The p53 pathway: positive and negative feedback loops

By S. Harris, Arnold J. Levine. Oncogene, 2005

2,085 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/f21fa906398b6f5af19de70da57b64c3c9a572a4

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Citations in the corpus

Network-based inference of protein activity helps functionalize the genetic landscape of cancer (2016, neutral): “6a) 37 .”
Senescence and aging: Causes, consequences, and therapeutic avenues (2018, background): “Conversely, p53 can regulate expression of ARF through a negative feedback loop, as demonstrated by elevated ARF expression in p53−/− mouse embryonic fibroblasts (Harris and Levine, 2005).”
MEG3 noncoding RNA: a tumor suppressor (2012, background): “Inhibition of MDM2 function plays a major role in p53 stabilization (see review Harris & Levine (2005)).”
p53-deficient cells rely on ATM- and ATR-mediated checkpoint signaling through the p38MAPK/MK2 pathway for survival after DNA damage. (2007, background): “The tumor suppressor protein p53 is a major downstream effector of these DNA-damage kinase pathways (Harris and Levine, 2005).”
Apoptosis as anticancer mechanism: function and dysfunction of its modulators and targeted therapeutic strategies (2016, background): “The p53 oncosuppressor protein is normally kept at low level because subject to negative regulation by MDM2dependent proteasome degradation [132]; in response to genotoxic stress, however, p53 undergoes posttranslational modifications that allow the protein to escape MDM2 control, accumulate, and be”
An integrated view of oxidative stress in aging: basic mechanisms, functional effects, and pathological considerations. (2007, background): “Tumor suppressor p53 is a 53-kD protein that controls cell cycle arrest, cell apoptosis, and senescence (97).”