TNFSF12

Protein-coding gene in the species Homo sapiens From Wikipedia, the free encyclopedia

Tumor necrosis factor ligand superfamily member 12 also known as TNF-related weak inducer of apoptosis (TWEAK) is a protein that in humans is encoded by the TNFSF12 gene.[5][6][7]

PDBOrtholog search: PDBe RCSB
AliasesTNFSF12, APO3L, DR3LG, TWEAK, TNLG4A, tumor necrosis factor superfamily member 12, TNF superfamily member 12
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TNFSF12
Available structures
PDBOrtholog search: PDBe RCSB
Identifiers
AliasesTNFSF12, APO3L, DR3LG, TWEAK, TNLG4A, tumor necrosis factor superfamily member 12, TNF superfamily member 12
External IDsOMIM: 602695; MGI: 1196259; HomoloGene: 7979; GeneCards: TNFSF12; OMA:TNFSF12 - orthologs
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_003809

NM_011614

RefSeq (protein)

NP_003800

NP_035744

Location (UCSC)Chr 17: 7.55 – 7.56 MbChr 11: 69.58 – 69.59 Mb
PubMed search[3][4]
Wikidata
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Function

TWEAK was discovered in 1997.[5] The protein encoded by this gene is a cytokine that belongs to the tumor necrosis factor (TNF) ligand family. This protein is a ligand for the FN14/TWEAKR receptor. This cytokine has overlapping signaling functions with TNF, but displays a much wider tissue distribution. Leukocytes are the main source of TWEAK including human resting and activated monocytes, dendritic cells and natural killer cells.[8] TWEAK can induce apoptosis via multiple pathways of cell death in a cell type-specific manner. This cytokine is also found to promote proliferation and migration of endothelial cells, and thus acts as a regulator of angiogenesis.[7]

Clinical significance

Excessive activation of the TWEAK pathway in chronic injury has been described to promote pathological tissue changes including chronic inflammation, fibrosis and angiogenesis.[9] In chronic liver disease, for example, TWEAK expression is enhanced and causes hepatic stellate cells, which are key regulators of liver fibrosis, to proliferate.[10]

References

Further reading

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