Mitochondrial p53 activates Bak and causes disruption of a Bak–Mcl1 complex

By J. Leu, P. Dumont, M. Hafey, M. Murphy, D. George. Nature Cell Biology, 2004

798 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/24a82cf9c1a2b697c27d36c223c7ea680521adf7

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Citations in the corpus

• The mitochondrial p53 pathway (2008, positive): “As discussed above, upon stress-induced p53 translocation, mitochondrial p53 directly interacts with and activates pro-apoptotic Bak in many cell types [16].”
• Regulation of reactive oxygen species generation in cell signaling (2011, background): “et al., 2004; 2005; Leu et al., 2004).”
• 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).”
• mir-29 regulates Mcl-1 protein expression and apoptosis (2007, background): “Either depletion of Mcl-1 (Nijhawan et al., 2003) or disruption of the interaction between Mcl-1 and Bak coincides with apoptosis following a cytotoxic stimulus (Leu et al., 2004).”
• Targeting p53 pathways: mechanisms, structures and advances in therapy (2023, background): “37,72 In addition, p53-driven miR34a expression may sensitize cells to apoptotic stimuli by decreasing Bcl-2 levels.”
• 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).”
• Proapoptotic Bak is sequestered by Mcl-1 and Bcl-xL, but not Bcl-2, until displaced by BH3-only proteins. (2005, methodology): “In healthy cells, Bak has also been shown to associate with Mcl-1 in the presence of CHAPS (Cuconati et al. 2003; Leu et al. 2004), an observation we have replicated with Mcl-1 (data not shown) and Bcl-xL (Supplementary Fig.”
• Diagnosing and exploiting cancer's addiction to blocks in apoptosis (2008, background): “For instance, the tumour suppressor p53 , which does not contain a BH3 domain, has been shown to activate BAX and BA”
• Tip60-dependent acetylation of p53 modulates the decision between cell-cycle arrest and apoptosis. (2006, background): “Although the transcription-independent mechanisms for p53-mediated apoptosis have been described (Manfredi, 2003; Chipuk et al., 2004; Leu et al., 2004; Mihara et al., 2003), the principal functions of p53 are mediated through its activity as a DNA-binding transcription factor.Indeed,anumberofgene”
• Apoptosis and Molecular Targeting Therapy in Cancer (2014, background): “As recently summarized, antiapoptotic proteins prevent Bax/Bak activation by sequestering/inhibiting “activator” BH3-only proteins and/or directly inhibiting Bax/Bak activation [33].”
• Targeting mitochondria for cancer therapy (2010, background): “Cytoplasmic p53 has also been suggested to directly activate BAX or to release BAX from inhibitory interactions with anti-apoptotic BCL-2 family members such as BCL-2 itself, BCL-X L and MCL1 (Ref”