p53 has a direct apoptogenic role at the mitochondria.

By M. Mihara, S. Erster, A. Zaika, O. Petrenko, T. Chittenden, P. Pančoška, U. Moll. Molecules and Cells, 2003

1,879 citations recorded by the source corpus.

Subfields: Biotechnology, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/279f7b0caae82418292c75d51b252d6cbea0f8ee

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Citations in the corpus

Calpain-mediated cleavage of Atg5 switches autophagy to apoptosis (2006, background): “For instance, recent studies demonstrated that a fraction of p53 translocates to mitochondria during stress-induced apoptosis, but not during growth arres”
p53 opens the mitochondrial permeability transition pore to trigger necrosis (2012, methodology): “One of them, called Lp53 (wt p53 fused to the mitochondrial import leader sequence of ornithine transcarbamylase) delivers p53 specifically and exclusively to the mitochondrial matrix, where the leader sequence gets cleaved off (Mihara et al., 2003) (Figure 6A left and Figure S6A).”
Targeted Apoptosis of Senescent Cells Restores Tissue Homeostasis in Response to Chemotoxicity and Aging (2017, background): “Moreover, p53 can induce apoptosis either through transactivating pro-apoptosis genes or in a transcription-independent manner by translocating to the mitochondria (Mihara et al., 2003).”
Mitochondrial outer membrane permeabilization during apoptosis: the innocent bystander scenario (2006, background): “Similar to a BH3-only protein, p53 can function to activate directly BAX, while it also has been described to bind to BCL-xL and BCL-2 similar to a de-repressor BH3-only protein”
The Bcl-2 apoptotic switch in cancer development and therapy (2007, background): “Multiple targets of this transcription factor have been implicated, and it has even been proposed that p53 has a direct apoptogenic role at the mitochondrion by engaging either Bcl-xL and Bcl-2 (Mihara et al., 2003) or Bax (Chipuk et al.”
Extrinsic versus intrinsic apoptosis pathways in anticancer chemotherapy (2006, background): “…of the outer mitochondrial membrane in a transcriptionindependent fashion through direct activation of proapoptotic Bcl-2 proteins Bax or Bak or through binding and inactivating of antiapoptotic Bcl-2 proteins such as Bcl-2 or Bcl-XL (Mihara et al., 2003; Chipuk et al., 2004; Moll et al., 2005).”
Regulating the p53 pathway: in vitro hypotheses, in vivo veritas (2006, background): “p53 might also induce apoptosis through non-transcriptional, cytoplasmic processe”
The BCL-2 Family Reunion (2010, background): “Cytosolic p53 can be sequestered by antiapoptotic BCL-2 proteins, and directly activates BAK and BAX (Chipuk et al., 2004; Leu et al., 2004; Mihara et al., 2003).”
Nutritional evaluation of cookies produced from pigeon pea, cocoyam and sorghum flour blends (2011, background): “It has also been shown to act directly upon mitochondria through a transcription-independent pathway (Mihara et al., 2003; Park et al., 2005).”
Hierarchical regulation of mitochondrion-dependent apoptosis by BCL-2 subfamilies (2006, background): “Notably, p53 is at least 1,000 times less potent than PUMA in inducing mitochondrial permeabilizatio”
The Cell-Cycle Arrest and Apoptotic Functions of p53 in Tumor Initiation and Progression. (2016, background): “A fraction of p53 protein can be detected at the mitochondria following DNA damage, preceding the loss of mitochondrial transmembrane potential and caspase activation (Marchenko et al. 2000; Mihara et al. 2003).”
Role of p53 in Cell Death and Human Cancers (2011, background): “found that, in response to DNA damage, a fraction of p53 is translocated from cell nucleus into mitochondria in cancer cells undergoing apoptosis [68].”
Apoptosis and Molecular Targeting Therapy in Cancer (2014, background): “Synthetic triterpenoids, such as CDDO and CDDOm, sensitize solid tumor cell lines to TRAIL and induce apoptosis as single agents in leukemia cells, through a caspase8-dependent mechanism that remains operative even in chemorefractory cells [235–237].”
Tip60-dependent acetylation of p53 modulates the decision between cell-cycle arrest and apoptosis. (2006, background): “In addition, p53 also transactivatesthemdm2genetoinitiatethep53-Mdm2feedback loop, which is crucial for restraining p53 function during the stress response ( Michael and Oren, 2002; Brooks and Gu, 2006).”
p53 ubiquitination: Mdm2 and beyond. (2006, background): “Moreover, movement of p53 into the cytoplasm may be important for transcription-independent functions of p53 such as interactions with mitochondrial proteins in the apoptosis response (Chipuk et al., 2004; Leu et al., 2004; Mihara et al., 2003).”
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).”