Mitochondria as the central control point of apoptosis.

By S. Desagher, J. Martinou. Trends in Cell Biology, 2000

1,987 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/28b356cb11097fa51aefdd772f3811e1b1c31a8f

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Citations in the corpus

Plant mitochondrial pathway leading to programmed cell death (2007, background): “…the intrinsic pathway is evolutionarily conserved in multicellular organisms and is characterised by signal sensing and amplification by mitochondria, mediated by the release of the mitochondrial apoptogenic factors (Desagher and Martinou 2000, Green and Kroemer 2004, Kroemer and Reed 2000).”
Neuronal Cell Death. (2018, positive): “mPTP opening results in 1) depolarization of the inner membrane, causing 2) cessation of ATP production by oxidative phosphorylation and 3) reversal of ATP synthase, hydrolyzing cytosolic ATP entering into the mitochondrial matrix, 4) hence depletion of all cellular ATP, 5) swelling of the mitochond”
Accumulation of mutant huntingtin fragments in aggresome-like inclusion bodies as a result of insufficient protein degradation. (2001, background): “It is well known that mitochondria play a crucial role in the activation of specific apoptotic pathways: under certain conditions they are concentrated in the perinuclear region (Desagher and Martinou, 2000).”
Mitochondrial reactive oxygen species in cell death signaling. (2002, background): “[5] S.”
Mitochondrial fusion and fission in mammals. (2006, background): “In several models of apoptosis, mitochondria fragment at the onset of cell death (Breckenridge et al. 2003, Desagher & Martinou 2000, Frank et al. 2001).”
Breaking the mitochondrial barrier (2001, background): “cgi?l=317">Apaf-1 (apoptotic protease-activating factor 1) and, in the presence of dATP or ATP, recruits and activates procaspase 9 to form a complex called the apoptosom”
Genetic Transformation and Hybridization (2002, neutral): “Normal HeLa cells display worm-like-shaped mitochondria, whereas cells in the process of Bax- or etoposide-induced death have punctiform mitochondria (Desagher and Martinou 2000).”
Heavy metal poisoning: the effects of cadmium on the kidney (2010, background): “…oxygen species (ROS) (Stohs et al. 2000), and mitochondrial disruption (Tang and Shaikh 2001) with release of cytochrome c (Thevenod 2003), leading to caspase activation, causing cell death by apoptosis and necrosis (Desagher and Martinou 2000; Thevenod et al. 2000; Tzirogiannis et al. 2003).”