Cyclophilin D-dependent mitochondrial permeability transition regulates some necrotic but not apoptotic cell death

By T. Nakagawa, S. Shimizu, Tetsuya Watanabe, O. Yamaguchi, K. Otsu, H. Yamagata, H. Inohara, T. Kubo, Y. Tsujimoto. Nature, 2005

1,550 citations recorded by the source corpus.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/3d5ac59514f5111364d0eb453c0d0dca262a3717

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Citations in the corpus

Cyclophilin D deficiency attenuates mitochondrial and neuronal perturbation and ameliorates learning and memory in Alzheimer's disease (2008, positive): “Moreover, recent studies show that a genetic deficiency in CypD protects from Ca 2+ - and oxidative stress–induced cell death and that CypD functions as a necessary component of the mPT”
Mitochondrial reactive oxygen species (ROS) and ROS-induced ROS release. (2014, background): “It can be raised by protective signaling [through preconditioning (218), cyclosporin A (180, 218), sanglofehrin (89), acidosis (47), cyclophilin D acetylation or its knockout (26, 34, 313, 387)] shown by a green dotted line.”
Calcium and apoptosis: ER-mitochondria Ca2+ transfer in the control of apoptosis (2008, background): “The availability of chemical mPTP inhibitors such as cyclosporine A and related compounds lacking the cytosolic inhibitory effect on calcineurin, as well as the development of cyclophilin D knockout mouse will help to clarify the role of mPTP in physiological and pathological condition and identify ”
Cellular and molecular mechanisms of mitochondrial function (2012, background): “60,61 Protection against a variety of pathologies has now been shown in the CypD knockout, including a reduction in stroke damage, and protection from experimental allergic encephalopathy.”
SIRT5 Deacetylates Carbamoyl Phosphate Synthetase 1 and Regulates the Urea Cycle (2009, positive): “Primary cultured hepatocytes were isolated from SIRT5 KO mice and their control littermates at 3-4 months of age using the retrograde two-step collagenase perfusion technique (Nakagawa et al., 2005).”
Necrotic death as a cell fate. (2006, background): “In CypD-deficient cells, cytochrome c release and caspase activation occur normally following apoptotic stimuli TNF , staurosporine, etoposide, and activation of proapoptotic Bcl-2 family members Bax, Bak, and tBid (Baines et al. 2005; Basso et al. 2005; Nakagawa et al. 2005; Schinzel et al. 2005).”
Cell death by necrosis: towards a molecular definition. (2007, positive): “In addition, CypD-deficient mice are resistant tocardiac injury by ischemia‐reperfusion [ 40 ,41] and focal cerebral ischemia [42].”
Caspase-independent cell death (2005, background): “In some modalities of pathogenic cell death, cyclophilin D–dependent mitochondrial permeability transition determines lethal MOM”
Superoxide Flashes in Single Mitochondria (2008, neutral): “Given significant limitations inherent in pharmacological manipulation of mPTP activity, we also determined the effect of RNA interference (siRNA) knockdown of cyclophilin D, a critical component of the mPTP (Baines et al., 2005; Basso et al., 2005; Nakagawa et al., 2005; Schinzel et al., 2005).”