Myc suppression of the p21Cip1 Cdk inhibitor influences the outcome of the p53 response to DNA damage

By J. Seoane, Hong-Van Le, J. Massagué. Nature, 2002

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Smad transcription factors. (2005, background): “Down-regulation of c-Myc by TGF relieves p15Ink4b and p21Cip1 from c-Myc-Miz1-mediated repression (Seoane et al. 2001, 2002), enabling activation of these genes by Smad–FoxO complexes bound to an upstream Smad-responsive region (Seoane et al. 2004).”
Tip60-dependent acetylation of p53 modulates the decision between cell-cycle arrest and apoptosis. (2006, background): “Interestingly, upon oncogene activation, c-Myc can influence the outcome of p53-mediated apoptosis by inhibiting p21 expression ( Seoane et al., 2002 ).”
Myc's broad reach. (2008, neutral): “2006) and in tumorigenesis (Seoane et al. 2002; Oskarsson et al. 2006).”
Apoptosis - the p53 network (2003, background): “This interaction effectively represses p21 induction by p53 and other activators (Herold et al., 2002; Seoane et al., 2002).”
ROS and p53: a versatile partnership. (2008, background): “, myc [17], hCAS/CSE1L [18], Hzf [19], and miR-34 [20]), can play a role in selective transactivation of p53 target genes that leads to different cellular outcomes.”
Intrinsic tumour suppression (2004, background): “Although Myc induces apoptosis, it also overrides cell-cycle arres”
Control of apoptosis by p53 (2003, background): “The underlying mechanism for this effect appears to depend on the ability of DNA damage to induce p21, the cyclindependent kinase inhibitor linked to p53-mediated arrest (Seoane et al., 2002).”