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TNFRSF6B (tumor necrosis factor receptor superfamily, member 6b, decoy)

Written2007-12Jiangping Wu, Bing Han
CHUM Research Center, University of Montreal, Canada

(Note : for Links provided by Atlas : click)

Identity

Alias_namestumor necrosis factor receptor superfamily
Alias_symbol (synonym)DcR3
DCR3
TR6
M68
HGNC (Hugo) TNFRSF6B
LocusID (NCBI) 8771
Atlas_Id 42628
Location 20q13.33  [Link to chromosome band 20q13]
Location_base_pair Starts at 62328004 and ends at 62330051 bp from pter ( according to hg19-Feb_2009)  [Mapping TNFRSF6B.png]

DNA/RNA

 
Description DNA sequence is located on chromosome 20. Transcription consists of 7 exons and 6 introns, spanning 3.6kb.
A shorter transcription variance (M68E) has been identified, and is transcribed from 3 exons and 2 introns spanning 1.9kb as illustrated above. The difference occurs at the 5' untranslated region, but the two transcripts encode the same isoform. Mice do not have a gene orthologue to human TNFRSF6B.
TNFRSF68B mRNA in Northen blot presents as a 1.2-knt band.

Protein

 
  A) Domains and Motifs. B) TNFRSF6B X-ray crystography
Description TNFRSF6B protein is 300-amino acid long, and has a molecular weight of 35 kD. Although TNFRSF6B belongs to the TNFR superfamily, it lacks the transmembrane and cytosolic domains in its sequence, and is a secreted protein. It contains 4 TNFR cystein-rich regions, as illustrated above.
TNFRSF6B can be easily cleaved between Arg218 and Ala219 in biological fluids and solutions. It has thus a very short (about 20 min) half-life in serum and in vivo. Mutation of arginine residue at position 218 to glutamine makes TNFRSF6B resistant to proteolysis, and significantly prolongs its half-life.
TNFRSF6B can bind to the TNF family members FasL, LIGHT and TL1A. It does not bind to other known TNF family members. Human TNFRSF6B can bind to mouse FasL, LIGHT and TL1A. This allows human DcR3/TNFRSF6B to function in mouse models both in vitro and in vivo.
The role of TNFRSF6B in apoptosis is obvious. FasL is a well-known molecule involved in apoptosis. LIGHT is a ligand for HVEM and LTbetaR, in addition to being a ligand for TNFRSF6B. LIGHT can induce apoptosis in cells expressing both HVEM and LTbetaR, or LTbetaR alone. TL1A, a member of the TNF family, can evoke apoptosis via its receptor, DR3. Consequently, the interaction of TNFRSF6B with FasL, LIGHT, and TL1A blocks apoptosis mediated by Fas, HVEM, LTbetaR and DR3.
Expression Normal tissue and cells express low-level TNFRSF6B, and healthy individuals have near-background serum TNFRSF6B levels. About 60% of malignant tumors of various tissue origins overexpress TNFRSF6B, and these patients have elevated serum TNFRSF6B levels. Serum TNFRSF6B levels of tumor patients are positively correlated to the degree of tumor malignancy and status of metastasis. It is hypothesized that malignant tumor cells secrete TNFRSF6B as a way to achieve survival advantage by blocking multiple apoptosis pathways.
Hepatocytes in liver cirrhosis have augmented TNFRSF6B expression and patients with liver cirrhosis have increased serum TNFRSF6B levels.
TNFRSF6B expression is low in resting T cells but is augmented in activated T cells, which probably represents a fine-tuning mechanism to balance the need for clonal expansion and subsequent massive activation-induced T cell death. About 40% of systemic lupus erythematosus patients have elevated serum TNFRSF6B levels.
TNFRSF6B expression in rheumatoid arthritis fibroblast-like synoviocytes is increased by TNFalpha
Localisation TNFRSF6B is a secreted protein, and is thus detected in body fluids. However, it can also be detected in cytoplasm before it is secreted.
Function As TNFRSF6B can block ligands from interacting with Fas, HVEM, LTbetaR, and DR3, all of which mediate apoptosis, it is thus can effectively inhibit apoptosis in many cell types. It is believed that many types of malignant tumors gain survival advantage by secreting TNFRSF6B which blocks tumor cell apoptosis.
Syngeneic islets transplanted to diabetes recipients survive better in the presence of administered exogenous human TNFRSF6B, due to the blockage of FasL-, LIGHT- and TL1A-triggered islets apoptosis. Transgenic expression of human TNFRSF6B in NOD mouse islets reduces diabetes pathogenesis, again, due to anti-apoptotic effect of TNFRSF6B.
The forward signaling from FasL to Fas, and from LIGHT to HVEM can provide costimulation signals to resting T cells. Blocking of these two signaling pathways reduces T cell responses to antigens. As LIGHT and FasL, although being ligands, are also transmembrane proteins, and are capable of reversely transducing costimulating signals into T cells, TNFRSF6B can also block such reverse signaling. The end result is that TNFRSF6B can reduce several costimulation pathways in T cells and inhibit T cell immune responses, such as cytokine secretion and proliferation in vitro, and cardiac allograft rejection in vivo in mouse models.
When human TNFRSF6B is linked to a transmembrane domain and is expressed on the mouse tumor cell surface, it can effectively trigger T cell costimulation via LIGHT and FasL reverse signaling, and cause effective tumor vaccination in mouse models.
When human TNFRSF6B is transgenically expressed in mice, it causes a systemic lupus erythrematosus-like syndrome. The expression of TNFRSF6B in bone marrow-derived cells is sufficient to induce this phenotype.
Recombinant human TNFRSF6B ameliorates an autoimmune crescentic glomerulonephritis model in mice.
TNFRSF6B can influence dendritic cells which in turn drive T cells to differentiate into Th2 cells.
TNFRSF6B can inhibit actin polymerization of T cells upon mitogen stimulation, and repress T-cell pseudopodium formation, which is known to be important for cell-cell interaction. As a consequence, T-cell aggregation after activation is suppressed by either soluble or solid phase TNFRSF6B.
Human T cells pretreated with soluble or solid-phase TNFRSF6B are compromised in migration in vitro and in vivo toward CXCL12. Mechanistically, a small GTPase Cdc42 fails to be activated after TNFRSF6B pretreatment of human T cells, and further downstream, p38 mitogen-activated protein kinase activation, actin polymerization, and pseudopodium formation are all down-regulated in the treated T cells.
Phagocytic activity toward immune complexes and apoptotic bodies as well as the production of free radicals and proinflammatory cytokines in response to lipopolysaccharide are impaired in TNFRSF6B-treated macrophages.

