Role for the p53 homologue p73 in E2F-1-induced apoptosis
By M. Irwin, M. Marin, A. Phillips, Ratnam S. Seelan, David I. Smith, Wanguo Liu, E. Flores, K. Tsai, T. Jacks, Karen H. Vousden and 1 more. Nature, 2000
694 citations recorded by the source corpus.
Subfields: Biotechnology, Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/035724c92a0ec13cc3430eff8786c4d52d1c0b32
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Citations in the corpus
- The E2F transcriptional network: old acquaintances with new faces (2005, background): “In cells lacking p53, the p53 family member, p73, has been shown to play a role in E2F-induced cell death (Irwin et al., 2000; Lissy et al., 2000; Stiewe and Putzer, 2000).”
- The E2F family: specific functions and overlapping interests (2004, background): “Among these are ARF, p73, APAF1, Casp3, Casp7 and several members of the BH3-only family (Irwin et al, 2000; Stiewe and Putzer, 2000; Moroni et al, 2001; Müller et al, 2001; Nahle et al, 2002).”
- p73: Friend or foe in tumorigenesis (2002, background): “E2F1 regulates p73 levels directly, by binding to E2F-binding sites within the TAp73 promote”
- Control of apoptosis by p53 (2003, background): “For example, E2F-1 (which activates p53 to promote apoptosis) can induce p73, leading to apoptosis in p53null cells (Irwin et al., 2000; Lissy et al., 2000; Stiewe and Putzer, 2000).”
- Regulation and mechanisms of mammalian double-strand break repair (2003, background): “It is also known that ATM directly phosphorylates the transcription factor E2F1, which results in increased P73 (a P53 analog) expression and apoptosis in the absence of P53 (Irwin et al., 2000; Lin et al., 2001).”