Gene interactions and pathways from curated databases and text-mining

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CDKN1A — E2F2

Pathways - manually collected, often from reviews:

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
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
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
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
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
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
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