Live or let die: the cell's response to p53

By Karen H. Vousden, Xin Lu. Nature Reviews. Cancer, 2002

3,519 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/2021e659d8fc698a4d547a579e1af858327ca9c1

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Citations in the corpus

Recent advances in the development of protein–protein interactions modulators: mechanisms and clinical trials (2020, background): “INHIBITORS OF PPIS Inhibitors of MDM2/p53 interaction (small molecules, peptides) The p53 is an important protein that regulates the cell cycle and functions as a tumor suppressor.(65) Studies showed ~50% human cancers have alterations in the p53 gene which results in the inactivation of p53 functio”
The interplay between the glucocorticoid receptor and nuclear factor-kappaB or activator protein-1: molecular mechanisms for gene repression. (2003, background): “Considering the transcription factor p53 as a paradigm for interrelated modifications (562), it will be a real challenge to map all GR, NF- B p65, and AP-1 modifications, as well as to understand their functional interplay in a spatiotemporal context.”
Intrinsically disordered proteins in human diseases: introducing the D2 concept. (2008, background): “The p53 protein is a transcription factor that targets genes involved in cell cycle regulation and apoptosis, among other functions (152).”
DNA damage-induced apoptosis (2004, background): “A detailed account of the role and regulation of p53 in apoptosis is beyond the scope of this paper, but excellent, more extensive reviews are available elsewhere (Shen and White, 2001; Vousden and Lu, 2002).”
Mutant p53: one name, many proteins. (2012, background): “Following activation, wild-type p53 normally functions as a sequence-specific transcription factor to inhibit cell cycle progression, promote senescence, or induce apoptotic cell death (Prives and Hall 1999; Vousden and Lu 2002; Vousden and Prives 2009).”
The Bcl-2 apoptotic switch in cancer development and therapy (2007, background): “The ability of wild-type p53 to elicit apoptosis is thought to be a major component of its tumor suppressor function (Vousden and Lu, 2002).”
TIGAR, a p53-inducible regulator of glycolysis and apoptosis. (2006, background): “The p53 tumor-suppressor protein plays a critical role in responding to cellular stress and inhibiting malignant development (Vousden and Lu, 2002).”
p53-deficient cells rely on ATM- and ATR-mediated checkpoint signaling through the p38MAPK/MK2 pathway for survival after DNA damage. (2007, background): “If the DNA damage is extensive, however, then p53-dependent pathways target the damaged cell for apoptotic cell death through both the intrinsic and extrinsic pathways (Fridman and Lowe, 2003; Vousden and Lu, 2002).”
The MDM2-p53 interaction. (2003, background): “p53 can kill cells via a dual transcription-dependent and -independent function in the nucleus and at the mitochondria (3, 4).”
ER stress triggers apoptosis by activating BH3-only protein Bim. (2007, background): “For example, noxa and puma/bbc3 were discovered as p53-inducible genes (Vousden and Lu, 2002) and are now known to be essential for DNA damage-induced apoptosis (Jeffers et al.”
ROS and p53: a versatile partnership. (2008, background): “Tumor suppressor protein p53 occupies a pivotal position in maintaining genomic integrity [14].”
Modeling the therapeutic efficacy of p53 restoration in tumors. (2006, methodology): “The frequent inactivation of p53 in human tumors (Vogelstein et al., 2000; Vousden and Lu, 2002) suggests that restoring p53 function in tumor cells might be an attractive and tumor cell-specific strategy for treating cancers.”