Functional interaction between Smad, CREB binding protein, and p68 RNA helicase

Cited2 modulates TGF-β-mediated upregulation of MMP9

“…The role for CBP/p300 as an essential co-activator in Smad driven gene expression has been well documented by observations that overexpression of E1A antagonizes the function of CBP/ p300, which leads to attenuation of Smad-driven transcription Nishihara et al, 1998;Pouponnot et al, 1998;Topper et al, 1998). However, coexpression of CBP/p300 has modest effects on Smadmediated transcription based on several promoter/ reporter assays Warner et al, 2004). The effects of p300 on Smad-driven transcription may rely on the recruitment of other co-activators to the Smad/p300 complex (Dennler et al, 2005).…”

Bone morphogenetic protein-2 down-regulates miR-206 expression by blocking its maturation process

“…Drosha-mediated pri-miRNA processing requires the DEAD-box RNA helicases p68 and p72 [28]. It has been reported that p68 interacts with Smad proteins [29]. More recently, the interaction of p68 with Smad2 was shown to promote the processing of pri-miR-21 into pre-miR-21 [20].…”

Dual role of the ddx5/ddx17 RNA helicases in the control of the pro-migratory NFAT5 transcription factor

“…For example, on one hand, as transcriptional coactivators of estrogen receptor alpha, they may contribute to the proliferative effect of estradiol on breast cancer cells (Wortham et al, 2009;Dutertre et al, 2010a) and, as coregulators of betacatenin, they may contribute to the epithelial to mesenchymal transition, which has been associated with breast cancer progression (Yang et al, 2006). On the other hand, as coactivators of p53 and Smad, ddx5/ ddx17 may exert tumor suppressor functions (Warner et al, 2004;Bates et al, 2005). However, oncogenic functions or tumor suppressor roles of ddx5 and ddx17 are still a matter of debate and could be contextdependent (Fuller-Pace and Moore, 2011).…”