RANKL

Tumor necrosis factor (ligand) superfamily, member 11
PDB rendering based on 1s55.
Available structures: 1s55
Identifiers
Symbol(s)	TNFSF11; ODF; CD254; OPGL; RANKL; TRANCE; hRANKL2; sOdf
External IDs	OMIM: 602642 MGI: 1100089 Homologene: 2744
Gene Ontology Molecular Function: • receptor activity • cytokine activity • tumor necrosis factor receptor binding • protein binding Cellular Component: • extracellular region • extracellular space • integral to plasma membrane • membrane Biological Process: • ossification • immune response • multicellular organismal development • organ morphogenesis • cell differentiation • bone resorption • positive regulation of osteoclast differentiation • protein homooligomerization
RNA expression pattern
Additional recommended knowledge Don't let static charges disrupt your weighing accuracy How to ensure accurate weighing results every day? Guide to balance cleaning: 8 simple steps More reference expression data
Orthologs
	Human	Mouse
Entrez	8600	21943
Ensembl	ENSG00000120659	ENSMUSG00000022015
Uniprot	O14788	Q059M3
Refseq	NM_003701 (mRNA) NP_003692 (protein)	NM_011613 (mRNA) NP_035743 (protein)
Location	Chr 13: 42.03 - 42.08 Mb	Chr 14: 77.01 - 77.04 Mb
Pubmed search	[1]	[2]

RANKL (Receptor Activator for Nuclear Factor κ B Ligand), also known as TNF-related activation-induced cytokine (TRANCE), osteoprotegerin ligand (OPGL), and ODF (osteoclast differentiation factor) is a molecule important in bone metabolism. This natural and necessary surface-bound molecule activates osteoclasts, cells involved in bone resorption. Overproduction of RANKL is implicated in a variety of degenerative bone diseases, such as rheumatoid arthritis and osteomyelitis.

RANKL also has a function in the immune system, where it is expressed by T helper cells and is thought to be involved in dendritic cell maturation. This protein was shown to be a dentritic cell survival factor and is involved in the regulation of T cell-dependent immune response. T cell activation was reported to induce expression of the RANKL gene and lead to an increase of osteoclastogenesis and bone loss. This protein was shown to activate antiapoptotic kinase AKT/PKB through a signaling complex involving SRC kinase and tumor necrosis factor receptor-associated factor (TRAF) 6, which indicated this protein may have a role in the regulation of cell apoptosis. Targeted disruption of the related gene in mice led to severe osteopetrosis and a lack of osteoclasts. The deficient mice exhibited defects in early differentiation of T and B lymphocytes, and failed to form lobulo-alveolar mammary structures during pregnancy. Two alternatively spliced transcript variants have been found.^[1]

See also

• RANK
• Osteoprotegerin
• Osteoimmunology

References

Further reading