Gene interactions and pathways from curated databases and text-mining

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CDKN1A — E2F1

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

Gartel et al., Oncogene 1998 : In contrast, HBP1 ( HMG-box protein-1 ), a novel retinoblastoma protein binding protein, can repress the p21 promoter and inhibit induction of p21 expression by E2F
Delavaine et al., Oncogene 1999 : The results suggest that p21 may control E2F activity through a pathway that acts independently of pRb
Gartel et al., Oncogene 2000 : A role for E2F1 in Ras activation of p21 ( WAF1/CIP1 ) transcription ... We recently reported that E2F1 could transactivate the p21 promoter via cis acting elements between -119 to +16 bp of the p21 gene ... In contrast, activated Ras was not able to induce the p21 promoter in E2F1-/- fibroblasts, suggesting that E2F1 is required for induction of the p21 promoter by activated Ras ... These data suggest that p53 independent induction of the p21 promoter by activated Ras is mediated at least in part by E2F1
Pruitt et al., J Biol Chem 2000 (Cell Transformation, Neoplastic) : Conversely, stable expression of activated Raf alone caused only a partial up-regulation of p21 and Rb hyperphosphorylation but no activation of E2F-responsive transcription or down-regulation of p27 in RIE-1 cells
Suzuki et al., Int J Cancer 2000 (Mouth Neoplasms...) : TSA enhanced the protein expression of p21 ( WAF1 ), CREB binding protein, cyclinE, cyclin A, Bak and Bax, while it reduced the expression of E2F-1 , E2F-4, HDAC1, p53 and hyperphosphorylated form of Rb
Park et al., Carcinogenesis 2001 (Prostatic Neoplasms) : Although expression of E2F-1 was reduced in three prostate cancer cell lines-PC-3, LNCaP and DU-145-the p21 and p27 protein levels were not increased in all the cell lines treated, suggesting that increase in p21 and p27 protein expression per se is not responsible for lovastatin mediated down-regulation of E2F-1
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
Yamada et al., Proc Natl Acad Sci U S A 2004 : Interestingly, M44KM64E mutant azurin protein failed to elicit inhibition of cell-cycle progression in MCF-7 cells, presumably because of mutation at the retinoblastoma tumor suppressor protein that allows functional E2F formation in MCF-7 cells even in the presence of high intracellular p21 level
Radhakrishnan et al., Oncogene 2004 : To further elucidate the consequences of E2F-1 regulated induction of p21 , we developed cell lines with a tamoxifen dependent form of E2F-1
Harr et al., Molecular cancer 2005 (Carcinoma, Bronchogenic) : E2F1 , an inducer of cell proliferation, directly upregulates p73 and in some systems upregulates p21 directly
Fandy et al., Neoplasia (New York, N.Y.) 2005 (Multiple Myeloma) : SAHA and TSA induced G1 phase cell cycle growth arrest by upregulating p21 ( WAF1 ) and p27 ( Kip1 ) expression and by inhibiting E2F transcriptional activity
Russell et al., Oncogene 2006 (Hyperplasia...) : While Arf inactivation impaired tumor suppression and p21 induction by E2F1 , it did not reduce the level of apoptosis observed in E2F1 transgenic mice
Bock et al., Mol Carcinog 2007 : Relative non-steroidal anti-inflammatory drug ( NSAID ) antiproliferative activity is mediated through p21 induced G1 arrest and E2F inhibition ... Cell cycle analysis showed that celecoxib and sulindac sulfide both induced a 3-fold increase in G ( 1 ) phase distribution, and this correlated with strong induction of p21 ( waf1/cip1 ), inhibition of cyclin D1, and hypophosphorylation of Rb. Celecoxib and sulindac sulfide treatment induced strong downstream inhibition of E2F transactivating activity as determined by a luciferase reporter assay
Chan et al., Mol Cancer Ther 2007 : Up-regulation of p21 by CCT129202 in HCT116 cells led to Rb hypophosphorylation and E2F inhibition, contributing to a decrease in thymidine kinase 1 transcription
Kim et al., Molecular cancer 2010 (Prostatic Neoplasms) : These findings suggest that upregulation of HOXB13 is associated with an additive growth advantage of prostate cancer cells in the absence of or low androgen concentrations, by the regulation of p21 mediated E2F signaling
Latini et al., BMC cancer 2011 (Neoplasms, Experimental...) : These responses were accompanied by the up-regulation of the cell cycle inhibitor p21 WAF1 and reduced ERK phosphorylation and E2F1 expression
Shiyanov et al., Mol Cell Biol 1996 : Since p21 is believed to be a mediator of p53, we speculated that the p21 mediated disruption of the cdk2 containing E2F-p130 complex plays a role in the growth suppression function of p53
Dimri et al., Mol Cell Biol 1996 : We show that p21 inhibits the activity of E2F , an essential growth-stimulatory transcription factor that is negatively regulated by unphosphorylated pRb ... p21 suppressed the activity of E2F-responsive promoters ( dihydrofolate reductase and cdc2 ), but E2F-unresponsive promoters ( c-fos and simian virus 40 early ) were unaffected ... Despite the central role for pRb in regulating E2F, p21 suppressed growth and E2F activity in cells lacking a functional pRb
Li et al., Cancer Res 1997 (Osteosarcoma) : Overexpression of p21waf1 leads to increased inhibition of E2F-1 phosphorylation and sensitivity to anticancer drugs in retinoblastoma negative human sarcoma cells ... Expression of p21waf1 reduced cyclin A-associated kinase activity and, surprisingly, resulted in inhibition of phosphorylation of E2F-1 and increased E2F-1 binding activity
Hiyama et al., Oncogene 1998 (Glioma) : Indeed, E2F induced levels of p21 protein during the G1/ S transition is consistent with the recent findings demonstrating that p21 acts as an assembly factor for kinase active cyclin/cdk/p21 complexes
Halaban et al., Oncogene 1998 : We conclude that neutralization of Rb by E2F1E132, but not the disruption of p16INK4A or p21WAF1/CIP1 , resulted in the accumulation of free E2F and cell cycle progression