Sentence examples for binding to the Smad from inspiring English sources

For example, activation of Xtwn requires Smad3 binding to the Smad binding elements (SBEs); c-myc activation needs Smad4 binding to the Lef/Tcf binding elements 1 (TBE1).

Opposing effects of Smad2 and Smad3 on transcriptional regulation of the goosecoid gene have been ascribed to competition between Smad3 and Smad4 for binding to the Smad binding element adjacent to the FAST2/Smad2 binding site [ 38].

Recent studies have shown that FOXG1 acts as a negative regulator of TGF- β signalling pathway by specifically binding to the Smad MH2 domain and associates with Smad -1, -2, -3 and -4 (Dou et al, 2000; Seoane et al, 2004).

Tgif1 was reported to act as a corepressor by binding to the activated Smad-complex (Smad2 and Smad3 can be bound) [ 70, 80].

In addition, the interaction between Smad2/3 and Smurf ubiquitin ligases can be enhanced by estrogen via Smad binding to the estrogen receptor (ER), causing estrogen-induced Smad degradation and inhibition of TGF-β signaling [ 24].

Following activation, TGF-β receptors are subject to negative regulation by the inhibitory Smads (I-Smad) Smad6 and Smad7, which act by competing for binding to the receptor with the activating Smads (e.g. Smad2, Smad3), and promoting receptor ubiquitination and degradation of type I receptors [ 34].

In addition to competing with R-Smads for binding to the activated type I TGF-β receptor, Smad7 can inhibit TGF-β signaling by recruiting phosphatases to the receptors and by inhibiting Smad binding to DNA [ 3, 4].

Activated BR-Smads bound to the Smad-binding element (SBE) of IL-11 gene promoter and formed complex with ΔFosB/JunD heterodimer via binding to the C-terminal region of JunD.

In neuroepithelial and glioblastoma cells, FoxO was found to bind specifically to the Smad proteins Smad3 and Smad4 to form a transcriptional activator complex that is targeted to a region of the p21cip1 promoter that contains a consensus forkhead binding element as well as a Smad-binding region [ 78].

These factors bind to Smad4 forming a heteromeric Smad complex which translocates to the nucleus and mediates gene transcription by binding to Smad binding elements (SBEs) in the promoters of target genes [4].

Two previous studies have reported the induction of LIF mRNA and/or protein by TGFβ in Schwann cells [ 22] and glioblastoma [ 23] and shown this upregulation to be Smad-dependant by binding to a Smad binding element in LIF promoter.