BNIP3 and Genetic Control of Necrosis-Like Cell Death through the Mitochondrial Permeability Transition Pore

By C. V. Velde, J. Cizeau, D. Dubik, J. Alimonti, T. Brown, S. Israels, R. Hakem, A. Greenberg. Molecular and Cellular Biology, 2000

625 citations recorded by the source corpus.

Subfields: Epidemiology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/4feb355910a6276d6bb1a790d1b76315bae25072

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Citations in the corpus

Necrosis: a specific form of programmed cell death? (2003, background): “[110] C.”
Self-eating and self-killing: crosstalk between autophagy and apoptosis (2007, result): “These findings are reminiscent of those obtained for BNIP3, a BH3-only protein induced by hypoxia that causes ΔP m dissipatio”
Response to myocardial ischemia/reperfusion injury involves Bnip3 and autophagy (2007, background): “However, other studies have reported that overexpression of Bnip3 in cell lines did not induce detectable release of cytochrome c from mitochondria and that Bnip3-mediated cell death occurred through a caspase-independent mechanism.(10,11) This variation could be due to the differences in the system”
HIF-1-dependent regulation of hypoxic induction of the cell death factors BNIP3 and NIX in human tumors. (2001, background): “mitochondrial permeability transition pore (20) and may be the pathway mediating hypoxia-induced necrotic cell death in cancer.”
Contrasting Properties of Hypoxia-Inducible Factor 1 (HIF-1) and HIF-2 in von Hippel-Lindau-Associated Renal Cell Carcinoma (2005, background): “BNip3 is a member of the Bcl-2 family of apoptosis-regulating proteins and activates caspase-independent necrosis-like cell death by opening the mitochondrial permeability transition pore ( 43 ).”
Mitophagy: mechanisms, pathophysiological roles, and analysis (2012, background): “In C. elegans , worms that carry the loss-of-function mutation in the insulin-like signaling pathway ( daf-2 ) display extended lifespans and induction of autophagy (Melendez et al. , 2003 ).”
Necrosis, a well-orchestrated form of cell demise: signalling cascades, important mediators and concomitant immune response. (2006, background): “In this respect, it was suggested that Bcl2 might act by binding BNIP3, a cytotoxic Bcl-2 family member [97], causing increased production of ROS and decreased mitochondrial membrane potential, without release of intermembrane space proteins [98,99].”
Regulation of Autophagy by Reactive Oxygen Species (ROS): Implications for Cancer Progression and Treatment (2009, positive): “On overexpression, BNIP3 induces a caspase-independent cell death that requires mitochondrial localization, loss of membrane potential, and increased ROS (113).”
The mitochondrion in apoptosis: how Pandora's box opens (2001, background): “cgi?l=664">BNIP3 , is prevented by cyclosporin A and bongkrekat”