Caspases 3 and 7: Key Mediators of Mitochondrial Events of Apoptosis

By S. Lakhani, Ali J Masud, K. Kuida, G. Porter, C. Booth, W. Mehal, I. Inayat, R. Flavell. Science, 2006

1,199 citations recorded by the source corpus.

Subfields: Epidemiology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/f0731f095478eb42412fd5f7aa258a3455eb3adf

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Citations in the corpus

Programmed Cell Death in Animal Development and Disease (2011, neutral): “Limiting this type of analysis, however, the inactivation of both of these caspases prevents mitochondrial and death receptormediated apoptosis, and these double-mutant animals die immediately after birth due to defective cardiac development (Lakhani et al., 2006).”
Caspase 3-mediated stimulation of tumor cell repopulation during cancer radiotherapy (2011, neutral): “To examine this hypothesis, we obtained mouse embryonic fibroblast (MEF) cells with genetic deletion of their Caspase 3 gene 12,13 and evaluated the ability of these cells to support the growth of a small number of Fluc-labeled tumor cells.”
Autophagy and apoptosis dysfunction in neurodegenerative disorders. (2014, neutral): “Engaged receptors trimerize, recruit adaptor molecules to their death domains and trigger the activation of caspase- 8, and subsequently caspase-3 and -7 that lead to cell death (Lakhani et al., 2006; Rashedi et al., 2007).”
The Bcl-2 apoptotic switch in cancer development and therapy (2007, background): “Furthermore, only a small proportion of Bax molecules may be required to launch the apoptotic program (Lakhani et al., 2006; Zhu et al., 2006).”
Cytochrome c: functions beyond respiration (2008, background): “In the absence of caspase-3 and caspase-7 , cytochrome c release is totally abolishe”
Synergism of TNF-α and IFN-γ Triggers Inflammatory Cell Death, Tissue Damage, and Mortality in SARS-CoV-2 Infection and Cytokine Shock Syndromes (2020, neutral): “Irf1–/– (Matsuyama et al., 1993), Stat1–/– (Durbin et al., 1996), Ripk3–/– (Newton et al., 2004), Ripk3–/–Fadd–/– (Dillon et al., 2012), Ripk3–/–Casp8–/– (Oberst et al., 2011), Apaf1–/– (JAX, #004373) (Honarpour et al., 2000), Nos2–/– (JAX, #002609) (Laubach et al., 1995), Casp7–/– (Lakhani et al., ”
A guide to cell death pathways (2023, positive): “The embryonic developmental defects seen in Apaf1 -null mice, Casp9 -null mice as well as Casp3 and Casp7 double-null mice demonstrate the functional importance of apoptosis in development 22 .”
Apoptosis and Molecular Targeting Therapy in Cancer (2014, background): “Caspase-3 and caspase-7 may participate in a feedback amplification loop to promote the mitochondrial apoptotic pathway [162].”
Mitochondrial outer membrane permeabilization during apoptosis: the innocent bystander scenario (2006, background): “from the caspase-3 and -7 double-knockout mice, which suggests that caspases may act to induce BAX translocation and cytochrome c release, there is a sustained and clear literature that supports the requirement for cytochrome c and APAF-1 in the activation of caspases.(59,60) Furthermore, numerous r”
Caspase-9, caspase-3 and caspase-7 have distinct roles during intrinsic apoptosis (2013, background): “Caspase-9 has been shown to uncouple the mitochondria and increase ROS production, while cells deficient in caspase-3 or caspase-7 show a delay in the mitochondrial events of intrinsic apoptosis [13,17,20].”
Apoptotic caspases prevent the induction of type I interferons by mitochondrial DNA (2014, methodology): “RESULTS Intrinsic Apoptosis Deficiency Confers Resistance to Viral Infection As mice with genetic deficiencies in the intrinsic pathway of apoptosis die perinatally (Hakem et al., 1998; Kuida et al., 1998; Lakhani et al., 2006; Yoshida et al., 1998), we generated mice with a floxed caspase-9 allele ”
IMMUNE TOLERANCE INDUCTION BY APOPTOTIC CELLS REQUIRES CASPASE-DEPENDENT OXIDATION OF HMGB1 (2008, methodology): “MEFs deficient in caspases 3 and 7 (Casp3 / Casp7 / ) and heterozygous MEFs deficient in caspases 3 and 7 (Casp3+/ Casp7+/ ) were obtained from Richard Flavell at Yale University (Lakhani et al., 2006).”