Selected-GenAtlas references SOURCE GeneCards NCBI Gene Swiss-Prot Orphanet Ensembl
HGNC UniGene Nucleotide OMIM UCSC
Home Page
FLASH GENE
Symbol TNFSF11 contributors: mct/shn - updated : 19-09-2017
HGNC name tumor necrosis factor (ligand) superfamily, member 11
HGNC id 11926
ASSOCIATED DISORDERS
corresponding disease(s) OPTB2
Other morbid association(s)
TypeGene ModificationChromosome rearrangementProtein expressionProtein Function
constitutional germinal mutation      
associated with bone mineral density at different skeletal sites in adult men, but not in women
constitutional     --over  
in keratinocytes of the inflamed skin (resulted in functional alterations of epidermal dendritic cells and systemic increases of regulatory CD4(+)CD25(+) T cells)
constitutional     --over  
significantly elevated in non-cirrhotic, chronic liver disease, which could modulate bone loss
constitutional     --over  
in rheumatoid arthritis subchondral bone tissue biopsies
Susceptibility
  • to modification of Camurati-engelmann disease (CED)
  • to Crohn disease
  • Variant & Polymorphism other
  • TNFSF11 variant associated with unique phenotype of CED
  • increasing the risk of Crohn disease
  • Candidate gene
    Marker
  • expression of TNFRSF11A, TNFSF11 and TNFRSF11B may be used as diagnostic markers to identify patients at high risk for aggressive Prostate carcinoma 6)
  • Therapy target
    SystemTypeDisorderPubmed
    allergy  
    . local induction of TNFSF11/TNFRSF11A in the skin could be used as a therapeutic approach for allergies as well for systemic autoimmunity through increasing regulatory T cells
    immunologyautoimmune 
    . local induction of TNFSF11/TNFRSF11A in the skin could be used as a therapeutic approach for allergies as well for systemic autoimmunity through increasing regulatory T cells
    osteoarticularboneothers
    . early TNFSF11 administration, as soluble RANKL treatment in mice, increases osteoclast number and stimulates bone resorption
    cancermetastases 
    . central role of TNFRSF11A/TNFSF11 pathway as potential therapeutic target not only in bone metastasis management, but also in the adjuvant setting
    cancerreproductiveprostate
    effective suppression of Prostate carcinoma cell migration by TNFRSF11B via the blockage of TNFSF11 activity represents a potential therapeutic strategy for interfering with prostate tumor metastasis and progression to bone
    ANIMAL & CELL MODELS
  • TRANCE-deficient mice showed severe osteopetrosis, with no osteoclasts, marrow spaces, or tooth eruption, and exhibited profound growth retardation at several skeletal sites, including the limbs, skull, and vertebrae
  • mice lacking RANK fail to form lobulo-alveolar mammary structures during pregnancy, resulting in death of newborns
  • RANKL overexpression in keratinocytes resulted in functional alterations of epidermal dendritic cells and systemic increases of regulatory CD4(+)CD25(+) T cells
  • Transgenic overexpression of TRANCE in lymphocytes of TRANCE-deficient mice rescued osteoclast development
  • deletion of RANK from the mammary epithelium results in a markedly decreased incidence and delayed onset of medroxyprogesterone acetate-driven mammary cancer
  • severe osteopetrotic phenotype observe in mice lacking RANKL specifically in osteocytes indicates that osteocytes are the major source of RANKL in bone remodeling