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

Tumor necrosis factor receptor superfamily, member 14

The protein encoded by this gene is a member of the TNF-receptor superfamily. This receptor was identified as a cellular mediator of herpes simplex virus (HSV) entry. Binding of HSV viral envelope glycoprotein D (gD) to this receptor protein has been shown to be part of the viral entry mechanism. The cytoplasmic region of this receptor was found to bind to several TRAF family members, which may mediate the signal transduction pathways that activate the immune response. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: CD45, CAN, BTLA, nectin-1, V1a
Papers using HVEM antibodies
A novel role for phagocytosis-like uptake in herpes simplex virus entry
Shukla Deepak et al., In The Journal of Cell Biology, 1980
... (nectin-1) and pBEC10 (HVEM); control vector pcDNA3 (Invitrogen); pNec1-EGFP or pHVEM-EGFP expressing full-length nectin-1 or HVEM fused with EGFP (pEGFP-N1 vector; BD Biosciences) and rat dynamin2 (wild-type, ...
Papers on HVEM
Recurrent somatic loss of TNFRSF14 in classical Hodgkin lymphoma.
Shendure et al., Seattle, United States. In Genes Chromosomes Cancer, Mar 2016
In eight cases (42%) we observed recurrent copy number loss of chr1:2,352,236-4,574,271, a region containing the candidate tumor suppressor TNFRSF14.
Immunotherapeutic targeting of LIGHT/LTβR/HVEM pathway fully recapitulates the reduced cytotoxic phenotype of LIGHT-deficient T cells.
Rodriguez-Barbosa et al., León, Spain. In Mabs, Feb 2016
Mouse LIGHT (TNFSF14) is a type II transmembrane protein with a C-terminus extracellular TNF homology domain (THD) that assembles in homotrimers and regulates the course of the immune responses by signaling through two receptors, the herpes virus entry mediator (HVEM, TNFSFR14) and the lymphotoxin β receptor (LTβR, TNFSFR3).
The Control of Tissue Fibrosis by the Inflammatory Molecule LIGHT (TNF Superfamily member 14).
Croft et al., Los Angeles, United States. In Pharmacol Res, Jan 2016
LIGHT acts through two receptors in the TNF receptor superfamily, HVEM (TNFRSF14) and LTβR (TNFRSF3), which are broadly expressed on hematopoietic and non-hematopoietic cells.
The histone lysine methyltransferase KMT2D sustains a gene expression program that represses B cell lymphoma development.
Wendel et al., New York City, United States. In Nat Med, Oct 2015
Notably, other KMT2D target genes include frequently mutated tumor suppressor genes such as TNFAIP3, SOCS3 and TNFRSF14.
Tumor necrosis factor superfamily in innate immunity and inflammation.
Ware et al., Los Angeles, United States. In Cold Spring Harb Perspect Biol, Apr 2015
The TNFSF and TNFRSF proteins lymphotoxins, LIGHT (homologous to lymphotoxins, exhibits inducible expression, and competes with HSV glycoprotein D for herpes virus entry mediator [HVEM], a receptor expressed by T lymphocytes), lymphotoxin-β receptor (LT-βR), and HVEM are used by embryonic and adult innate lymphocytes to promote the development and homeostasis of lymphoid organs.
Herpesvirus entry mediator on radiation-resistant cell lineages promotes ocular herpes simplex virus 1 pathogenesis in an entry-independent manner.
Longnecker et al., Chicago, United States. In Mbio, 2014
Herpesvirus entry mediator (HVEM), a widely expressed tumor necrosis factor (TNF) receptor superfamily member with diverse roles in immune signaling, facilitates viral entry through interactions with viral glycoprotein D (gD) and is important for HSV-1 pathogenesis.
Myocyte-derived Tnfsf14 is a survival factor necessary for myoblast differentiation and skeletal muscle regeneration.
Chen et al., Urbana, United States. In Cell Death Dis, 2014
We find that Tnfsf14, as well as its cognate receptors herpes virus entry mediator (HVEM) and lymphotoxin β receptor (LTβR), are expressed in both differentiating myocytes and regenerating myofibers.
HVEM is a TNF Receptor with Multiple Regulatory Roles in the Mucosal Immune System.
Kronenberg et al., Los Angeles, United States. In Immune Netw, 2014
The herpes virus entry mediator (HVEM) is a member of the tumor necrosis factor receptor superfamily (TNFRSF), and therefore it is also known as TNFRSF14 or CD270 (1,2).
