TRAFs in RANK signaling
- PMID: 17633024
- DOI: 10.1007/978-0-387-70630-6_12
TRAFs in RANK signaling
Abstract
Members of the tumor necrosis factor (TNF) family govern many diverse physiological and cellular responses including cellular proliferation, differentiation, and apoptosis. Ligands of this family interact through a distinct set of specific receptors that lack enzymatic activity and therefore are dependent on the association of adaptor molecules. One receptor/ligand pair known as receptor activator of nuclear factor-kappa B (RANK) and RANK ligand (RANKL) regulates bone remodeling, mammary gland development, and lymph node organogenesis. RANK interacts with five members of the TNF receptor-associated factor (TRAF) family, of which TRAF6 is indispensable for its signaling capability. An accumulation of evidence from various research laboratories indicates TRAFs, but more importantly TRAF6, is the key to understanding how RANKL links cytoplasmic signaling to the nuclear transcriptional program.
Similar articles
-
Biology of RANK, RANKL, and osteoprotegerin.Arthritis Res Ther. 2007;9 Suppl 1(Suppl 1):S1. doi: 10.1186/ar2165. Arthritis Res Ther. 2007. PMID: 17634140 Free PMC article. Review.
-
The role of TNF-receptor family members and other TRAF-dependent receptors in bone resorption.Arthritis Res. 2001;3(1):6-12. doi: 10.1186/ar134. Epub 2000 Nov 2. Arthritis Res. 2001. PMID: 11178122 Free PMC article. Review.
-
Physiology and pathophysiology of the RANKL/RANK system.Biol Chem. 2010 Dec;391(12):1365-70. doi: 10.1515/BC.2010.149. Biol Chem. 2010. PMID: 21087090 Review.
-
TNF receptor (TNFR)-associated factor (TRAF) 3 serves as an inhibitor of TRAF2/5-mediated activation of the noncanonical NF-kappaB pathway by TRAF-binding TNFRs.Proc Natl Acad Sci U S A. 2005 Feb 22;102(8):2874-9. doi: 10.1073/pnas.0500187102. Epub 2005 Feb 11. Proc Natl Acad Sci U S A. 2005. PMID: 15708970 Free PMC article.
-
TRAF-mediated TNFR-family signaling.Curr Protoc Immunol. 2009 Nov;Chapter 11:11.9D.1-11.9D.19. doi: 10.1002/0471142735.im1109ds87. Curr Protoc Immunol. 2009. PMID: 19918944 Review.
Cited by
-
Osteopetrosis in TAK1-deficient mice owing to defective NF-κB and NOTCH signaling.Proc Natl Acad Sci U S A. 2015 Jan 6;112(1):154-9. doi: 10.1073/pnas.1415213112. Epub 2014 Dec 22. Proc Natl Acad Sci U S A. 2015. PMID: 25535389 Free PMC article.
-
NF-κB-Mediated Regulation of Osteoclastogenesis.Endocrinol Metab (Seoul). 2015 Mar 27;30(1):35-44. doi: 10.3803/EnM.2015.30.1.35. Endocrinol Metab (Seoul). 2015. PMID: 25827455 Free PMC article. Review.
-
TAK1 is essential for osteoclast differentiation and is an important modulator of cell death by apoptosis and necroptosis.Mol Cell Biol. 2013 Feb;33(3):582-95. doi: 10.1128/MCB.01225-12. Epub 2012 Nov 19. Mol Cell Biol. 2013. PMID: 23166301 Free PMC article.
-
Inflammation, cancer, and bone loss.Curr Opin Pharmacol. 2009 Aug;9(4):427-33. doi: 10.1016/j.coph.2009.06.007. Epub 2009 Jul 2. Curr Opin Pharmacol. 2009. PMID: 19577517 Free PMC article. Review.
-
TRAF6 promotes osteogenesis in ADSCs through Raf-Erk-Merk-Hif1-a pathway.Adipocyte. 2023 Dec;12(1):2193280. doi: 10.1080/21623945.2023.2193280. Adipocyte. 2023. PMID: 37005742 Free PMC article.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
