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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

Poliovirus receptor

poliovirus receptor, CD155, nectin-2
The protein encoded by this gene is a transmembrane glycoprotein belonging to the immunoglobulin superfamily. The external domain mediates cell attachment to the extracellular matrix molecule vitronectin, while its intracellular domain interacts with the dynein light chain Tctex-1/DYNLT1. The gene is specific to the primate lineage, and serves as a cellular receptor for poliovirus in the first step of poliovirus replication. Multiple transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Oct 2008] (from NCBI)
Top mentioned proteins: CAN, CD226, nectin-1, ACID, CD45
Papers on poliovirus receptor
Five of five VHHs neutralizing poliovirus bind the receptor-binding site.
Hogle et al., Boston, United States. In J Virol, Feb 2016
All VHHs bind the capsid in the canyon at sites that extensively overlap the poliovirus receptor binding site.
Identification of CD112R as a novel checkpoint for human T cells.
Edil et al., Hangzhou, China. In J Exp Med, Feb 2016
UNASSIGNED: T cell immunoglobulin and ITIM domain (TIGIT) and CD226 emerge as a novel T cell cosignaling pathway in which CD226 and TIGIT serve as costimulatory and coinhibitory receptors, respectively, for the ligands CD155 and CD112.
HTLV-1 bZIP Factor Impairs Anti-viral Immunity by Inducing Co-inhibitory Molecule, T Cell Immunoglobulin and ITIM Domain (TIGIT).
Matsuoka et al., Kyoto, Japan. In Plos Pathog, Jan 2016
When CD4+ T cells from HBZ-Tg mice were stimulated with TIGIT's ligand, CD155, their production of the inhibitory cytokine IL-10 was enhanced.
Melanoma Cells Control Antimelanoma CTL Responses via Interaction between TIGIT and CD155 in the Effector Phase.
Shimada et al., Japan. In J Invest Dermatol, Jan 2016
In this study, we demonstrated that melanoma cells control antimelanoma cytotoxic T lymphocyte responses via the TIGIT-CD155 interaction in the effector phase.
TIGIT-CD155 Interactions in Melanoma: A Novel Co-Inhibitory Pathway with Potential for Clinical Intervention.
Enk et al., Heidelberg, Germany. In J Invest Dermatol, Jan 2016
describe a novel immunosuppressive mechanism in melanoma that is triggered by the interaction between CD155 (expressed by melanomas) and T-cell Ig and ITIM domain (TIGIT) (expressed by tumor infiltrating lymphocytes).
Monocyte trafficking across the vessel wall.
Ley et al., Los Angeles, United States. In Cardiovasc Res, Sep 2015
The emerging roles of endothelial junctional molecules like vascular endothelial-cadherin and the junctional adhesion molecule family, adhesion molecules such as intercellular adhesion molecule-1, molecules localized to the lateral border recycling compartment like cluster of differentiation 99, platelet/endothelial cell adhesion molecule-1, and poliovirus receptor (CD155), as well as other cell surface molecules such as cluster of differentiation 146 and ephrins in transendothelial migration are discussed.
Pathological consequences of systemic measles virus infection.
Duprex et al., Boston, United States. In J Pathol, 2015
The identification of poliovirus receptor-like 4 (PVRL4) as the second natural receptor for measles virus (MV) has closed a major gap in our understanding of measles pathogenesis, and explains how this predominantly lymphotropic virus breaks through epithelial barriers to transmit to a susceptible host.
The receptors CD96 and CD226 oppose each other in the regulation of natural killer cell functions.
Smyth et al., Melbourne, Australia. In Nat Immunol, 2014
In contrast, the role of CD96, which shares the ligand CD155 with CD226 and TIGIT, has remained unclear.
The DNA Damage Response: A Common Pathway in the Regulation of NKG2D and DNAM-1 Ligand Expression in Normal, Infected, and Cancer Cells.
