Oxygen sensing requires mitochondrial ROS but not oxidative phosphorylation.

By J. Brunelle, Eric L. Bell, N. Quesada, K. Vercauteren, V. Tiranti, M. Zeviani, R. Scarpulla, Navdeep S. Chandel. Cell Metabolism, 2005

758 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/ce9499ce38f2b6d8be9de50cb54b12fd12c2ec23

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cancer Research

1. G. Semenza
2. C. V. Dang
3. Navdeep S. Chandel
4. Ralph J. Deberardinis
5. Craig B. Thompson
6. M. V. Vander Heiden
7. Ping Gao
8. P. Schumacker

In Molecular Biology

1. G. Semenza
2. C. V. Dang
3. Navdeep S. Chandel
4. Ralph J. Deberardinis
5. Craig B. Thompson
6. M. V. Vander Heiden
7. Ping Gao
8. P. Schumacker

In Physiology

1. G. Semenza
2. M. C. Simon
3. P. Schumacker
4. R. Guzy
5. C. V. Dang
6. Jung-whan Kim
7. Lucas B. Sullivan
8. Ping Gao

Citations in the corpus

• Oxygen sensing by mitochondria at complex III: the paradox of increased reactive oxygen species during hypoxia (2006, background): “In subsequent studies, we have further confirmed that ρ cells that are free from microbial contamination fail to respond to hypoxia, but are still capable of responding to anoxia (Guzy et al. 2005; Mansfield et al. 2005; Brunelle et al. 2005).”
• The interplay between MYC and HIF in cancer (2008, background): “In hypoxic conditions, decreased molecular oxygen diminishes the activity of PHDs and these are further inhibited by reactive oxygen species (ROS) released from inefficiently respiring mitochondri”
• HIF-1 regulates cytochrome oxidase subunits to optimize efficiency of respiration in hypoxic cells. (2007, positive): “In considering the factors that determine how respiratory chain function is optimized at any given O 2 concentration, we hypothesize that a balance is maintained between transfer of electrons to O 2 at complex IV to form water as opposed to premature electron transfer at complex I or complex III to ”
• HIF-1-mediated expression of pyruvate dehydrogenase kinase: a metabolic switch required for cellular adaptation to hypoxia. (2006, methodology): “This model is compatible with findings that hypoxia-induced mitochondrial ROS is necessary and sufficient for the stabilization of HIF-1 (Brunelle et al., 2005; Guzy et al., 2005; Kaelin, 2005), which would in turn activate PDK1 and thereby attenuate the persistence of potentially lethal ROS.”
• The Impact of Oxidative Stress and Inflammation on RPE Degeneration in Non-neovascular AMD (2017, background): “ROS signal a wide range of cellular responses that protect the RPE, such as feedback regulation after excess metabolism (Brunelle et al., 2005; Guzy et al., 2005), response to hypoxia via HIF-1α (Guzy et al., 2005), regulation of autophagy through ATF4 (Scherz-Shouval et al., 2007), and regulation…”
• The biology of cancer: metabolic reprogramming fuels cell growth and proliferation. (2008, background): “During hypoxia, prolyl hydroxylation is inhibited by a process involving reactive oxygen species (ROS) generated in the mitochondria, resulting in stabilization of the HIF-1a protein and transcriptional activity of the HIF-1 complex (Brunelle et al., 2005; Guzyet al., 2005; Mansfield et al., 2005).”
• Tumor suppressors and cell metabolism: a recipe for cancer growth. (2009, background): “HIF1a accumulation can also result from reactive oxygen species (ROS) generated from mitochondrial OXPHOS, which inhibit prolyl hydroxylase activity to promote HIF1a stabilization (Brunelle et al. 2005; Guzy et al. 2005; Mansfield et al. 2005).”
• Reductive carboxylation supports growth in tumor cells with defective mitochondria (2011, methodology): “Methods Summary WT 143B, CYTB 143B, UOK262, CCL16-B2 and CCL16-NDI1 cells were cultured as describe”
• Mitochondrial dysfunction resulting from loss of cytochrome c impairs cellular oxygen sensing and hypoxic HIF-alpha activation. (2005, positive): “This, along with other emerging genetic models (Brunelle et al., 2005 [this issue of Cell Metabolism]; Guzy et al., 2005 [this issue of Cell Metabolism]), will provide valuable tools for investigating the role of the mitochondria in other hypoxic phenomena.”
• Nox proteins in signal transduction (2009, neutral): “There is evidence to support both mitochondrial [41] and NADPH oxidasederived [42] ROS in oxygen sensing, but overall, the mechanisms are not well understood.”
• Hydrogen peroxide sensing, signaling and regulation of transcription factors (2014, background): “Furthermore, the high levels of mitochondria-derived reactive oxygen species generated by hypoxia were considered to be essential for HIF-1α stabilization and this effect was reversed upon overexpression of either catalase or glutathione peroxidase 1 [134][234][235].”