Mitochondria and neuronal survival.
By D. Nicholls, S. Budd. Physiological Reviews, 2000
1,278 citations recorded by the source corpus.
Subfields: Cellular and Molecular Neuroscience, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/6bf6af6c3e8b678c6de6881d726b024dd982f381
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Cellular and Molecular Neuroscience
- Jennifer Lippincott-Schwartz
- S. Gandhi
- Oliver Kann
- M. Beal
- M. Duchen
- R. Kovács
- A. Abramov
- Chunyan Guo
In Molecular Biology
- A. Abramov
- M. Duchen
- S. Gandhi
- Oliver Kann
- R. Kovács
- Roger Tsien
- M. Beal
- Jennifer Lippincott-Schwartz
Citations in the corpus
- Changes in intramitochondrial and cytosolic pH: early events that modulate caspase activation during apoptosis (2000, background): “Recognizing that this H + pump can operate bidirectionall”
- Mitochondrial dynamics regulates migration and invasion of breast cancer cells (2012, background): “The proton ionophore m-chlorophenylhydrazone (CCCP) disperses this proton gradient, thereby uncoupling mitochondrial respiration from ATP synthesis (30).”
- ROS and ROS-Mediated Cellular Signaling (2016, background): “In this review paper, we particularly focus on the pattern of the generation and homeostasis of intracellular ROS, the mechanisms and targets of ROS impacting on cell-signaling proteins (NF-𝜅B, MAPKs, Keap1-Nrf2-ARE, and PI3K-Akt), ion channels and transporters (Ca2+ and mPTP), and modifying…”
- A hyperfused mitochondrial state achieved at G1–S regulates cyclin E buildup and entry into S phase (2009, background): “A predictable decrease in mitochondrial potential after membrane depolarization by the protonophore carbonyl cyanide p-trifluoromethoxyphenylhydrazone (FCCP) (14) is observed.”
- Mitochondria and neuronal activity. (2007, background): “Indeed, mitochondrial ROS formation at its major sites, namely, complex III and complex I, was shown to be decreased or completely inhibited by depolarization of the mitochondrial membrane (158, 206, 216).”
- Disruption of the uncoupling protein-2 gene in mice reveals a role in immunity and reactive oxygen species production (2000, background): “Other reports have described a relationship between mitochondrial uncoupling and production of ROS (ref”
- Mitochondrial α-Ketoglutarate Dehydrogenase Complex Generates Reactive Oxygen Species (2004, background): “Reactive oxygen species (ROS) are thought to contribute to neuronal cell death caused by ischemia, excitotoxicity, and various acute and chronic neurological disorders (Dykens, 1994; Fiskum et al., 1999; Murphy et al., 1999; Fiskum, 2000; Nicholls and Budd, 2000).”
- Mitochondrial transport in neurons: impact on synaptic homeostasis and neurodegeneration (2012, neutral): “jpg"/> Mitochondria are essential for neuronal function and surviva”
- Oxidative stress, mitochondrial damage and neurodegenerative diseases (2013, background): “and Na + -K + -adenosine triphosphate synthases at the plasma membrane and consequently the activity of Na + -coupled plasma membrane transporters [43] .”
- Calcium, ATP, and ROS: a mitochondrial love-hate triangle. (2004, background): “Although the mechanism of DCD is still under debate, it is agreed that the speed of DCD is strongly dependent on the magnitude of [Ca2 ]m AJP-Cell Physiol • VOL 287 • OCTOBER 2004 • www.ajpcell.org by 10.220.32.247 on O ctober 4, 2017 http://ajpcell.physiology.org/ D ow nloaded from accumulation, su”
- PINK1-Associated Parkinson's Disease Is Caused by Neuronal Vulnerability to Calcium-Induced Cell Death (2009, background): “Thus, repetitive rises in cytosolic calcium result in mitochondrial calcium overload, leading to premature opening of the PTP, profound mitochondrial depolarization, and ultimately cell death (Crompton, 1999; Nicholls and Budd, 2000).”
- Mitochondrial membrane potential probes and the proton gradient: a practical usage guide. (2011, background): “Szabadkai G, Duchen MR. Mitochondria: the hub of cellular Ca2+ signaling.”