Apoptosis: controlled demolition at the cellular level

By Rebecca C. Taylor, Sean P. Cullen, Seamus J. Martin. Nature reviews. Molecular cell biology, 2008

2,697 citations recorded by the source corpus.

Subfields: Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/01b670b5dc91a2b40ae836d852eea45612437290

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Citations in the corpus

Human Coronavirus: Host-Pathogen Interaction. (2019, background): “In the extrinsic pathway, binding of the death ligands [such as FasL and tumor necrosis factor-α (TNF-α)] to the cell surface death receptors (such as Fas and TNF receptor 1) leads to the formation of death-inducing signaling complex and activation of caspase 8, which either directly activates effec”
Radiation-induced cell death mechanisms (2010, background): “The resulting activation of caspase-8/10 leads to cleavage and activation of effector caspase-3, caspase-6, caspase-7, which subsequently cleave cell death substrates [ 65 ].”
Biogenesis of extracellular vesicles (EV): exosomes, microvesicles, retrovirus-like vesicles, and apoptotic bodies (2013, neutral): “During normal development, most apoptotic bodies are phagocytosed by macrophages [94, 97, 101] and are cleared locally.”
Anoikis: an emerging hallmark in health and diseases (2012, background): “Autoactivated caspase-8 then proteolytically activates caspase-3 and -7, culminating in substrate proteolysis and cell death [16,31].”
Focus on Extracellular Vesicles: Introducing the Next Small Big Thing (2016, background): “Apoptotic cells undergo a series of distinct changes, such as chromatin condensation, internucleosomal DNA fragmentation, nuclear rupture, mitochondrial swelling and cytochrome c release, proteolytic cleavage of the cytoskeleton and focal adhesion complexes, PS externalization, PM blebbing, disrupti”
Necroptosis: a regulated inflammatory mode of cell death (2018, background): “It is well known that involvement of receptor like Fas, TNF, and TRAIL can lead to cell death through the recruitment of caspase-8 leading to initiation of extrinsic apoptotic pathway [5].”
Tumour suppression by p53: a role for the DNA damage response? (2009, background): “p53 can also suppress tumour development by initiating apoptosis, the major form of programmed cell death, which involves the ordered and rapid destruction of the cell in the absence of an inflammatory respons”
Essential versus accessory aspects of cell death: recommendations of the NCCD 2015 (2014, background): “Apparently at odds with the role of PARP1 in the execution of parthanatos, both the Parp1 / genotype and the administration of (relatively unselective) PARP inhibitors have been associated with bona fide cytoprotection in rodent models of ischemia/reperfusion injury and retinal degeneration.318–321 ”
Cleavage of DFNA5 by caspase-3 during apoptosis mediates progression to secondary necrotic/pyroptotic cell death (2017, positive): “However, both pathways converge on the activation of the executioner caspases (caspase-3, 6 and 7), which target 4 600 substrates to orchestrate morphological changes associated with apoptosis 14 .”
Caspases in Cell Death, Inflammation, and Gasdermin-Induced Pyroptosis (2020, background): “This in turn proteolytically activates effector caspases, which facilitate the systematic dismantling of cellular components, leading to characteristic intracellular changes including DNA degradation, nuclear shrinkage (pyknosis) and fragmentation (karyorrhexis), membrane blebbing, and release of ap”
Caspase 3-mediated stimulation of tumor cell repopulation during cancer radiotherapy (2011, positive): “Therefore, we hypothesized that caspases, the proteases that were involved in both the initiation and the execution of programmed cell death 11 , might be involved in regulating the growth-promoting properties of dying cells.”
Lysosomal membrane permeabilization in cell death (2008, background): “Caspases can be activated after MOMP or independently of MOMP (Taylor et al., 2008).”
Caspase-8 induces cleavage of gasdermin D to elicit pyroptosis during Yersinia infection (2018, background): “the shedding of apoptotic bodies and the retention of membrane integrity during cell death to promote efferocytosis over secondary necrosis and the release of cytosolic contents (28).”
The flavonoid quercetin in disease prevention and therapy: facts and fancies. (2012, background): “In this case, Bcl-2 family members play a key role including factors possessing proapoptotic (Bax, Bak, PUMA, NOXA, Bim, Bid) or anti-apoptotic activities (Bcl-2, Mcl-1, Bcl-xL, Bfl-1/A1) [52].”
Apoptotic caspases prevent the induction of type I interferons by mitochondrial DNA (2014, background): “One of the best-described mechanisms of programmed cell death is apoptosis, which is mediated through the activation of members of the caspase family of proteases (Fuchs and Steller, 2011; Kumar, 2007; Taylor et al., 2008).”