomegalovirus (CMV) and in renal allograft rejection. Serpin-B9 and SPI-6 expression in immune-privileged cells, APCs, and CTLs protect these cells against the actions of granzyme B, and when expressed in tumor cells or virally infected hepatocytes, confers resistance to killing by CTL and NK cells. Expression of increasing levels of Serpin-B9 ( CAP-3 PI-9 ) in target cells may progressively inhibit immune surveillance by blocking NK and CTL-induced cytotoxicity through the perforin granzyme pathway and then through the Fas FasL pathway. Serpin-B9 ( CAP-3 PI-9 ) is selectively up-regulated in hepatocytes in response to infiltration of the liver by NK cells that express perforin and enzymatically active granzyme B. Upregulated expression of Serpin-B9 ( CAP-3 PI-9 ) in NSCLC cells may serve to protect them from apoptosis induced by GrB.