Blinded by the Light: The Growing Complexity of p53.

By Karen H. Vousden, Carol Prives. Cell, 2009

3,199 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/018e8ed8c8694d45cfd9ffaf967368345fe22af6

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Citations in the corpus

Programmed cell senescence during mammalian embryonic development. (2013, positive): “Together with senescence, apoptosis is the other main cellular response to damage, and both processes can share common triggers, such as DNA damage or oncogenic stress, and common mediators, most notably p53 (Campisi and d’Adda di Fagagna, 2007; Collado et al., 2007; Vousden and Prives, 2009).”
Non-cell-autonomous tumor suppression by p53 (2013, background): “…and Prives, 2009). p53 binds DNA in a sequence-specific manner and controls the expression of target genes that mediate its diverse effects (Vousden and Prives, 2009). p53 can limit the propagation of premalignant cells by promoting cell-cycle exit or apoptosis, though p53 has other…”
Glutaminase 2, a novel p53 target gene regulating energy metabolism and antioxidant function (2010, background): “In response to stress, p53 selectively regulates the expression of its target genes, which results in cell cycle arrest, apoptosis, or senescence (1, 2).”
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 Cell-Cycle Arrest and Apoptotic Functions of p53 in Tumor Initiation and Progression. (2016, background): “Given the ability of p53 to induce both cellcycle arrest and cell death, the regulation of cell fate decision has been the focus of numerous studies (Vousden and Prives 2009).”
iRegulon: From a Gene List to a Gene Regulatory Network Using Large Motif and Track Collections (2014, background): “…study the gene regulatory network downstream of the p53 tumor suppressor. p53 functions mainly, if not exclusively, as a TF which regulates the expression of hundreds of genes that in turn mediate its biological activities including induction of cell-cycle arrest, senescence and apoptosis [55,56].”
The Achilles’ heel of senescent cells: from transcriptome to senolytic drugs (2015, background): “Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd. p21 and PAI-1, both regulated by p53, are implicated in protection of cancer and other cell types from apoptosis (Gartel & Radhakrishnan, 2005; Kortlever et al., 2006; Schneider et al., 2008; Vousden & Prives, 2009).”