p53 in health and disease
By Karen H. Vousden, David P. Lane. Nature reviews. Molecular cell biology, 2007
2,332 citations recorded by the source corpus.
Subfields: Biotechnology, Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/af77fbadb1348429349230ab80ca3539355a6268
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Citations in the corpus
- MicroRNA and cancer (2012, background): “There are also important transcriptionindependent functions of p53 in the induction of apoptosis and, as discussed above, in regulating the biogenesis of several miRNAs under damage conditions (Suzuki et al., 2009; Vousden and Lane, 2007) (Figure 2C).”
- Molecular mechanisms of cisplatin resistance (2012, background): “Oncogene (2012) 31, 1869–1883; doi:10.1038/onc.2011.384; published online 5 September 2011 Keywords: ATP7B; CTR1; ERCC1; glutathione; metallothioneins; TP53”
- Tumour suppression by p53: a role for the DNA damage response? (2009, background): “jpg" NDATA ITEM> ]> p53 is a short-lived transcription factor that has been most extensively studied in its capacity to mediate innate tumour suppression”
- Linking functional decline of telomeres, mitochondria and stem cells during ageing (2010, neutral): “The cellular consequences of p53 activation include growth arrest and repair or apoptosis and senescence, depending on the degree of activatio”
- Awakening guardian angels: drugging the p53 pathway (2009, background): “MDM2 also inhibits p53 function by modulating its transcriptional activity and by preventing its interaction with the general transcription machiner”
- Regulation of autophagy by cytoplasmic p53 (2008, background): “The most extensively characterized tumour suppressor protein is p53, a master regulator with pleiotropic effects on metabolism, anti-oxidant defence, genomic stability, proliferation, senescence and cell deat”
- Regulation of cell signalling by uPAR (2010, background): “Loss of p53 function is, of course, a frequent event in tumorigenesi”
- Cellular Stress Responses: Cell Survival and Cell Death (2010, background): “Once DSBs are generated, ataxia telangiectasia mutated (ATM) is recruited by the MRE-11-Rad50-NBS1 (MRN) complex to sites of broken DNA and phosphorylates downstream substrates such as checkpoint kinase 2 (Chk2) and p53 [175, 178] (Figure 3). p53 induces transcriptional activation of different funct”
- Blinded by the Light: The Growing Complexity of p53. (2009, background): “…layer specification (Piccolo, 2008). p53 even makes a subtle but important contribution to several aspects of normal growth and development in mice, where the p53 family members p63 and p73 shoulder the bulk of the developmental functions (Aranda-Anzaldo and Dent, 2007; Vousden and Lane, 2007).”
- p53 target genes sestrin1 and sestrin2 connect genotoxic stress and mTOR signaling. (2008, neutral): “In addition to cell proliferation, p53 also inhibits cell growth, a function that is important for preventing the wasteful buildup of proteins and other cellular building blocks during periods of stress (Vousden and Lane, 2007).”
- Acetylation is indispensable for p53 activation. (2008, background): “p53 is regulated by a variety of posttranslational modifications, including phosphorylation, acetylation, methylation, ubiquitination, sumoylation ,and neddylation (Vousden and Lane, 2007; Brooks and Gu, 2006; Berger, 2007).”
- Integrative Transcriptome Analysis Reveals Common Molecular Subclasses of Human Hepatocellular Carcinoma (2009, background): “immunohistochemistry for p53, wherein nuclear accumulation of p53 protein is well known to reflect inactivating p53 mutation (28).”
- Self-eating and self-killing: crosstalk between autophagy and apoptosis (2007, background): “However, accumulating evidence suggests that p53 has a positive role in cell survival in response to physiological (as opposed to genotoxic) stress; for example, by stimulating antioxidant pathway”