Control of apoptosis by p53
By J. Fridman, Scott W. Lowe. Oncogene, 2003
1,468 citations recorded by the source corpus.
Subfields: Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/ad8d8fcc773687213110f7ead4372ab03ca1d253
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Citations in the corpus
- Crosstalk between apoptosis, necrosis and autophagy. (2013, background): “[112]).”
- 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).”
- Identification of a novel senolytic agent, navitoclax, targeting the Bcl‐2 family of anti‐apoptotic factors (2016, background): “Much like cancer cells, senescent cells are resistant to apoptosis (Wang, 1995; Fridman & Lowe, 2003), potentially protecting them from their own pro-inflammatory secretions, reactive metabolites, and activated DNA damage response.”
- Intrinsic tumour suppression (2004, background): “Suppression of c-Myc-induced apoptosis by Ras signalling through PI(3)K and PKB.”
- Transcription factor YY1: structure, function, and therapeutic implications in cancer biology (2006, background): “Moreover, the same molecular components are targets for oncogenic changes that frequently drive cell proliferation to cooperate with those that uncouple proliferation from apoptosis during transformation and tumorigenesis (Evan and Vousden, 2001; Fridman and Lowe, 2003).”
- The Achilles’ heel of senescent cells: from transcriptome to senolytic drugs (2015, background): “…Center, Audie L. Murphy VA Hospital South Texas Veterans Health Care System, San Antonio, TX, USA 5Department of Biochemistry and Molecular Biology, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA 6Department of Metabolism and Aging, The Scripps Research Institute, Jupiter, FL, USA”