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

◀ Back to TP53

E2F1 — TP53

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

Yamasaki et al., Biochim Biophys Acta 1999 (Neoplasms) : At sites where E2F-1 contributes mainly to proliferation and p53 levels remain low, loss of E2F-1 expression may lead to tissue atrophy and overexpression may lead to hyperplasia or tumors
Hale et al., J Biol Chem 1999 : Our studies indicate that E2F binding is not essential for activation of the p53 promoter but that ETF is
Bist et al., Biochemistry 2000 : Overexpression of E2F or p53 increased E2F binding to the -148 to -141 bp site, increased FC efflux, and inhibited cell division
García et al., Cell Growth Differ 2000 : Furthermore, we observed an E2F1 dependent increase of p53 protein levels during the process of thymic clonal deletion, which suggests that E2F1 regulates activation induced apoptosis of self-reactive thymocytes by a p53 dependent mechanism
James et al., Prog Cell Cycle Res 2000 : This provides a link between the Rb and p53 pathways and a mechanism whereby inactivation of Rb and release of E2F will lead to the stabilisation and functional activation of p53
Chen et al., Invest Ophthalmol Vis Sci 2000 : Expression of either E2F1 or E2F2 was sufficient to induce the transcription of cyclins ( A2, B1, and E ), as well as p53 and Bax in the lens fibercells
Nip et al., Oncogene 2001 : E2F-1 induces the stabilization of p53 but blocks p53 mediated transactivation ... E2F-1 induces p53 accumulation and E2F-1 and p53 form a physical complex, which affects the ability of E2F-1 to activate transcription ... Radiolabeling pulse/chase analysis demonstrated that E2F-1 caused post-translational stabilization of p53 ... Although E2F-1 caused the stabilization of p53 , E2F-1 expression impaired p53 dependent transactivation
Nip et al., Cell Biochem Biophys 2000 : Enforced expression of E2F-1 led to accumulation of p53 protein ... An E2F-1 mutant that is defective in inducing cell cycle progression also induced p53 , suggesting that p53 was responding directly to E2F, and not to secondary events caused by inappropriate cell cycle progression ( i.e., DNA damage )
Russell et al., Mol Cell Biol 2002 : E2F1 induces the accumulation of p53 in the absence of ARF, and this is associated with the phosphorylation of p53 on several residues
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
Wunderlich et al., Oncogene 2002 : Mdm2 inhibition of p53 induces E2F1 transactivation via p21 ... Using a set of cell lines with differing p53 and Rb status we determined that Mdm2 induction of E2F1 transactivation was p53 dependent , resulting from release of repression by p53 ... While Mdm2 association with p53 was required to increase E2F1 transactivation, Mdm2 mediated degradation of p53 was not ... Consistent with Mdm2 activation of E2F1 via an inhibition of p53 transactivation we demonstrate a concomitant reduction in p21 protein levels with Mdm2 overexpression
Rogoff et al., Mol Cell Biol 2002 : E2F1 induces phosphorylation of p53 that is coincident with p53 accumulation and apoptosis
Berkovich et al., Oncogene 2003 : This is accompanied by an E2F induced increase in p53 phosphorylation
Choi et al., IUBMB Life 2002 : E2F1 activates the human p53 promoter and overcomes the repressive effect of hepatitis B viral X protein ( Hbx ) on the p53 promoter ... E2F1 activated the p53 promoter through E2F1 binding site
Lindström et al., Oncogene 2003 : Myc and E2F1 induce p53 through p14ARF independent mechanisms in human fibroblasts ... Both Myc and E2F1 activation rapidly induced p53 phosphorylation at Ser-15, p53 protein accumulation, and upregulation of the p53 target genes MDM2 and p21 ... Our results indicate that p53 phosphorylation, but not p14ARF, plays a major role for the induction of p53 in response to Myc and E2F1 activation in normal human fibroblasts
Sola et al., J Biol Chem 2003 : Moreover, in the absence of TGF-beta1, UDCA prevented induction of p53 and Bax by overexpression of E2F-1 and p53, respectively ( p < 0.05 )
Powers et al., Mol Cancer Res 2004 : In primary human fibroblasts lacking functional ATM, the ability of E2F1 to induce the phosphorylation of p53 and apoptosis is impaired
Ramalho et al., J Neurochem 2004 : Notably, TUDCA modulated Abeta induced apoptosis, E2F-1 induction , p53 stabilization and Bax expression ... Notably, TUDCA modulated Abeta induced apoptosis, E2F-1 induction , p53 stabilization and Bax expression ... Further, TUDCA protected PC12 cells against p53- and Bax dependent apoptosis induced by E2F-1 and p53 overexpression, respectively
Garcia et al., Mutat Res 2004 (Breast Neoplasms) : These pathways are related, for instance, p73 is also downstream of E2F-1, since E2F-1 induces p73 mediated apoptosis in the absence of p53
Darbinian et al., Anticancer Res 2004 (Glioblastoma...) : However ectopic E2F-1 overexpression activates p53 and inhibits growth
Hershko et al., Cell Death Differ 2005 : However, it is not known how E2F directs p53 activity towards apoptosis rather than growth arrest ... We demonstrate that activation of E2F1 leads to phosphorylation of p53 on serine 46 and this modification is important for E2F1-p53 cooperation in apoptosis