Mutations

Note Not reported yet.

Implicated in

Note
Entity Malignant tumors
Disease Oncogenesis
TNFRSF6B is overexpressed in about 60% of various malignant tumors. Its anti-apoptotic effect provides the tumors a survival advantage, and its role in reducing T cell costimulation favors tumor evasion from the immune surveillance. No TNFRSF6B gene amplification in tumors has been identified.
Diagnosis and prognosis
TNFRSF6B in sera or tumor can be used as a parameter for tumor diagnosis and prognosis. The degree of tumor malignancy is correlated to TNFRSF6B levels. When a TNFRSF6B-expressing tumor is resected, serum TNFRSF6B levels will decrease to near-zero level. The re-arising of serum TNFRSF6B in such patients will indicate tumor reoccurrence.
Therapeutics
When TNFRSF6B is anchored on tumor cell surface, it can increase the antigenicity of the tumor, and such TNFRSF6B-expressing tumors can be used as tumor vaccine.
  
Entity Systemic lupus erythematosus (SLE)
Disease Pathogenesis
About 50% of SLE patients have elevated serum TNFRSF6B levels, and the levels augment during SLE flare-up. In animal models, human TNFRSF6B overexpression in mouse cells of hematopoietic origin leads to a SLE-like syndrome, suggesting a pathogenic role of TNFRSF6B in SLE.
Diagnosis
Serum TNFRSF6B can be used as a diagnostic parameter for SLE and SLE disease activity.
Therapeutics
Due to the pathogenic effect of TNFRSF6B on SLE, it is speculated that neutralizing TNFRSF6B might have therapeutic effect on a subpopulation of SLE patients, who are serum TNFSF6B positive.
  
Entity Islet primary nonfunction during islet transplantation
Disease Therapeutics
Due to the anti-apoptotic effect of TNFRSF6B, it can effectively protect islets from apoptosis during their isolation, transportation, and primary non-function after transplantation.
  

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Citation

This paper should be referenced as such :
Wu, J ; Han, B
TNFRSF6B (tumor necrosis factor receptor superfamily, member 6b, decoy)
Atlas Genet Cytogenet Oncol Haematol. 2008;12(4):334-338.
Free journal version : [ pdf ]   [ DOI ]
On line version : http://AtlasGeneticsOncology.org/Genes/TNFRSF6BID42628ch20q13.html


