SMAD2

SMAD2

A gene on chromosome 18q21.1 that encodes a SMAD family protein, named for their similarity to the Drosophila gene Mothers Against Decapentaplegic (MAD), which are signal transducers and transcription modulators of multiple signalling pathways. SMAD2 mediates the signal of transforming growth factor (TGF)-beta, and thus regulates multiple cellular processes—e.g., cell proliferation, apoptosis and differentiation. In response to the binding of TGF-beta, SMAD2 is phosphorylated and dissociated from the SMAD anchor for receptor activation (SARA) protein and forms a complex with SMAD4, resulting in transcription regulation.
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It was also found that the phosphorylation level of Smad3 was slightly higher than that of Smad2 after treated with TGF-[[beta].
There are many tumor suppressor genes encoded at this locus (DCC, SMAD4, SMAD2, and CABLES
TGF-[beta] signaling through Smad2 and Smad3 is associated with enhanced chondrogenesis in murine mesenchymal stem cells (Yu and Xing 2006).
Results We found that Lycopus suppressed rhTGF-[beta]1-induced Smad2 and ERK1/2 activation, down-regulated the expression of TGF-[beta]RI, TGF-[beta]RII, Smad4 and Smad7 in SV40 MES13 cells without inhibiting cell viability.
Smad2 is translocated from the cytoplasm to the nucleus when cells are stimulated with TGF-[beta].
On transforming growth factor [beta]/activin receptor activation, SMAD2 and SMAD3 proteins are phosphorylated and heterodimerize with the SMAD4 protein.
Smad2, Smad3, and Smad4 were used as receptors and intracellular signal-transducing proteins by TGF-[beta] to regulate extracellular matrix homeostasis, apoptosis, cell proliferation, and others (Lawrence, 1996; ten Dijke et al.
These data resulted in inhibition of the cell growth of HSC-T6 in a dose-dependent manner and a reduction in TRI, smad2 and smad3 expressed proteins in the presence of PR on TGF-[beta]1-treated HSC-T6 cells, while smad7 levels were downregulated.
Mutations in the tumor suppressors Smad2 and Smad4 inactivate transforming growth factor [beta] signaling by targeting Smads to the ubiquitin-proteasome pathway.
Receptor activation triggers the phosphorylation and activation of its downstream signaling molecules, Smad2 and Smad3.
2007) reported that hypoxia treatment significantly increased phosphorylation of the Smad2 protein with the up-regulation of TGF-[beta]1, VEGF, and HIF-1[alpha] mRNA expression in human hepatic stellate cells.