Fogal et al., EMBO J 2005 : E2F1 binds residues 347-370 of p53 and enhances nuclear retention of Ser315 phosphorylated p53 ... This regulation of p53 by E2F1 is cell cycle dependent, as the cellular distribution of Ser315 phosphorylated p53 is associated with the periodic expression of E2F and cyclin A throughout the cell cycle ... This is the first demonstration that the activities of p53 are regulated during the cell cycle by E2F/p53 interactions and that phosphorylation of p53 at Ser315 is required for this regulation
Hallstrom et al., Genes Dev 2006 : Cells depleted of Jab1 are deficient for both E2F1 induced apoptosis and induction of p53 accumulation
Ruiz et al., Cell cycle (Georgetown, Tex.) 2006 (Carcinoma, Squamous Cell...) : In particular, we characterized the aberrant p53 activation mediated by E2F/p19(ARF) and other transduction pathways
Lara et al., Mol Carcinog 2007 (Carcinoma, Squamous Cell...) : Detailed biochemical analyses have indicated that, in the absence of pRb, multiple pathways, including the aberrant p53 activation mediated by E2F/p19(ARF) , are activated leading to increased tumor apoptosis
Rizos et al., Cell cycle (Georgetown, Tex.) 2007 (Genetic Predisposition to Disease) : p14ARF regulates E2F-1 ubiquitination and degradation via a p53 dependent mechanism
Danielian et al., Oncogene 2008 : E2f3 mutant mice typically die around birth and E2f3-deficient cells have a proliferation defect that correlates with impaired E2f target gene activation and also induction of p19(Arf) and p53
Ye et al., Zhonghua Yu Fang Yi Xue Za Zhi 2008 (Mechanotransduction, Cellular) : And p53 could regulate p21 expression positively, but not E2F-1
Zhang et al., J Cell Biochem 2010 : In turn, ARF may target E2F for its degradation via a p53 dependent mechanism
Guo et al., Mol Immunol 2010 (Burkitt Lymphoma) : Analysis of the expression pattern of a key set of cell cycle regulators revealed that the expression of Zta and Rta substantially interfered with the cell cycle regulatory machinery in Raji cells, strongly inhibiting the expression of Rb and p53 and inducing the expression of E2F1
Lin et al., PloS one 2011 : H-eag1antisense antagonized the growth stimulating effects and the upregulation of h-eag1 expression in SHSY5Y cells, induced by knockdown of miR-34, E2F1 overexpression, or inhibition of p53 activity ... H-eag1antisense antagonized the growth stimulating effects and the upregulation of h-eag1 expression in SHSY5Y cells, induced by knockdown of miR-34, E2F1 overexpression, or inhibition of p53 activity
Kanaan et al., Hum Mutat 2012 (Colitis, Ulcerative...) : Using two human colon cancer cell lines ( HT-29 and HCT-116 ), E2F1 , an upstream regulator of TP53 , was downregulated in both cell lines transfected with let-7e ( P < 0.05 ) as well as in HCT-116 cells transfected with miR-17 ( P < 0.05 ) ... Using two human colon cancer cell lines ( HT-29 and HCT-116 ), E2F1 , an upstream regulator of TP53 , was downregulated in both cell lines transfected with let-7e ( P < 0.05 ) as well as in HCT-116 cells transfected with miR-17 ( P < 0.05 )
Hiebert et al., Mol Cell Biol 1995 : E2F-1:DP-1 induces p53 and overrides survival factors to trigger apoptosis ... In the absence of IL-3, E2F-1 alone was sufficient to induce apoptosis, and p53 levels were diminished ... In the presence of IL-3, levels of endogenous wild-type p53 increased in response to E2F-1 , and coexpression of DP-1 further augmented p53 levels
O'Connor et al., EMBO J 1995 : The expression of wild-type p53 can inhibit the transcriptional activity of E2F , and the expression of both E2F1 and DP1 can also downregulate p53 dependent transcription ... The transcriptional activity of p53 is known to be inhibited by the direct binding of mdm2, but we demonstrate here that both E2F1 and DP1 can inhibit p53 transcriptional activity independently of mdm2
Nip et al., Mol Cell Biol 1997 : Although E2F-1 alone induces moderate levels of p53 and treatment with drugs markedly increased p53, the deleterious effects of etoposide in E2F-1 overexpressing cells were independent of p53 accumulation
Fan et al., Oncogene 1997 (Cell Transformation, Viral...) : In addition, in VA13 cells, induction of E2F97 resulted in down-regulation of the tumor suppressor protein p53
Hunt et al., Cancer Res 1997 (Breast Neoplasms...) : Adenovirus mediated overexpression of the transcription factor E2F-1 induces apoptosis in human breast and ovarian carcinoma cell lines and does not require p53
Kowalik et al., Cell Growth Differ 1998 : Although this could represent a response to aberrant cell cycle progression, we show that only E2F1 induces apoptosis and that this coincides with an ability of E2F1 to induce accumulation of p53 protein ... We also find that coexpression of Mdm2, which is known to regulate p53 activity, blocks the E2F1 mediated induction of apoptosis and also blocks the E2F1 mediated accumulation of p53
Frank et al., Clin Cancer Res 1998 (Carcinoma, Squamous Cell...) : Ample data exist contending that wild-type p53 and E2F-1 cooperate to mediate apoptosis, that E2F-1 mediated apoptosis is p53 dependent in some situations, and that E2F-1 can induce accumulation of p53 in mammalian cells