Organelle-specific initiation of cell death pathways
By K. Ferri, Guido Kroemer. Nature Cell Biology, 2001
1,513 citations recorded by the source corpus.
Subfields: Cell Biology, Epidemiology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/3fb5781c0d1ed072c190dec38baf8be30ec18c44
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In Cell Biology
In Epidemiology
- Guido Kroemer
- R. Kaufman
- Beth Levine
- John Calvin Reed
- Craig B. Thompson
- D. Ron
- Jerry M. Adams
- P. Codogno
In Molecular Biology
- Guido Kroemer
- R. Kaufman
- D. Ron
- Jerry M. Adams
- H. Harding
- John Calvin Reed
- Junying Yuan
- Craig B. Thompson
Citations in the corpus
- Ways of dying: multiple pathways to apoptosis. (2003, background): “Stress to the ER produced by disturbed glycosylation, misfolded proteins, perturbed calcium homeostasis, or glucose deprivation provokes the unfolded protein response, and persistence of this response induces necrosis or apoptosis (Ferri and Kroemer 2001; Kaufman 2002).”
- Endoplasmic Reticulum Stress and the Unfolded Protein Response in Cellular Models of Parkinson's Disease (2002, background): “Such changes can result in rescue from distress or, if the damage is excessive, to cell death (Ferri and Kroemer, 2001).”
- Inhibition of Macroautophagy Triggers Apoptosis (2005, background): “, caspase12 in the endoplasmic reticulum and caspase-2 in the nucleus) (16, 40, 52).”
- Roles of CHOP/GADD153 in endoplasmic reticulum stress (2004, background): “The fourth is apoptosis, which occurs when functions of the ER are severely impaired, to protect the organism by eliminating the damaged cells.(16,17)”
- Structural and functional features and significance of the physical linkage between ER and mitochondria (2006, background): “…and relay points in intracellular Ca2+ signaling, contributing to a spectrum of cellular events ranging from oxidative ATP generation (Hajnoczky et al., 1995; Robb-Gaspers et al., 1998; Jouaville et al., 1999) to apoptotic cell death (Ferri and Kroemer, 2001; Demaurex and Distelhorst, 2003).”
- Bcl-2 family proteins and cancer (2008, background): “…proteins do not appear to insert into lysosomal membranes to an appreciable degree, they have been reported to suppress downstream sequeli of lysosomal enzyme release into the cytosol, particularly as pertains to effects on mitochondria (reviewed by Ferri and Kroemer, 2001; Kroemer et al., 2007).”
- Caspase-dependent immunogenicity of doxorubicin-induced tumor cell death (2005, background): “Although apoptosis is itself nonuniform with respect to the programmed signaling events responsible for cell death (3, 4), it is morphologically defined as a uniform type of cell death accompanied by chromatin condensation (pyknosis) and nuclear fragmentation (karyorhexis) occurring within an intact”
- Lysosomes in cell death (2004, background): “For many years, lysosomes have been thought to be solely involved in necrotic and autophagic cell death, with their role in apoptosis being limited to the digestion of engulfed apoptotic bodies (Ferri and Kroemer, 2001a; Leist and Jaattela, 2001a).”
- Cell death by mitotic catastrophe: a molecular definition (2004, background): “This places Cdk1 upstream of the Bcl-2-regulated mitochondrial changes that define apoptosis (Kroemer and Reed, 2000; Ferri and Kroemer, 2001b).”
- Chaperone-mediated coupling of endoplasmic reticulum and mitochondrial Ca2+ channels (2006, background): “…intertwined endomembrane networks, and their dynamic interaction controls metabolic fl ow, protein transport, intracellular Ca2+ signaling, and cell death (Ferri and Kroemer, 2001; Berridge et al., 2003; Szabadkai and Rizzuto, 2004; Yi et al., 2004; Brough et al., 2005; Levine and Rabouille, 2005).”