Santoni et al., Roma, Italy. In Front Immunol, 2014
Their ligands - MICA, MICB, ULBP1-6 for NKG2D, PVR/CD155 and Nectin-2/CD112 for DNAM-1 - can be constitutively expressed at low levels in some normal cells, but they are more often defined as "stress-induced," since different stimuli can positively regulate their expression.
Natural killer cells and neuroblastoma: tumor recognition, escape mechanisms, and possible novel immunotherapeutic approaches.
Castriconi et al., Genova, Italy. In Front Immunol, 2013
PVR (Poliovirus Receptor) and B7-H3 are promising targets, since they are expressed by most high-risk NB, are upregulated in tumor vasculature and are essential for tumor survival/invasiveness.
Lck availability during thymic selection determines the recognition specificity of the T cell repertoire.
Singer et al., Bethesda, United States. In Cell, 2013
Transgenic TCR with MHC-independent specificity for CD155 utilized coreceptor-free Lck to signal thymic selection in the absence of MHC, unlike any transgenic TCR previously described.
The human immunodeficiency virus type 1 Nef and Vpu proteins downregulate the natural killer cell-activating ligand PVR.
Doria et al., Roma, Italy. In J Virol, 2012
the PVR downmodulation by Nef and Vpu is a strategy evolved by HIV-1 to prevent NK cell-mediated lysis of infected cells.
Necl-5/poliovirus receptor interacts with VEGFR2 and regulates VEGF-induced angiogenesis.
Rikitake et al., Kōbe, Japan. In Circ Res, 2012
Necl-5/poliovirus receptor interacts with VEGFR2 and regulates VEGF-induced angiogenesis.
αβ T cell receptors that do not undergo major histocompatibility complex-specific thymic selection possess antibody-like recognition specificities.
Singer et al., Bethesda, United States. In Immunity, 2012
Instead of recognizing peptide-MHC complexes, the two αβTCRs studied here resembled antibodies in recognizing glycosylation-dependent conformational epitopes on a native self-protein, CD155, and they did so with high affinity independently of MHC molecules.
The toll-like receptor 3-mediated antiviral response is important for protection against poliovirus infection in poliovirus receptor transgenic mice.
Koike et al., Tokyo, Japan. In J Virol, 2012
The TLR3-TRIF mediated antiviral response is important for protection against poliovirus infection in poliovirus receptor transgenic mice.
Receptors for hyaluronic acid and poliovirus: a combinatorial role in glioma invasion?
Pilkington et al., Portsmouth, United Kingdom. In Plos One, 2011
This investigation has enhanced understanding of cell invasion and confirmed CD44 to play a more significant role in this biological process than CD155.
The TLR3/TICAM-1 pathway is mandatory for innate immune responses to poliovirus infection.
Seya et al., Sapporo, Japan. In J Immunol, 2011
The host TICAM-1 pathway, particularly in macrophages, serves as a source of type I interferon induction that protects poliovirus (PV) receptor-bearing transgenic mice from PV infection and paralytic death.
The surface protein TIGIT suppresses T cell activation by promoting the generation of mature immunoregulatory dendritic cells.
Grogan et al., San Francisco, United States. In Nat Immunol, 2009
Poliovirus receptor, which is expressed on dendritic cells, bound TIGIT with high affinity.
Molecular aspects of poliovirus pathogenesis.
Nomoto, Tokyo, Japan. In Proc Jpn Acad Ser B Phys Biol Sci, 2007
The development of a transgenic mouse model carrying the human poliovirus receptor has made it possible to investigate the molecular mechanisms of the viral dissemination process in a whole organism.
Downregulation of natural killer cell-activating ligand CD155 by human cytomegalovirus UL141.
Wilkinson et al., Cardiff, United Kingdom. In Nat Immunol, 2005
Evasion of NK cell killing was mediated by human cytomegalovirus UL141 blocking surface expression of CD155
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