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CDKN1A — SMAD1

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
Pouliot et al., J Endocrinol 2002 (Breast Neoplasms) : Role of Smad1 and Smad4 proteins in the induction of p21WAF1,Cip1 during bone morphogenetic protein induced growth arrest in human breast cancer cells ... p21 promoter activity required both Smad1 and Smad4 and was induced by either BMP-2 or constitutively active type I BMP receptors
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
Wu et al., Br J Pharmacol 2008 (Adenocarcinoma...) : Knockdown of BMP receptor II abolished Smad1/5/8 phosphorylation, the induction of p21 ( Waf1/Cip1 ) and p27 ( Kip1 ) and inhibition of cell proliferation induced by MG-132
Wu et al., Biochem Biophys Res Commun 2008 (Adenocarcinoma...) : Knockdown of BMP receptor II by RNA interference abolished Smad1/5/8 phosphorylation, p21 ( Waf1/Cip1 ) induction , and the inhibition of cell proliferation induced by MG-132
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