Cytoplasmic functions of the tumour suppressor p53

By Douglas R. Green, Guido Kroemer. Nature, 2009

1,111 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Epidemiology, Oncology

View Paper: https://www.semanticscholar.org/paper/afc759f0d2baa48417d61b9fca12e8afb323af0e

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Citations in the corpus

p53 opens the mitochondrial permeability transition pore to trigger necrosis (2012, background): “In addition, p53 protein can directly promote mitochondrial outer membrane permeabilization (MOMP) to trigger apoptosis by modulating the MOMP governing Bcl-2 family (Green and Kroemer, 2009; Vaseva and Moll, 2009).”
p53 regulates biosynthesis through direct inactivation of glucose-6-phosphate dehydrogenase (2011, neutral): “dtd" [ ]> Cancer cells consume large quantities of glucose and primarily use glycolysis for ATP production, even in the presence of adequate oxyge”
Autophagy and the integrated stress response (2010, positive): “By contrast, the apoptosis-associated activation of proteases such as calpain and caspase-3 may destroy autophagy-specific factors (Atg4D, Beclin 1, or Atg5), thereby suppressing autophagy. leads to increased autophagic targeting of intracellular bacteria (Gutierrez et al., 2004).”
The Tumor Suppressor p53 Limits Ferroptosis by Blocking DPP4 Activity. (2017, positive): “…1692–1704, August 15, 2017 ª 2017 The Autho This is an open access article under the CC BY-NC-ND license (http:// arrest and apoptosis under different stress stimuli through transcriptional and transcription-independent mechanisms (Bieging et al., 2014; Green and Kroemer, 2009; Khoo et al., 2014).”
Crosstalk between apoptosis, necrosis and autophagy. (2013, background): “Overall, these ﬁ ndings indicate that p53 modulates autophagy depending on its subcellular localization [55].”
The p53 protein and its molecular network: modelling a missing link between DNA damage and cell fate. (2014, background): “However, p53 can also play a part outside of the nucleus, notably as a transcription-independent factor involved in apoptosis induction [4,20].”
When NRF2 Talks, Who's Listening? (2010, positive): “p53 regulates a host of processes within the cell, both directly, including the induction of apoptosis through the permeabilization of the outer mitochondrial membrane through interaction with proapoptotic factors (43, 89, 100), and indirectly, through the transcription of genes that effect changes ”
Tumor suppressive functions of p53. (2009, background): “Hence, p53 can be activated in response to DNA damage, oncogene activation, or hypoxia, in which it subsequently orchestrates biological outputs such as apoptosis, cell-cycle arrest, senescence, or modulation of autophagy (Yee and Vousden 2005; Riley et al. 2008; Green and Kroemer 2009).”
Oxidative Stress in Ischemic Brain Damage: Mechanisms of Cell Death and Potential Molecular Targets for Neuroprotection (2011, background): “The p53 gene transcription product, PUMA, is a critical mediator of apoptosis induced by a wide variety of stimuli.”