TNFRSF13C

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Tumor necrosis factor receptor superfamily, member 13C

PDB rendering based on 1oqe.
Available structures
PDB Ortholog search: PDBe, RCSB
Identifiers
Symbols TNFRSF13C ; BAFF-R; BAFFR; BROMIX; CD268; CVID4; prolixin
External IDs OMIM606269 MGI1919299 HomoloGene49897 GeneCards: TNFRSF13C Gene
Orthologs
Species Human Mouse
Entrez 115650 72049
Ensembl ENSG00000159958 ENSMUSG00000068105
UniProt Q96RJ3 Q9D8D0
RefSeq (mRNA) NM_052945 NM_028075
RefSeq (protein) NP_443177 NP_082351
Location (UCSC) Chr 22:
42.32 – 42.32 Mb
Chr 15:
82.22 – 82.22 Mb
PubMed search [1] [2]

Tumor necrosis factor receptor superfamily member 13C also known as B-cell-activating factor receptor or BAFF receptor is a protein that in humans is encoded by the TNFRSF13C gene.[1][2]

Function[edit]

B-cell-activating factor (BAFF) enhances B-cell survival in vitro and is a regulator of the peripheral B-cell population. The protein encoded by this gene is a receptor for BAFF and is a type III transmembrane protein containing a single extracellular phenylalanine-rich domain. It is thought that this receptor is the principal receptor required for BAFF-mediated mature B-cell survival.[2]

Clinical signifance[edit]

Overexpression of Baff in mice results in mature B-cell hyperplasia and symptoms of systemic lupus erythematosus (SLE). Also, some SLE patients have increased levels of BAFF in serum. Therefore, it has been proposed that abnormally high levels of BAFF may contribute to the pathogenesis of autoimmune diseases by enhancing the survival of autoreactive B cells.[2]

References[edit]

  1. ^ Thompson JS, Bixler SA, Qian F, Vora K, Scott ML, Cachero TG, Hession C, Schneider P, Sizing ID, Mullen C, Strauch K, Zafari M, Benjamin CD, Tschopp J, Browning JL, Ambrose C (Sep 2001). "BAFF-R, a newly identified TNF receptor that specifically interacts with BAFF". Science 293 (5537): 2108–11. doi:10.1126/science.1061965. PMID 11509692. 
  2. ^ a b c "Entrez Gene: TNFRSF13C tumor necrosis factor receptor superfamily, member 13C". 

Further reading[edit]

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