Caspase-independent cell death

By Guido Kroemer, Seamus J. Martin. Nature Medicine, 2005

850 citations recorded by the source corpus.

Subfields: Epidemiology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/32f636bce3cd66e48d664876f1af17b69e73d42b

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Citations in the corpus

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”
Mitochondrial membrane permeabilization in cell death. (2007, background): “Importantly, cell death that usually occurs with an apoptotic morphology can be shifted to a more necrotic phenotype when caspase activation is inhibited by pharmacological inhibitors or by the elimination of essential caspase activators such as APAF-1 (257, 407).”
Death by design: apoptosis, necrosis and autophagy. (2004, background): “Following an apoptotic stimulus, such as the expression of Bax or treatment with tumor necrosis factor (TNF) or Fas ligand, cells will die even in the presence of non-specific caspase inhibitors such as zVAD-fmk or antiapoptotic molecules like Bcl-XL that prevent caspase activation [2,4].”
Suppression of interleukin-33 bioactivity through proteolysis by apoptotic caspases. (2009, background): “Because caspases do not become activated during necrotic cell death (Kroemer and Martin, 2005), IL-33 is therefore likely to be released from necrotic cells as a full-length active molecule.”
Cancer despite immunosurveillance: immunoselection and immunosubversion (2006, background): “Both pathways culminate in the activation of caspases and caspase-independent cell-death pathway”
Cell death by necrosis: towards a molecular definition. (2007, background): “Preclinical experiments indicate that inhibition of PARP, RIP1, CypD, calpains and cathepsins can inhibit necrotic cell death in vivo in models of acute cell loss [ 18 ].”
Mixed lineage kinase domain-like protein mediates necrosis signaling downstream of RIP3 kinase. (2012, neutral): “As important as caspase activity is for apoptosis, inhibiting caspases often delays but does not prevent cell death in mammalian cells if the death is through the mitochondrial pathway (Kroemer and Martin, 2005).”
Molecular definitions of cell death subroutines: recommendations of the Nomenclature Committee on Cell Death 2012 (2011, background): “Thus, at least in vitro, caspase activation is not a strict requirement for multiple cases of apoptosis (see below).(16,17) Similarly, phosphatidylserine (PS) exposure, which is widely considered as an early marker of apoptotic cell death,(18) reportedly does not occur in autophagy-deficient cells s”