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 Essential Laboratory Skills Guide Don't let static charges disrupt your weighing accuracy Daily Sensitivity Test 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