Requirement for Caspase-2 in Stress-Induced Apoptosis Before Mitochondrial Permeabilization

By P. Lassus, Ximena Opitz-Araya, Y. Lazebnik. Science, 2002

762 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/51ef4738da1c89e39a298312b8d3484720a07aa9

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Citations in the corpus

A decade of caspases (2003, methodology): “In that respect, caspase-2 was found to cause the release of apoptogenic factors from mitochondria directly, a process which may be mediated in part by caspase-2 cleavage of Bid (Guo et al., 2002; Lassus et al., 2002; Robertson et al., 2002).”
Ways of dying: multiple pathways to apoptosis. (2003, background): “Caspase-2 must act upstream, because it was required for Bax translocation to mitochondria and cytochrome c release (Lassus et al. 2002; Robertson et al. 2002).”
Apoptosis and melanoma chemoresistance (2003, background): “Interestingly, while most studies indicate that caspases act primarily downstream cyt c release, recent evidence supports the requirement of caspase activation upstream of the mitochondria (Guo et al., 2002; Lassus et al., 2002; Robertson et al., 2002).”
The Bcl-2 family: roles in cell survival and oncogenesis (2003, background): “As discussed further elsewhere (Adams, 2003), the initiators implicated in different situations include caspase-1 (Marsden et al., 2002), caspase-2 (Lassus et al., 2002) and caspase-12 (Nakagawa et al., 2000), but none can be the sole initiator because no general defects in apoptosis have appeared…”
Regulation of apoptosis by endoplasmic reticulum pathways (2003, background): “Given that initiator procaspase-2 has been implicated upstream of mitochondrial dysfunction during druginduced apoptosis (Lassus et al., 2002) and that this caspase is located at Golgi and ER membranes in some cell types (Mancini et al., 2000), however, it is conceivable that procaspase-2 is also…”
Cytochrome c binds to inositol (1,4,5) trisphosphate receptors, amplifying calcium-dependent apoptosis (2003, background): “Alternatively, calcium release through InsP 3 R may function as an apoptotic signal amplifier, as suggested for cytochrome c”
Caspases in apoptosis and beyond (2008, background): “Caspase-2 is a long prodomain initiator caspase involved in stress-induced apoptosis (Lassus et al., 2002).”
Translational control in stress and apoptosis (2005, background): “As APAF1 is essential for the progression of the intrinsic apoptotic pathwa”
DNA damage-induced apoptosis (2004, background): “This and subsequent studies showed that, in response to DNA damage, activation of caspase-2 is indeed required before mitochondrial permeabilization and apoptosis can take place (Guo et al., 2002; Lassus et al., 2002; Paroni et al., 2002; Robertson et al., 2002).”
Apoptosis defects and chemotherapy resistance: molecular interaction maps and networks (2004, background): “At least in response to DNA-damaging agents, caspase-2 could play a role upstream of the mitochondria, but the mechanism of its activation remains only partially known (Lassus et al., 2002).”
Caspase-independent cell death (2005, background): “, caspase-8 in the DISC or caspase-2 in the piddosome) may interrupt proapoptotic signaling at an upstream level and hence inhibit cell deat”