Molecular pathogenesis of follicular lymphoma.
Nishikori et al., Kyoto, Japan. In J Clin Exp Hematop, 2013
With recent advances in the technology for DNA analysis, recurrent gene aberrations such as TNFRSF14, EPHA7, EZH2, CREBBP, EP300, MLL2 and MEF2B have been identified.
T cell co-stimulatory molecules: a co-conspirator in the pathogenesis of eosinophilic esophagitis?
Eroglu et al., Cleveland, United States. In Dig Dis Sci, 2013
In this review, we will discuss the growing evidence of co-stimulatory molecules including OX40, Light, and HVEM in the pathogenesis of Th2-driven EoE.
Interfering with coinhibitory molecules: BTLA/HVEM as new targets to enhance anti-tumor immunity.
Olive et al., Marseille, France. In Immunol Lett, 2013
Here we summarize the recent advances made on PD1/PD1 ligands expression in cancer and we discuss about another couple of inhibitory molecules, BTLA and its ligand HVEM and their potential role in immune escape.
BTLA expression contributes to septic morbidity and mortality by inducing innate inflammatory cell dysfunction.
Ayala et al., Providence, United States. In J Leukoc Biol, 2012
These findings support role for BTLA and/or HVEM as potential, novel diagnostic markers of innate immune response/status and as therapeutic targets of sepsis.
HVEM signalling at mucosal barriers provides host defence against pathogenic bacteria.
Kronenberg et al., Los Angeles, United States. In Nature, 2012
results pinpoint HVEM as an important orchestrator of mucosal immunity, integrating signals from innate lymphocytes to induce optimal epithelial Stat3 activation, which indicates that targeting HVEM with agonists could improve host defence
B and T lymphocyte attenuator mediates inhibition of tumor-reactive CD8+ T cells in patients after allogeneic stem cell transplantation.
Dolstra et al., Nijmegen, Netherlands. In J Immunol, 2012
HVEM-B and T lymphocyte attenuator (BTLA) interactions impair minor histocompatibility antigen (MiHA)-specific T cell functionality, providing a rationale for interfering with BTLA signaling in post-stem cell transplantation.
Selective blockade of herpesvirus entry mediator-B and T lymphocyte attenuator pathway ameliorates acute graft-versus-host reaction.
Rodriguez-Barbosa et al., León, Spain. In J Immunol, 2012
Combined blockade of HVEM and B-and-T- lymphocyte attenuator (BTLA) does not inhibit donor T cell infiltration into graft-versus-host reaction organs; instead, it decreases the functional activity of the alloreactive T cells.
The soluble amino-terminal region of HVEM mediates efficient herpes simplex virus type 1 infection of gD receptor-negative cells.
Kwon et al., Seoul, South Korea. In Virol J, 2011
These results suggest that the C-terminal portion of the soluble HVEM ectodomain inhibits herpes simplex virus type 1 gD activation and that this effect is neutralized in the full-length form of HVEM in normal infection.
Multiple common variants for celiac disease influencing immune gene expression.
van Heel et al., London, United Kingdom. In Nat Genet, 2010
Variants from 13 new regions reached genome-wide significance (P(combined) < 5 x 10(-8)); most contain genes with immune functions (BACH2, CCR4, CD80, CIITA-SOCS1-CLEC16A, ICOSLG and ZMIZ1), with ETS1, RUNX3, THEMIS and TNFRSF14 having key roles in thymic T-cell selection.
Slow down and survive: Enigmatic immunoregulation by BTLA and HVEM.
Murphy et al., Saint Louis, United States. In Annu Rev Immunol, 2009
Its ligand, herpesvirus entry mediator (HVEM), is a tumor necrosis factor receptor superfamily member.
Common variants at CD40 and other loci confer risk of rheumatoid arthritis.
Plenge et al., Cambridge, United States. In Nat Genet, 2008
Finally, we identified evidence of association at four additional gene loci: MMEL1-TNFRSF14 (rs3890745, P = 0.0035 replication, P = 1.1 x 10(-7) overall), CDK6 (rs42041, P = 0.010 replication, P = 4.0 x 10(-6) overall), PRKCQ (rs4750316, P = 0.0078 replication, P = 4.4 x 10(-6) overall), and KIF5A-PIP4K2C (rs1678542, P = 0.0026 replication, P = 8.8 x 10(-8) overall).
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