Title : Mechanisms involved in suppression of osteoclast supportive activity by transforming growth factor-β1 via the ubiquitin-proteasome system.

Pub. Date : 2022

PMID : 35196318






4 Functional Relationships(s)
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1 The current study investigated the effect of TGF-beta1 on receptor activator of nuclear factor kappa-B ligand (RANKL) expression in stromal cells induced by 1alpha,25(OH)2D3 (D3) and dexamethasone (Dex). Cholecalciferol tumor necrosis factor (ligand) superfamily, member 11 Mus musculus
2 The current study investigated the effect of TGF-beta1 on receptor activator of nuclear factor kappa-B ligand (RANKL) expression in stromal cells induced by 1alpha,25(OH)2D3 (D3) and dexamethasone (Dex). Cholecalciferol tumor necrosis factor (ligand) superfamily, member 11 Mus musculus
3 TGF-beta1 downregulated the expression of RANKL induced by D3 and Dex in mouse bone marrow stromal lineage, ST2 cells. Cholecalciferol tumor necrosis factor (ligand) superfamily, member 11 Mus musculus
4 These results indicated that TGF-beta1 downregulates RANKL expression and the osteoclast-supporting activity of osteoblasts/stromal cells induced by D3 and Dex through the degradation of the RXR-alpha protein mediated by ubiquitin-proteasome system. Cholecalciferol tumor necrosis factor (ligand) superfamily, member 11 Mus musculus