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FLASH GENE

Symbol

TNFSF11

contributors: mct/shn - updated : 19-09-2019

HGNC name	tumor necrosis factor (ligand) superfamily, member 11
HGNC id	11926

FLASH GENE DNA RNA EXPRESSION PROTEIN DISORDER ANIMAL & CELL MODELS

ASSOCIATED DISORDERS

corresponding disease(s)

OPTB2

Other morbid association(s)

Type Gene Modification Chromosome rearrangement Protein expression Protein 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
	System Type Disorder Pubmed 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 immunology autoimmune   . 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 osteoarticular bone others . early TNFSF11 administration, as soluble RANKL treatment in mice, increases osteoclast number and stimulates bone resorption cancer metastases   . central role of TNFRSF11A/TNFSF11 pathway as potential therapeutic target not only in bone metastasis management, but also in the adjuvant setting cancer reproductive prostate 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