2006
DOI: 10.4161/cc.5.12.2859
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CDK2 Is Required By MYC to Induce Apoptosis

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Cited by 19 publications
(14 citation statements)
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“…Importantly, CDK2 activation was recently found necessary for Myc-induced apoptosis in murine and human fibroblasts. 24 In good agreement with our findings, this was not the case when the authors induced apoptosis with etoposide instead of Myc overexpression. Although the molecular function of CDK2 in this context remains unclear, this appears to be of outstanding importance as CDC25A was also described as a transcriptional target of Myc and as a key effector of Mycinduced apoptosis.…”
Section: Discussionsupporting
confidence: 91%
“…Importantly, CDK2 activation was recently found necessary for Myc-induced apoptosis in murine and human fibroblasts. 24 In good agreement with our findings, this was not the case when the authors induced apoptosis with etoposide instead of Myc overexpression. Although the molecular function of CDK2 in this context remains unclear, this appears to be of outstanding importance as CDC25A was also described as a transcriptional target of Myc and as a key effector of Mycinduced apoptosis.…”
Section: Discussionsupporting
confidence: 91%
“…Synergy between MYC and Cdk-2 relies in part on Cdk-2-dependent MYC phosphorylation at Ser62 by Cdk-2, a critical MYC residue normally phosphorylated in response to Ras activation (Sears et al 2000;Hydbring et al 2010). The ability of Cdk-2 to dictate the cellular responses to MYC deregulation seems to also be supported by the observation that this kinase is also essential for MYCdependent apoptosis (Deb-Basu et al 2006). …”
Section: Replication Stress and Preneoplasiamentioning
confidence: 97%
“…20 Thus, if active CDKs are required for apoptotic processes, one would expect to find elevated CDK activities under those conditions. Indeed apoptosis induction by a variety of death stimuli correlated in a number of reports with increased CDK activities, [21][22][23][24] and inhibition of these activities by pharmacological compounds or dominant-negative CDK mutants or simply by siRNA-mediated downregulation of their expression impaired or delayed for instance thymocyte apoptosis following IR, dexamethasone, heat shock or etoposide, 23 apoptosis induced by c-myc, 25 proteasome inhibition, 26 TNF and staurosporine 27 as well as camptothecin-induced death of neuronal cells. 28 Although in most cases inhibition of CDK activity prevented several manifestations of apoptotic death, including chromatin condensation and DNA fragmentation, the exact hierarchical point of CDK intervention in these processes remained either unresolved or controversial.…”
Section: P21 Protects Cells From Apoptosis Via Inhibition Of Cdksmentioning
confidence: 98%