Apaf-1 is a transcriptional target for E2F and p53

By M. Moroni, E. Hickman, E. L. Denchi, G. Caprara, Elena Colli, F. Cecconi, Heiko Müller, K. Helin. Nature Cell Biology, 2001

640 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/065f2d60fec4bd88b223459cae5999ab92529c1b

How researchers see this paper

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In Molecular Biology

1. K. Helin
2. A. Bracken
3. Diego Pasini
4. Uri Alon
5. Alon Zaslaver
6. S. Mangan
7. Scott W. Lowe
8. Moshe Oren

In Oncology

1. Scott W. Lowe
2. Ricky W. Johnstone
3. K. Helin
4. Moshe Oren
5. J. Campisi
6. Arnold J. Levine

Citations in the corpus

• Apoptosis - the p53 network (2003, background): “This induction by p53 is boosted by E2F1, which induces APAF-1 expression, and activates p53 in an ARF-dependent manner (Moroni et al., 2001).”
• The E2F family: specific functions and overlapping interests (2004, background): “Indeed studies that evaluated the effect of E2F3 overexpression for a prolonged period of time have shown that E2F3 also triggers apoptosis (Moroni et al, 2001; Lazzerini Denchi and Helin, unpublished results).”
• Apoptosis as anticancer mechanism: function and dysfunction of its modulators and targeted therapeutic strategies (2016, background): “, Apaf-1, caspase-6, and Bid) does not efficiently induce apoptosis per se but rather sensitizes cancer cells to the effects of chemotherapeutic agents, improving the apoptotic outcome [124-127].”
• Decision making by p53: life, death and cancer (2003, background): “sites for each of these two transcription factors, as perhaps best illustrated for the Apaf1 gene.(42) This is probably an example of a broader generic mechanism, where the”
• EZH2 is downstream of the pRB‐E2F pathway, essential for proliferation and amplified in cancer (2003, methodology): “Supplementary Material and Methods Plasmids The retroviral vectors pBabeHAER-E2F1, pBabeHAER-E2F2, pBabeHAERE2F3,pBabeHAER-E2F1(E132) and pBabe HAER-E2F1(1-374) have been described previously (Vigo et al. 1999; Moroni et al. 2001).”
• Apoptosis A Link between Cancer Genetics and Chemotherapy (2002, background): “…lead to in- Given the importance of Bcl-2 family members in regulating the intrinsic apoptotic pathway, it is not surprisingcreases in reactive oxygen species (ROS) (Hwang et al., 2001; Moroni et al., 2001; Ryan et al., 2001; Stambolic et that these genes are altered in tumor samples (Table 1).”
• GATHER: a systems approach to interpreting genomic signatures (2006, background): “…assembled a gene expression signature of 231 genes representing E2F activation from standard biochemical experiments (DeGregori et al., 1995; Ohtani et al., 1996; Leone et al., 1998; Moroni et al., 2001) and gene expression microarrays (Ishida et al., 2001; Muller et al., 2001; Black et al., 2003).”
• The coherent feedforward loop serves as a sign-sensitive delay element in transcription networks. (2003, background): “An example in human cells is E2F, which regulates p73 (and indirectly also p53), and both regulate apoptosis genes such as apaf-1.(32) An additional example involves interferon-g induction in T-cells.”
• Cellular mechanisms controlling caspase activation and function. (2013, background): “It is interesting to note that Apaf-1, the adapter protein for caspase-9, can also be transcriptionally regulated by E2F1 and p53 (Fortin et al. 2001; Moroni et al. 2001; Furukawa et al. 2002; Johnson et al. 2007).”