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CDKN1A — SMAD6

Text-mined interactions from Literome

Pardali et al., J Biol Chem 2000 : Role of Smad proteins and transcription factor Sp1 in p21 ( Waf1/Cip1 ) regulation by transforming growth factor-beta
Medrano et al., Oncogene 2003 (Melanoma...) : SKI also facilitates cell-cycle progression by targeting the RB pathway by at least two ways : it directly associates with RB and represses its activity when expressed at high levels, and indirectly, it represses Smad mediated induction of p21 ( Waf-1 ) This results in increased CDK2 activity, RB phosphorylation, and inactivation
Pardali et al., J Cell Physiol 2005 : Based on the previously known ability of c-Myc to block p21 expression and epithelial growth arrest in response to TGF-beta1, we demonstrate that ectopic c-Myc expression can abrogate Smad mediated p21 induction by all TGF-beta and BMP receptors
Kim et al., Arch Pharm Res 2007 : Although it has been demonstrated that p21WAF1/Cip1 could be induced by transforming growth factor-beta1 ( TGF-beta1 ) in a Smad dependent manner, the cross-talk of Smad signaling pathway with other signaling pathways still remains poorly understood
Lo et al., Molecular cancer 2010 : In response to TGFbeta stimulation, LMP1 does not abolish SMAD phosphorylation but inhibits p21 protein expression
Yilmaz et al., EMBO J 2011 (Melanoma, Experimental) : Dlx2 counteracts TGFß induced cell-cycle arrest and apoptosis in mammary epithelial cells by at least two molecular mechanisms : Dlx2 acts as a direct transcriptional repressor of TGFß receptor II ( TGFßRII ) gene expression and reduces canonical, Smad dependent TGFß signalling and expression of the cell-cycle inhibitor p21 ( CIP1 ) and increases expression of the mitogenic transcription factor c-Myc