Status
Please wait ...

Details for messenger / hormone: RANKL

EndoNet ID: ENH00409

To link to the content of EndoNet use the EndoNet ID that is given on the detail pages in the format ENX0000, where X is a place holder for the type of the component (e. g. R for receptor or C for anatomical structure).
As URL for the linking append this ID to the detail page for this type of component.
For an hormone that would be: 

http://endonet.bioinf.med.uni-goettingen.de/hormone/ENH00000

It is also possible to use the search of EndoNet to link to the right detail page. The URL should look like 

http://endonet.bioinf.med.uni-goettingen.de/search/ENC00000
If the search pattern is unambigious the user is directed to the corresponding detail page.

Synonyms

  • receptor activator of nuclear factor kappa-B ligand
  • tumor necrosis factor ligand superfamily member 11
  • RANKL
  • osteoprotegerin ligand
  • OPGL
  • osteoclast differentiation factor
  • ODF
  • CD254 antigen
  • TNFSF11
  • receptor activator of nuclear factor kappa B ligand
  • TNF-related activation-induced cytokine
  • TRANCE

General information

  • RANKL secretion by activated T cells may induce osteoclastogenesis via a mechanism enhanced by several cytokines (TNF-alpha, IL-1, and IL-17) that promote both inflammation and bone resorption. [1]
  • Cytokine that binds to TNFRSF11B/OPG and to TNFRSF11A/RANK. Osteoclast differentiation and activation factor. Augments the ability of dendritic cells to stimulate naive T-cell proliferation. [2]
  • Osteoclast precursors express RANK, and the interaction between RANKL and RANK (which is inhibited by OPG) is the major determinant of osteoclast formation. [3]

Classification

Hormone function

  • development and growth
    • growth stimulation
    • immune response
      • activation

      Chemical classification

      • hormone
        • genome-encoded
          • cytokines

      Composition

      soluble form

      Sequence 
      IRAEKAMVD GSWLDLAKR SKLEAQPFA 
HLTINATDI PSGSHKVSL SSWYHDRGW 
AKISNMTFS NGKLIVNQD GFYYLYANI 
CFRHHETSG DLATEYLQL MVYVTKTSI 
KIPSSHTLM KGGSTKYWS GNSEFHFYS 
INVGGFFKL RSGEEISIE VSNPSLLDP 
DQDATYFGA FKVRDID

      Links to other resources

      UniProt O14788
      Ensembl ENST00000239849
      KEGG hsa:8600

      • Anatomical structure: osteoblast

        • PTH and VD3 (calcitriol) increase the expression of RANKL on the surface of osteoblasts and bone marrow stem cells. [4]

        Influenced by:

        • VDR
          in osteoblast
        • PTHR1
          in osteoblast

      • Anatomical structure: hematopoietic_stem_cell

        • PTH and VD3 (calcitriol) increase the expression of RANKL on the surface of osteoblasts and bone marrow stem cells. [4]

        Influenced by:

        • PTHR1
          in hematopoietic_stem_cell
        • VDR
          in hematopoietic_stem_cell

      • Anatomical structure: stromal_cell_of_bone_marrow

        Influenced by:

        • PTHR1
          in stromal_cell_of_bone_marrow
          • Stromal cells and osteoblasts express RANKL and M-CSF, which are up-regulated by osteoclastogenic molecules such as PTH. [5]

      • Anatomical structure: T-lymphocyte

        • Activated T cells can directly trigger osteoclastogenesis through OPGL (RANKL). Systemic activation of T cells in vivo leads to an OPGL-mediated increase in osteoclastogenesis and bone loss. [6]

      • Anatomical structure: blood_vessel

      • Anatomical structure: thymus

      • Anatomical structure: osteoclast

      • Anatomical structure: right_coronary_artery

      • Anatomical structure: left coronary artery

      Targets

      CellOPGRANK
      osteoblast Present
      osteoclast Present
      Phenotypes
      • inhibition of osteoclast differentation
      		Present
      Reference