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Lyons, "BMP canonical Smad signaling through Smad1 and Smad5 is required for endochondral bone formation," Development, vol.
In PBC&PSC, we observed that aberrant Ca2+ levels could activate RYR2 to facilitate SMAD5 to induce TP53 activated by UBC in the WNT and the MAPK signaling pathways, causing dysregulation of H3F3A.
To date, eight mammalian Smad proteins have been characterized and are grouped into three functional classes: receptor-activated Smads (R-Smads) including Smad1, Smad2, Smad3, Smad5, and Smad8, common mediator Smad (Smad4), and inhibitory Smads (I-Smads) including Smad6 and Smad7.
The results of Blast in GenBank showed that they shared high homologies with SMAD5 (95%), COL6A3 (95%), SLC17A5 (93%), TPM4 (99%) and HMGB1 (98%), respectively.
[43.] Rai D, Kim SW, McKeller MR, Dahia PL, Aguiar RC (2010) Targeting of SMAD5 links microRNA-155 to the TGF-beta pathway and lymphomagenesis.
The primers for SMAD5, ALP, and GAPDH were synthesized by Sangon Biotech, Shanghai, China.
Different ligands can bind to TGF-[sz] receptors on the cell surface, allowing regulatory messages to be transferred into the cell by activating the signaling effectors and the Sma- and Mad-related proteins (Smads) and ultimately interacting with deoxyribonucleic acid.[sup][7] Both Smad2 and Smad3 are activated by TGF-[sz], myostatin, or activin whereas Smad1, Smad5, and Smad8 are activated by bone morphogenetic proteins; the activation of these proteins results in the interaction with Smad4, leading to the modulation of target gene expression.
Smad5 and DPC4 are key molecules in mediating BMP-2-induced osteoblastic differentiation of the pluripotent mesenchymal precursor cell line C2C12.
El receptor de BMP tipo II fosforila al receptor de BMP tipo I, permitiendo a su vez la fosforilacion de Smads (Smad1, Smad5, o Smad8).
Cistanches Herba aqueous extract affecting serum BGP and TRAP and bone marrow Smad1 mRNA, Smad5 mRNA, TGF-beta1 mRNA and TIEG1 mRNA expression levels in osteoporosis disease.
Runx2 is a common target of transforming growth factor betal and bone morphogenetic protein 2, and cooperation between Runx2 and Smad5 induces osteoblast-specific gene expression in the pluripotent mesenchymal precursor cell line C2C12.
Overexpression of Smurf1 negatively regulates mouse embryonic lung branching morphogenesis by specifically reducing Smad1 and Smad5 proteins.