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April 1, 2004Molecular Cancer ResearchOpen Access

E2F1 Uses the ATM Signaling Pathway to Induce p53 and Chk2 Phosphorylation and Apoptosis

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Authors

JPJohn T. PowersThe University of Texas at AustinSHSungKi HongThe University of Texas MD Anderson Cancer CenterCMChristopher N. MayhewCincinnati Children's Hospital Medical Center

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Powers et al. (2004) studied this question.

synapsesocial.com/papers/6a740b5f50d38cf5d4cdeeedhttps://doi.org/10.1158/1541-7786.203.2.4
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1E2F1 overexpression in quiescent fibroblasts leads to induction of cellular DNA synthesis and apoptosis1995 · 420 citations
  2. 2Chk2 Is a Tumor Suppressor That Regulates Apoptosis in both an Ataxia Telangiectasia Mutated (ATM)-Dependent and an ATM-Independent Manner2002 · 418 citations
  3. 3Ataxia-telangiectasia-mutated (ATM) and NBS1-dependent Phosphorylation of Chk1 on Ser-317 in Response to Ionizing Radiation2003 · 301 citations
  4. 4Atm Is Dispensable for p53 Apoptosis and Tumor Suppression Triggered by Cell Cycle Dysfunction1999 · 42 citations
  5. 5Chk2/hCds1 functions as a DNA damage checkpoint in G<sub>1</sub>by stabilizing p532000 · 793 citations