Tumor Necrosis Factor Receptor Superfamily, Member 11b Proteine (TNFRSF11B)

Human Tumor Necrosis Factor Receptor Superfamily, Member 11b (TNFRSF11B) Interaktionspartner

1. MMP-2 and OPG may be involved in the pathogenesis of atherosclerosis in patients with chronic kidney disease and could potentially be of use as biomarkers of subclinical atherosclerosis in these patients.

2. rs3102724 polymorphism associated with external apical root resorption

3. higher concentrations of butyric acid generated by periodontal and root canal microorganisms may potentially induce bone destruction and impair bone repair by the alteration of OPG/RANKL expression/secretion, 8-isoprostane, MMP-2 and OPN secretion, and affect cell viability.

4. Plasma TNFRSF11B levels were significantly associated with the presence of OSA and its severity

5. Changes in cerebrospinal fluid levels of the RANKL/RANK/OPG axis are associated with multiple sclerosis, particularly at disease onset.

6. Higher pre-diagnosis endogenous concentrations of the decoy receptor for RANKL, OPG, appear to increase risk of death after a breast cancer diagnosis especially in those diagnosed with ER+ disease.

7. Meta-analysis demonstrates that A163G might be associated with the femoral hip and total hip bone mineral density (BMD), G1181C and T950C might be associated with the lumbar spine and total hip BMD. And, T245G has no effect on BMD in postmenopausal women.

8. REVIEW: role of osteoprotegerin in the crosstalk between vessels and bone: circulating OPG levels could be used as independent biomarkers of cardiovascular disease in patients with acute or chronic cardiometabolic disease and thus an improved prognosis

9. OPG is one promising susceptibility gene of bone mineral density or osteoporotic fractures.

10. The concentration of circulating osteoprotegerin can be a biomarker for both medial artery calcification and atherosclerosis in patients with chronic kidney disease (CKD); OPG might be an early indicator of all-cause mortality in CKD patients with advanced medial arterial calcification

11. We conclude that non-small cell lung cancer patients have a higher content of OPG in bronchoalveolar lavage fluid than healthy people.

12. positive correlation of OPG with age and an inverse correlation with IGF-I favor the compensatory response of OPG against bone loss in the aging skeleton

13. The results indicated that mice treated with low levels of human recombinant OPG may have a more stable aneurysmal phenotype due to compensatory production of collagen and increased vessel wall thickness of the aorta, potentially protecting the aneurysm from rupture.

14. TNF-alpha, DKK1, and OPG have roles in pathogenesis of knee osteoarthritis

15. OPG mRNA expression was higher in tumour tissue from patients with metastatic prostate cancer compared to local disease. The RANKL/OPG ratio was low in normal prostate tissue and high in tumours with bone metastases. Expression was high in BPH tissue but did not exceed as much as in the tumour tissue.

16. results of this study concluded that the RANK, RANK-L and OPG system participates in bone remodeling after RME

17. In cardiovascular risks, OPG serum level might increase as a preventive compensatory mechanism to neutralize the RANKL level increment. The determination of the OPG-RANKL system is a diagnostic indicator for the intensity of vascular calcification and atherosclerosis in SSc patients.

18. Demonstrate that rs3134069 in TNFRSF11B increases risk of ischemic stroke by decreasing TNFRSF11B expression.

19. sRANKL and OPG may play a role in the pathogenesis of diabetes as well as metabolic disturbance

20. The study revealed an enhanced sensitivity of aortic valve interstitial cells to osteogenic inductors in aortic stenosis patients, which indicates probable implication of OPN, OPG, and BMP2 genes in pathogenesis of aortic valve calcification.

Mouse (Murine) Tumor Necrosis Factor Receptor Superfamily, Member 11b (TNFRSF11B) Interaktionspartner

1. intact dimerization interface is essential for the biological activity of OPG.

2. lactation increases physiological maxillary bone remodeling and orthodontic tooth movement, and both require activation of RANK/RANKL/OPG system

3. Hdac3-depletion in osteoblasts increases expression of Opg, subsequently preserving insulin sensitivity.

4. Epithelial rests of Malassez may be associated with root resorption via OPG, thus helping to explain the mechanism underlying root resorption.

5. findings demonstrate that mTORC1 activation-stimulated RANKL expression in B cells is sufficient to induce bone loss and osteoporosis. The study also established a link between mTORC1 and the RANKL/OPG axis via negative regulation of beta-catenin.

6. RANK/RANKL signaling is involved in the androgen deprivation therapy-induced acceleration of bone metastasis in castration-insensitive prostate cancer and is inhibited by osteoprotegerin to prevent bone metastasis.

7. endocortical resorption is driven by reduced OPG rather than elevated RANKL expression

8. Diabetes significantly increased OPG and the OPG/TRAIL ratio expression in the aorta, while dyslipidemia was the major determinant of the changes observed in the heart, where it significantly increased OPG and reduced TRAIL expression, thus increasing cardiac OPG/TRAIL ratio.

9. These discoveries strongly suggest that Heparan Sulfate plays an active role in regulating OPG-RANKL interaction and osteoclastogenesis.

10. OPG plays an important role in regulating bone marrow mesenchymal stem cells differentiation and bone marrow adipogenesis.

11. These data suggested that OPG played an important role in maintaining the homeostasis of articular cartilage of femoral head.

12. Data show that p38alpha mitogen-activated protein kinase (MAPK) in paired related homeobox 1 protein (Prx1+) bone marrow-derived mesenchymal stromal cells acts to preserve the bone by sustaining osteoprotegerin (OPG) production.

13. OPG expression in chondrocyte increases bone mass in the proximal metaphysis of tibiae through negative regulation of osteoclast formation.

14. the generation of Rag2GFP+ regulatory T cells is unaltered in Tnfrsf11b(-/-) mice

15. identify osteoprotegerin as a HIF target gene capable of directing osteoblast-mediated osteoclastogenesis to regulate bone homeostasis

16. Osteoprotegerin is increased in metabolic syndrome and promotes adipose tissue proinflammatory changes.

17. Osteoprotegerin inhibits vascular calcification by regulating the procalcific effects of RANKL and Il6 on vascular smooth muscle cells.

18. These results indicate that OPG derived either from the bone marrow or from the vessel wall is sufficient to slow down lesion progression and vascular calcification independent of bone turnover.

19. High concentrations of alendronate decrease the expressions of OPG and RANKL in cultured osteoblasts.

20. In a xenograft model, increased osteoprotegerin expression correlated with a delay to pathologic fracture suggesting a potential role for mTOR inhibitors in the treatment of neuroblastoma bone metastases.

Rabbit Tumor Necrosis Factor Receptor Superfamily, Member 11b (TNFRSF11B) Interaktionspartner

1. The OPG expression levels decreased while those of RANKL and RUNX2 increased during orthodontic tooth movement, which suggested that they play a role in the osteogenesis process and the reconstruction of periodontal tissue.

2. Low-frequency vibration may promote the osteogenic differentiation capability of BMSC probably through regulating the OPG/RANKL mRNA expression.

Pig (Porcine) Tumor Necrosis Factor Receptor Superfamily, Member 11b (TNFRSF11B) Interaktionspartner

1. Regional variation of periosteal activity at the mandibular ramus is regulated by differential expression of osteoprotegerin.