LIGHT (protein)

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TNFSF14
Available structures
PDB Ortholog search: PDBe RCSB
Identifiers
Aliases TNFSF14, CD258, HVEML, LIGHT, LTg, TR2, TNLG1D, tumor necrosis factor superfamily member 14
External IDs MGI: 1355317 HomoloGene: 2822 GeneCards: TNFSF14
Genetically Related Diseases
multiple sclerosis[1]
RNA expression pattern
PBB GE TNFSF14 207907 at fs.png
More reference expression data
Orthologs
Species Human Mouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_003807
NM_172014

NM_019418

RefSeq (protein)

NP_003798
NP_742011

NP_062291.1
NP_062291

Location (UCSC) Chr 19: 6.66 – 6.67 Mb Chr 17: 57.19 – 57.19 Mb
PubMed search [2] [3]
Wikidata
View/Edit Human View/Edit Mouse

LIGHT, also known as tumor necrosis factor superfamily member 14 (TNFSF14), is a secreted protein of the TNF superfamily.[4][5][6] It is recognized by herpesvirus entry mediator (HVEM), as well as decoy receptor 3.

Nomenclature[edit]

LIGHT stands for "homologous to lymphotoxin, exhibits inducible expression and competes with HSV glycoprotein D for binding to herpesvirus entry mediator, a receptor expressed on T lymphocytes". In the cluster of differentiation terminology it is classified as CD258.

Function[edit]

The protein encoded by this gene is a member of the tumor necrosis factor (TNF) ligand family. This protein is a ligand for TNFRSF14, which is a member of the tumor necrosis factor receptor superfamily, and which is also known as a herpesvirus entry mediator ligand (HVEML). This protein may function as a costimulatory factor for the activation of lymphoid cells and as a deterrent to infection by herpesvirus. This protein has been shown to stimulate the proliferation of T cells, and trigger apoptosis of various tumor cells. This protein is also reported to prevent tumor necrosis factor alpha mediated apoptosis in primary hepatocyte. Two alternatively spliced transcript variant encoding distinct isoforms have been reported.[5]

Interactions[edit]

LIGHT has been shown to interact with TNFRSF14,[7][8] TNFRSF6B,[7][8][9] BIRC2,[10] TRAF2[10] and TRAF3.[10]

Role in herpes simplex virus[edit]

Similar to how CD4 is the primary mediating receptor in HIV infection, the HSV glycoprotein (gD) binds to the HVEM receptor which is demanded by TNFSF14/LIGHT lowering the ability for LIGHT to activate the NFκB pathway. NFκB is a survival factor helping to inhibit apoptosis which triggers a pathway inhibiting caspase 8. When gD from HSV binds to HVEM, LIGHT is non-competitively inhibited from binding, encouraging apoptosis in the infected cell.[6]

References[edit]

  1. ^ "Diseases that are genetically associated with TNFSF14 view/edit references on wikidata". 
  2. ^ "Human PubMed Reference:". 
  3. ^ "Mouse PubMed Reference:". 
  4. ^ Mauri DN, Ebner R, Montgomery RI, Kochel KD, Cheung TC, Yu GL, Ruben S, Murphy M, Eisenberg RJ, Cohen GH, Spear PG, Ware CF (January 1998). "LIGHT, a new member of the TNF superfamily, and lymphotoxin alpha are ligands for herpesvirus entry mediator". Immunity. 8 (1): 21–30. doi:10.1016/S1074-7613(00)80455-0. PMID 9462508. 
  5. ^ a b "Entrez Gene: TNFSF14 tumor necrosis factor (ligand) superfamily, member 14". 
  6. ^ a b Ware, Carl (2008). "Chapter 25: TNF-Related Cytokines in Immunity". In Paul, William. Fundamental Immunology (Book) (6th ed.). Philadelphia: Lippincott Williams & Wilkins. pp. 776–801. ISBN 0-7817-6519-6. 
  7. ^ a b Zhang J, Salcedo TW, Wan X, Ullrich S, Hu B, Gregorio T, Feng P, Qi S, Chen H, Cho YH, Li Y, Moore PA, Wu J (June 2001). "Modulation of T-cell responses to alloantigens by TR6/DcR3". The Journal of Clinical Investigation. 107 (11): 1459–68. doi:10.1172/JCI12159. PMC 209323Freely accessible. PMID 11390428. 
  8. ^ a b Yu KY, Kwon B, Ni J, Zhai Y, Ebner R, Kwon BS (May 1999). "A newly identified member of tumor necrosis factor receptor superfamily (TR6) suppresses LIGHT-mediated apoptosis". The Journal of Biological Chemistry. 274 (20): 13733–6. doi:10.1074/jbc.274.20.13733. PMID 10318773. 
  9. ^ Hsu TL, Chang YC, Chen SJ, Liu YJ, Chiu AW, Chio CC, Chen L, Hsieh SL (May 2002). "Modulation of dendritic cell differentiation and maturation by decoy receptor 3". Journal of Immunology. 168 (10): 4846–53. doi:10.4049/jimmunol.168.10.4846. PMID 11994433. 
  10. ^ a b c Kuai J, Nickbarg E, Wooters J, Qiu Y, Wang J, Lin LL (April 2003). "Endogenous association of TRAF2, TRAF3, cIAP1, and Smac with lymphotoxin beta receptor reveals a novel mechanism of apoptosis". The Journal of Biological Chemistry. 278 (16): 14363–9. doi:10.1074/jbc.M208672200. PMID 12571250. 

Further reading[edit]

External links[edit]

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