Herpesvirus entry mediator

Last updated
TNFRSF14
Protein TNFRSF14 PDB 1jma.png
Available structures
PDB Ortholog search: PDBe RCSB
Identifiers
Aliases TNFRSF14 , ATAR, CD270, HVEA, HVEM, LIGHTR, TR2, tumor necrosis factor receptor superfamily member 14, TNF receptor superfamily member 14
External IDs OMIM: 602746 MGI: 2675303 HomoloGene: 2833 GeneCards: TNFRSF14
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_001297605
NM_003820

NM_178931

RefSeq (protein)

NP_001284534
NP_003811

NP_849262

Location (UCSC) Chr 1: 2.56 – 2.57 Mb Chr 4: 155.01 – 155.01 Mb
PubMed search [3] [4]
Wikidata
View/Edit Human View/Edit Mouse

Herpesvirus entry mediator (HVEM), also known as tumor necrosis factor receptor superfamily member 14 (TNFRSF14), is a human cell surface receptor of the TNF-receptor superfamily [5] [6] [7] [8] encoded by the TNFRSF14 gene. [7]

Contents

Nomenclature

This protein was originally known as herpesvirus entry mediator A (HveA); HveB and HveC are structurally unrelated proteins of the immunoglobulin superfamily. It is also known as CD270 in the cluster of differentiation classification. Moreover, it is also referred to as ATAR (another TRAF-associated receptor).

Function

The protein encoded by this gene is a member of the TNF-receptor superfamily. The cytoplasmic region of this receptor was found to bind to several TNF receptor associated factor (TRAF) family members, which may mediate the signal transduction pathways that activate the immune response. [7]

In melanocytic cells TNFRSF14 gene expression may be regulated by MITF. [9]

Interactions

TNFRSF14 has been shown to interact with TRAF2, [10] [11] TNFSF14 [12] [13] and TRAF5. [10] [11]

Clinical relevance

Mutations in this gene have been recurrently been associated to cases of diffuse large B-cell lymphoma [14] [15] and pediatric-type follicular lymphoma. [16]

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. [7]

Related Research Articles

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References

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Further reading

This article incorporates text from the United States National Library of Medicine, which is in the public domain.