Apoptotic DNA fragmentation.

By S. Nagata. Experimental Cell Research, 2000

964 citations recorded by the source corpus.

Subfields: Immunology, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/c06bb6c1ecab4c2570f5021c2ab16eb02a745bf3

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Citations in the corpus

Prevalence of exposure of heavy metals and their impact on health consequences (2018, background): “Researchers observed that these effects were due to generation of ROS where DNA was observed to be cleaved into internucleosomal fragments.(251) Investigations were also conducted on other nanoparticles which summarizes that the key role player is oxidative stress.”
DNA fragments in the blood plasma of cancer patients: quantitations and evidence for their origin from apoptotic and necrotic cells. (2001, background): “The spectrum of multiples of 180-bp fragments is reminiscent of the oligonucleosomal DNA ladder characteristic for apoptotic cell death when cellular chromatin is degraded by a caspase-activated DNase (35).”
Apoptosis in neurodegenerative disorders (2000, background): “Effector caspases can also be activated in response to mitochondrial changes and cytochrome c release; these caspases can then activate a DNase that cleaves DNA into oligonucleosome-sized fragment”
The biochemistry of apoptosis (2000, background): “In an elegant series of experiments, the groups of Wang and Nagata showed that the DNA ladder nuclease (now known as caspase-activated DNase, or CAD) pre-exists in living cells as an inactive complex with an inhibitory subunit, dubbed ICAD (ref”
Extrinsic versus intrinsic apoptosis pathways in anticancer chemotherapy (2006, neutral): “E-mail: simone.fulda@uniklinik-ulm.de Oncogene (2006) 25, 4798–4811 & 2006 Nature Publishing Group All rights reserved 0950-9232/06 $30.00 www.nature.com/onc ments (Nagata, 2000).”
On the origin, evolution, and nature of programmed cell death: a timeline of four billion years (2002, background): “Some of the caspases, termed effector or executionary caspases, such as caspase 3, 6 and 7, are involved in cell death through their cleavage of numerous nuclear and cytoplasmic proteins, thereby inducing several of the typical features of apoptosis.(19,86) The activation of these effector caspases ”
Caspase‐1‐dependent pore formation during pyroptosis leads to osmotic lysis of infected host macrophages (2006, background): “Salmonella -infected macrophages Degradation of chromosomal DNA is a terminal event in the life of a cell and a hallmark of cell death (Zhang and Xu, 2002).”
Pattern Recognition Receptors and the Host Cell Death Molecular Machinery (2018, background): “Indeed the apoptotic process reduce cell immunogenicity by diverse ways including, (1) preservation of intracellular structures and plasma membrane, thereby blocking the release of DAMPS; (2) reduction of cellular volume, by condensation of the nucleus and shedding of small vesicles, which favors it”