Apoptosis initiated by Bcl-2-regulated caspase activation independently of the cytochrome c/Apaf-1/caspase-9 apoptosome

By Vanessa S. Marsden, L. O’Connor, L. O’Reilly, J. Silke, D. Metcalf, P. Ekert, David C. S. Huang, F. Cecconi, K. Kuida, K. Tomaselli and 6 more. Nature, 2002

596 citations recorded by the source corpus.

Subfields: Molecular Biology, Nutrition and Dietetics

View Paper: https://www.semanticscholar.org/paper/49ec4b073a4e208821cda3ebb2da8ffda018be68

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Citations in the corpus

Apoptotic Caspases Suppress mtDNA-Induced STING-Mediated Type I IFN Production (2014, unknown): “In contrast, Apaf-1- or caspase-deficient cells exhibit only short-term resistance to apoptotic stimuli and do not retain clonogenic potential (Ekert et al., 2004; Marsden et al., 2002; van Delft et al., 2010).”
The Bcl-2 family: roles in cell survival and oncogenesis (2003, background): “Rather, the Apaf-1/cytochrome c/ caspase-9/caspase-3 apoptosome appears to be an amplifier of caspase activity, and death of some cell types (such as developing neurons), but not others (such as lymphocytes) requires the higher levels of activity it generates (Marsden et al., 2002).”
Toxic proteins released from mitochondria in cell death (2004, background): “…setting that allows the in vivo reconstitution of the haematopoietic system from foetal liver stem cells, Andreas Strasser and his team showed that neither Apaf-1 nor caspase-9 deficiency affected the differentiation, homeostasis and apoptotic responses of lymphocytes (Marsden et al., 2002).”
Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018 (2018, background): “Accordingly, blocking post-mitochondrial caspase activation by genetic means or with specific pharmacological inhibitors, such as to N-benzyloxycarbonyl-Val-Ala-Asp(O-Me) fluoromethylketone (Z-VAD-fmk) and (3S)-5-(2,6-difluorophenoxy)-3-[[(2S)-3-methyl-1-oxo-2-[(2-quinolinylcarbonyl)amino]butyl]amin”
Control of apoptosis by p53 (2003, background): “Conversely, thymocytes lacking Apaf-1 respond normally to irradiation (Marsden et al., 2002).”
Apoptosis - the p53 network (2003, background): “This comparison revealed an impaired response, but neither protection from apoptosis nor normal sensitivity to IR-induced death (Marsden et al., 2002).”
A decade of caspases (2003, background): “…for by caspase-8 (Le et al., 2002); inactivation of caspase-9 may lead to loss of caspase-3 and -6 activation, but not caspase-7 processing (Marsden et al., 2002); caspase-9 can replace caspase-2 (Troy et al., 2001); deletion of caspase-3 and - 9 results in the compensatory activation of…”