https://www.ncbi.nlm.nih.gov/gene/8600
- Also known as
- ODF; OPGL; sOdf; CD254; OPTB2; RANKL; TNLG6B; TRANCE; hRANKL2
- Summary (Suomennosta)
- Tämä geeni koodaa TNF- sytokiiniperheen jäsentä, joka toimii osteoprotegeriinin ligandina ja on avain tekijä osteokalstein erilaistumisessa ja aktivoitumisessa. Tämä RANKL- proteiini näyttää olevan dendriittisolujen elossapysymisfaktori ja se osallistuu T-solusta riippuvaiseen immuunivasteeseen. T-solujen aktivoituminen indusoi RANKL- geenin ilmenemän ja johtaa lisäntyneeseen osteoklastigeneesiin ja luukatoon. Tämä proteiini näyttää aktivoivan antiapoptoottisen kinaasin AKT/PKB:n Srckinaasi/TRAF6-signaalikompleksin kautta, mikä viittaa siihen, että tällä proteiinilla on osuutta solun apoptoosin säätelyssä. Jos hiirellä kohdennetusti tätä proteiinia vastaava geeni irrotetaan, seuraa vaikea osteopetroosi ja osteoklastien puute. Geenipuutteinen hiiri ilmentää T- ja B-imusolujen varhaiserilaistumisen defektejä ja raskauden aikana siltä puuttui kyky muodosta lobuloalveolaarista rintarauhasstruktuuria. Geenistä on kaksi vaihtoehtoispleissauksella syntyvää transkriptia. Geeniä ilmenee imusolmukkeisssa, umpilisäkkeessä ja 6 muussa kudoksessa.
- This gene encodes a member of the tumor necrosis factor (TNF) cytokine family which is a ligand for osteoprotegerin and functions as a key factor for osteoclast differentiation and activation. 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 this 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. [provided by RefSeq, Jul 2008]
- Expression
- Biased expression in lymph node (RPKM 4.9), appendix (RPKM 2.0) and 6 other tissues See more
(Lisätietoja) Related articles in PubMed
- The Expression of Matrix Metalloproteinases in Receptor Activator of Nuclear Factor Kappa-B Ligand (RANKL)-expressing Cancer of Apocrine Origin. Kambayashi Y, et al. Anticancer Res, 2018 Jan. PMID 29277763
- Effects of Osteogenic-Conditioned Medium from Human Periosteum-Derived Cells on Osteoclast Differentiation. Park HC, et al. Int J Med Sci, 2017. PMID 29200953, Free PMC Article
- RANKL-mediated harmonious dialogue between fetus and mother guarantees smooth gestation by inducing decidual M2 macrophage polarization. Meng YH, et al. Cell Death Dis, 2017 Oct 12. PMID 29022922, Free PMC Article
- Circulating RANKL and RANKL/OPG and Breast Cancer Risk by ER and PR Subtype: Results from the EPIC Cohort. Sarink D, et al. Cancer Prev Res (Phila), 2017 Sep. PMID 28701332, Free PMC Article
- -643C > T RANKL gene polymorphism is associated with osteoporosis in Tunisian postmenopausal women. Sassi R, et al. Climacteric, 2017 Aug. PMID 28453307
GeneRIFs: Gene References Into FunctionsWhat's a GeneRIF?
- The -643C>T RANKL polymorphism, through its significant influence on body weight and BMI value, may contribute to the development of Osteoporosis in Postmenopausal women.
- In the present study, we measured expression of RANKL in human periosteum-derived cells(hPDCs) undergoing osteoblastic differentiation and found that expression of RANKL mRNA was markedly increased in these cells in a time-dependent manner.RANKL protein expression was also significantly enhanced in osteogenic-conditioned media from hPDCs undergoing osteoblastic differentiation
- MiR-217 is a useful diagnostic biomarker and is involved in human podocyte cells apoptosis via targeting TNFSF11 in membranous nephropathy.
- rs9525641 might contribute to bone mineral density
- Vascular smooth cells are a significant source of osteoprotegerin within the vasculature but that RANKL, once present, downregulates this production and appears capable of preventing the "protective" upregulation of OPG seen with VSMCs exposed to physiological levels of cyclic strain.
- receptor activator for nuclear factor-kappa B ligand (RANKL), secreted by human embryonic trophoblasts and maternal decidual stromal cells, polarizes decidual macrophages toward a M2 phenotype.
- There were no significant associations involving the RANKL gene. Thus, it is suggested that alterations in the OPG and RANK genes are primarily responsible for altering the function and expression of the RANKL ligand, resulting in a predisposition to chronic arthralgia and comorbid temporomandibular OA.
- Vitamin D, tumor necrosis factor (TNF)-alpha, receptor activator of nuclear factor-KB ligand (RANKL), and OPG levels were determined in GCF and serum. Baseline clinical parameters were similar in all periodontitis groups (P > 0.05) but were higher than that in controls
- study demonstrated the association of the -643C > T polymorphism with bone mineral density variation and osteoporosis risk in postmenopausal Tunisian women
- down-regulated miR-143-5p promotes the differentiation of DPSCs into odontoblasts by enhancing Runx2 expression via the OPG/RANKL signaling pathway.
