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UCSC Genome Browser Gene Interaction Graph
Gene interactions and pathways from curated databases and text-mining

◀ Back to CDKN1A

CDKN1A — SMAD2

Pathways - manually collected, often from reviews:

  • KEGG Cell cycle: Complex of SMAD2-SMAD3-SMAD4 → CDKN1A (gene expression, expression)

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
Zhang et al., J Neurosurg 2006 (Glioma) : Overall, the expression of the Smad2 and Smad3 proteins was low in the glioma cell lines, the phosphorylation and nuclear translocation of Smad2 and Smad3 were impaired, and the TGFbeta receptor signal did not affect the expression of the SnoN, p21 , p15, cyclin D1, and CDK4 proteins
Kayed et al., Int J Oncol 2006 (Carcinoma, Pancreatic Ductal...) : GPC1 down-regulation resulted in a slightly altered response towards TGF-beta1, activin-A and BMP-2 in terms of growth, p21 induction and Smad2 phosphorylation
Chuang et al., J Cell Biochem 2007 : We concluded that high glucose induced hypertrophy via Sp1-Smad2/3 dependent activation of p21 ( WAF1 ) gene transcription in LLC-PK ( 1 ) cells
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
Moustakas et al., Proc Natl Acad Sci U S A 1998 : Smad3/4 and to a much lesser extent Smad2/4 caused high levels of transcriptional activation of the p21 promoter