External links

Nomenclature
HGNC (Hugo)TNFRSF6B   11921
Cards
AtlasTNFRSF6BID42628ch20q13
Entrez_Gene (NCBI)TNFRSF6B  8771  tumor necrosis factor receptor superfamily member 6b
AliasesDCR3; DJ583P15.1.1; M68; M68E; 
TR6
GeneCards (Weizmann)TNFRSF6B
Ensembl hg19 (Hinxton)ENSG00000243509 [Gene_View]  chr20:62328004-62330051 [Contig_View]  TNFRSF6B [Vega]
Ensembl hg38 (Hinxton)ENSG00000243509 [Gene_View]  chr20:62328004-62330051 [Contig_View]  TNFRSF6B [Vega]
ICGC DataPortalENSG00000243509
TCGA cBioPortalTNFRSF6B
AceView (NCBI)TNFRSF6B
Genatlas (Paris)TNFRSF6B
WikiGenes8771
SOURCE (Princeton)TNFRSF6B
Genetics Home Reference (NIH)TNFRSF6B
Genomic and cartography
GoldenPath hg19 (UCSC)TNFRSF6B  -     chr20:62328004-62330051 +  20q13.33   [Description]    (hg19-Feb_2009)
GoldenPath hg38 (UCSC)TNFRSF6B  -     20q13.33   [Description]    (hg38-Dec_2013)
EnsemblTNFRSF6B - 20q13.33 [CytoView hg19]  TNFRSF6B - 20q13.33 [CytoView hg38]
Mapping of homologs : NCBITNFRSF6B [Mapview hg19]  TNFRSF6B [Mapview hg38]
OMIM603361   
Gene and transcription
Genbank (Entrez)AF104419 AF134240 AF217794 AW204999 AY124378
RefSeq transcript (Entrez)NM_003823 NM_032945
RefSeq genomic (Entrez)NC_000020 NC_018931 NT_011362 NW_004929419
Consensus coding sequences : CCDS (NCBI)TNFRSF6B
Cluster EST : UnigeneHs.434878 [ NCBI ]
CGAP (NCI)Hs.434878
Alternative Splicing GalleryENSG00000243509
Gene ExpressionTNFRSF6B [ NCBI-GEO ]   TNFRSF6B [ EBI - ARRAY_EXPRESS ]   TNFRSF6B [ SEEK ]   TNFRSF6B [ MEM ]
Gene Expression Viewer (FireBrowse)TNFRSF6B [ Firebrowse - Broad ]
SOURCE (Princeton)Expression in : [Datasets]   [Normal Tissue Atlas]  [carcinoma Classsification]  [NCI60]
GenevisibleExpression in : [tissues]  [cell-lines]  [cancer]  [perturbations]  
BioGPS (Tissue expression)8771
GTEX Portal (Tissue expression)TNFRSF6B
Protein : pattern, domain, 3D structure
UniProt/SwissProtO95407   [function]  [subcellular_location]  [family_and_domains]  [pathology_and_biotech]  [ptm_processing]  [expression]  [interaction]
NextProtO95407  [Sequence]  [Exons]  [Medical]  [Publications]
With graphics : InterProO95407
Splice isoforms : SwissVarO95407
PhosPhoSitePlusO95407
Domaine pattern : Prosite (Expaxy)TNFR_NGFR_1 (PS00652)    TNFR_NGFR_2 (PS50050)   
Domains : Interpro (EBI)TNFR/NGFR_Cys_rich_reg   
Domain families : Pfam (Sanger)TNFR_c6 (PF00020)   
Domain families : Pfam (NCBI)pfam00020   
Domain families : Smart (EMBL)TNFR (SM00208)  
Conserved Domain (NCBI)TNFRSF6B
DMDM Disease mutations8771
Blocks (Seattle)TNFRSF6B
PDB (SRS)3K51    3MHD    3MI8    4J6G    4KGG    4KGQ    4MSV   
PDB (PDBSum)3K51    3MHD    3MI8    4J6G    4KGG    4KGQ    4MSV   
PDB (IMB)3K51    3MHD    3MI8    4J6G    4KGG    4KGQ    4MSV   
PDB (RSDB)3K51    3MHD    3MI8    4J6G    4KGG    4KGQ    4MSV   
Structural Biology KnowledgeBase3K51    3MHD    3MI8    4J6G    4KGG    4KGQ    4MSV   
SCOP (Structural Classification of Proteins)3K51    3MHD    3MI8    4J6G    4KGG    4KGQ    4MSV   
CATH (Classification of proteins structures)3K51    3MHD    3MI8    4J6G    4KGG    4KGQ    4MSV   
SuperfamilyO95407
Human Protein AtlasENSG00000243509
Peptide AtlasO95407
HPRD04527
IPIIPI00646641   IPI00442342   
Protein Interaction databases
DIP (DOE-UCLA)O95407
IntAct (EBI)O95407
FunCoupENSG00000243509
BioGRIDTNFRSF6B
STRING (EMBL)TNFRSF6B
ZODIACTNFRSF6B
Ontologies - Pathways
QuickGOO95407
