Gene interactions and pathways from curated databases and text-mining

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CDKN1A — RB1

Pathways - manually collected, often from reviews:

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Zarrilli et al., Gastroenterology 1999 : Nocodazole treatment of constitutive IGF-II expressing cells stimulated p21 expression in the presence of hyperphosphorylated pRb
Nakanishi et al., Biochem Biophys Res Commun 1999 : These findings suggest that pRb may be dynamically regulated by the relative binding and activities of p21 and Cdks
Turovets et al., Genetika 1999 : Protein p21WAF is transactivated by p53 and is responsible for the cell block in the G1 phase of the damaged cells ; protein pRb is a target for p21WAF which controls the G1-S-phase transition ; and p19ARF protein is responsible for p53 activation in cells with certain anomalies
Liberto et al., Cancer Lett 2000 (Breast Neoplasms) : EGCG induced p21 ( CIP1/WAF1/SDI1 ), inhibited cyclin D1-associated pRB kinase activity, and impaired pRB phosphorylation
Kuhn et al., Biochim Biophys Acta 2002 : However, as experiments in p53 deficient cell lines indicated, the decrease of pRb and E2F-1 is independent of p53 and p21 expression
Huang et al., J Cell Physiol 2004 : Down-regulation of p21 ( WAF1 ) by antisense caused an increase in the phosphorylation and inactivation of pRb
Tsukada et al., J Biochem 2004 (Carcinoma, Hepatocellular...) : These results suggest that the decrease in cyclin A expression and increase in p21 ( Cip1 ) expression through a high-intensity ERK signal by HGF lead to suppression of the phosphorylation of pRb by Cdk2, which contributes to the cell cycle arrest at G1 in HepG2 cells by HGF
Balsitis et al., J Virol 2005 (Hyperplasia...) : E7-induced p21 upregulation was also pRb dependent , and genetic Rb inactivation was sufficient to reproduce this effect ... These data show that E7 upregulates the expression of p53 and p21 via pRb dependent mechanisms distinct from the proposed p19-Mdm2 pathway
Rosato et al., Mol Pharmacol 2006 (Leukemia) : Exposure of U937 cells to a low concentration of LAQ824 ( 30 nM ) resulted in a delayed ( 2 h ) increase in reactive oxygen species ( ROS ), induction of p21 ( WAF1/CIP1 ), pRb dephosphorylation, growth arrest of cells in G ( 0 ) /G ( 1 ) phase, and differentiation
Sawant et al., Toxicology 2007 (Carbon Tetrachloride Poisoning...) : Furthermore, higher TGFbeta1 expression and p21 activation may also contribute to decreased p-pRB in DB rats compared to non-DB rats
Jia et al., J Cell Mol Med 2009 : Overexpression of phosphatase and tensin homologue deleted on chromosome 10 ( PTEN ) in SV SMCs followed by IGF-1 activation significantly decreased the expression of cyclin E and pRb and induced p27 expression in SV SMCs, while, pRb levels were markedly decreased and p27 levels were significantly increased in IMA SMCs. Silencing the PTEN gene by siRNA transfection of IMA SMCs significantly induced the expression of pRb and inhibited p27 expression, while, the expression levels of cyclin E, pRb, p21 and p27 were unaffected by the silencing of PTEN in SV SMCs
Jeong et al., J Cell Biochem 2009 : Quercetin induced p21 CDK inhibitor with a concomitant decrease of phosphorylation of pRb , which inhibits the G ( 1 ) /S cell cycle progression by trapping E2F1
Goldberg et al., Oncogene 1996 (Adenocarcinoma...) : Sulindac and sulindac sulfide decrease the levels of mitotic cyclins, induce the levels of p21WAF-1/cip1 , and reduce the total levels of pRB , with a relative increase in the amount of the underphosphorylated form of pRB in a time- and concentration dependent manner
Tomida et al., Oncogene 1996 : A23187, compared with the other stressors, caused extreme pRb hypophosphorylation, suggesting that p21WAf1 is involved in the regulation of pRb phosphorylation in the stressed cells
Doherty et al., Oncogene 1997 : In cells grown at 32 degrees C, LT expession led to cell proliferation and phosphorylation of pRB in the presence of p21
Hermanns et al., J Virol 1997 : From these data, we conclude that the major effect of AAV2 infection on primary human fibroblasts appears to be upregulation of p21WAF1 gene expression and thus cell cycle arrest by the suppression of pRB family protein phosphorylation
Chelliah et al., Biochem Pharmacol 1997 : The actions of c-myc AS-ODN did not stem from proximal G1 arrest/differentiation or biochemical events, since they were not associated with a reduction in the S-phase cell fraction, p21 ( WAF1/CIP1 ) induction , pRb hypophosphorylation, or alterations in ara-C metabolism