2000
DOI: 10.1101/gad.813200
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The Rb/E2F pathway: expanding roles and emerging paradigms

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Cited by 1,059 publications
(931 citation statements)
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References 167 publications
(230 reference statements)
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“…59,60 However, a growing body of evidence supports an alternative view where E2Fs co-operate with Rb in active repressor complexes that regulate cell cycle progression through association with cofactors, such as HDAC or BRG/BRM, and the subsequent modulation of chromatin. 60,61 In support of the latter, interference with E2F-mediated transcriptional regulation through a dominant-negative mutant caused a general derepression of E2F-responsive genes, implying a predominant repressor role of endogenous E2Fs in cultured cells. 25,36,62 Moreover, Myc-induced p53-dependent apoptosis is increased in the epithelium of mice lacking E2F1, 63 while the role of E2F1 in mediating tumorigenesis can be explained by its ability to suppress rather than induce apoptosis.…”
Section: Discussionmentioning
confidence: 88%
“…59,60 However, a growing body of evidence supports an alternative view where E2Fs co-operate with Rb in active repressor complexes that regulate cell cycle progression through association with cofactors, such as HDAC or BRG/BRM, and the subsequent modulation of chromatin. 60,61 In support of the latter, interference with E2F-mediated transcriptional regulation through a dominant-negative mutant caused a general derepression of E2F-responsive genes, implying a predominant repressor role of endogenous E2Fs in cultured cells. 25,36,62 Moreover, Myc-induced p53-dependent apoptosis is increased in the epithelium of mice lacking E2F1, 63 while the role of E2F1 in mediating tumorigenesis can be explained by its ability to suppress rather than induce apoptosis.…”
Section: Discussionmentioning
confidence: 88%
“…In cancer cells, the pRB brakes are often defective, resulting in E2F-dependent G 1 -S gene expression even in the absence of mitogens [14]. This may arise as a result of activating tumourigenic mutations which have been identified in diverse tumours at all levels in the mitogenic signalling pathways from ligands and receptors (eg HER2/ErbB2/neu receptor mutations or HER2 gene amplification) to downstream signalling networks (eg Ras-Raf-MAPK or PI3K-Akt signalling pathways) and also for the cell cycle-regulated genes themselves (eg CYCLIND1 and CDK4 gene amplification) [15][16][17].…”
Section: Introductionmentioning
confidence: 99%
“…This dual function necessitates that E2F-1 activity is tightly regulated during the cell cycle, which is accomplished in a variety of ways. For example, E2F-1 can upregulate its own transcription, its activity is modulated by interacting proteins, protein turnover is tightly controlled and E2F-1 is regulated by post-translational modifications (Dyson, 1998;Harbour and Dean, 2000;.…”
Section: Introductionmentioning
confidence: 99%
“…The inhibition of E2F-1 activity, which occurs as a consequence of this interaction, coincides with the ability of pRb to arrest cells in G1 (Harbour and Dean, 2000). During the cell cycle, as cells progress from the G1 to S phase, the sequential phosphorylation of pRb by cyclin/cyclindependant kinase (Cdk) complexes causes the release of E2F-1 and the activation of genes required for the entry into S phase (Sherr, 2000;Classon and Harlow, 2002;Longworth and Dyson, 2010).…”
Section: Introductionmentioning
confidence: 99%