Ontology : AmiGOreceptor activity  tumor necrosis factor-activated receptor activity  protein binding  extracellular region  extracellular space  integral component of plasma membrane  inflammatory response  immune response  multicellular organism development  response to lipopolysaccharide  tumor necrosis factor-mediated signaling pathway  regulation of cell proliferation  negative regulation of apoptotic process  positive regulation of MAPK cascade  apoptotic signaling pathway  
Ontology : EGO-EBIreceptor activity  tumor necrosis factor-activated receptor activity  protein binding  extracellular region  extracellular space  integral component of plasma membrane  inflammatory response  immune response  multicellular organism development  response to lipopolysaccharide  tumor necrosis factor-mediated signaling pathway  regulation of cell proliferation  negative regulation of apoptotic process  positive regulation of MAPK cascade  apoptotic signaling pathway  
Pathways : KEGGCytokine-cytokine receptor interaction   
REACTOMEO95407 [protein]
REACTOME PathwaysR-HSA-5669034 TNFs bind their physiological receptors [pathway]
NDEx NetworkTNFRSF6B
Atlas of Cancer Signalling NetworkTNFRSF6B
Wikipedia pathwaysTNFRSF6B
Orthology - Evolution
OrthoDB8771
GeneTree (enSembl)ENSG00000243509
Phylogenetic Trees/Animal Genes : TreeFamTNFRSF6B
HOVERGENO95407
HOGENOMO95407
Homologs : HomoloGeneTNFRSF6B
Homology/Alignments : Family Browser (UCSC)TNFRSF6B
Gene fusions - Rearrangements
Polymorphisms : SNP and Copy number variants
NCBI Variation ViewerTNFRSF6B [hg38]
dbSNP Single Nucleotide Polymorphism (NCBI)TNFRSF6B
dbVarTNFRSF6B
ClinVarTNFRSF6B
1000_GenomesTNFRSF6B 
Exome Variant ServerTNFRSF6B
ExAC (Exome Aggregation Consortium)TNFRSF6B (select the gene name)
Genetic variants : HAPMAP8771
Genomic Variants (DGV)TNFRSF6B [DGVbeta]
DECIPHER (Syndromes)20:62328004-62330051  ENSG00000243509
CONAN: Copy Number AnalysisTNFRSF6B 
Mutations
ICGC Data PortalTNFRSF6B 
TCGA Data PortalTNFRSF6B 
Broad Tumor PortalTNFRSF6B
OASIS PortalTNFRSF6B [ Somatic mutations - Copy number]
Somatic Mutations in Cancer : COSMICTNFRSF6B  [overview]  [genome browser]  [tissue]  [distribution]  
Mutations and Diseases : HGMDTNFRSF6B
LOVD (Leiden Open Variation Database)Whole genome datasets
LOVD (Leiden Open Variation Database)LOVD - Leiden Open Variation Database
LOVD (Leiden Open Variation Database)LOVD 3.0 shared installation
BioMutasearch TNFRSF6B
DgiDB (Drug Gene Interaction Database)TNFRSF6B
DoCM (Curated mutations)TNFRSF6B (select the gene name)
CIViC (Clinical Interpretations of Variants in Cancer)TNFRSF6B (select a term)
intoGenTNFRSF6B
NCG5 (London)TNFRSF6B
Cancer3DTNFRSF6B(select the gene name)
Impact of mutations[PolyPhen2] [SIFT Human Coding SNP] [Buck Institute : MutDB] [Mutation Assessor] [Mutanalyser]
Diseases
OMIM603361   
Orphanet
MedgenTNFRSF6B
Genetic Testing Registry TNFRSF6B
NextProtO95407 [Medical]
TSGene8771
GENETestsTNFRSF6B
Huge Navigator TNFRSF6B [HugePedia]
snp3D : Map Gene to Disease8771
BioCentury BCIQTNFRSF6B
ClinGenTNFRSF6B
Clinical trials, drugs, therapy
Chemical/Protein Interactions : CTD8771
Chemical/Pharm GKB GenePA36614
Clinical trialTNFRSF6B
Miscellaneous
canSAR (ICR)TNFRSF6B (select the gene name)
Probes
Litterature
PubMed115 Pubmed reference(s) in Entrez
GeneRIFsGene References Into Functions (Entrez)
CoreMineTNFRSF6B
EVEXTNFRSF6B
GoPubMedTNFRSF6B
iHOPTNFRSF6B
REVIEW articlesautomatic search in PubMed
Last year publicationsautomatic search in PubMed

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