Mitochondrial dysfunction resulting from loss of cytochrome c impairs cellular oxygen sensing and hypoxic HIF-alpha activation.

By Kyle D Mansfield, R. Guzy, Yi Pan, Regina M. Young, T. Cash, P. Schumacker, M. C. Simon. Cell Metabolism, 2005

634 citations recorded by the source corpus.

Subfields: Cancer Research, Genetics, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/2fdbbb2439513d0098d060d77928d08e83eb1a25

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Citations in the corpus

Hypoxia and mitochondrial oxidative metabolism. (2010, background): “On the contrary, experiments carried out on genetic models consisting of either cells lacking cytochrome c or ρ cells both could evidence the essential role of mitochondrial respiration to stabilize HIF-1α [74].”
Regulation of reactive oxygen species generation in cell signaling (2011, background): “Hypoxic HIF-1α activation was also suppressed in cells lacking Cyt c, and exogenous treatment with H2O2 recovered HIF-1α stability (Mansfield et al., 2005).”
HIF-2alpha promotes hypoxic cell proliferation by enhancing c-myc transcriptional activity. (2007, methodology): “Second, to use a defined genetic system that is relatively undifferentiated and unlikely to have the mutational load of a human tumor cell line, we produced embryonic ECs (Mansfield et al., 2005) from day 8.5 embryos harboring targeted deletions of Hif-1a (Carmeliet et al., 1998) or Hif-2a (Comperno”
Oxygen sensing by mitochondria at complex III: the paradox of increased reactive oxygen species during hypoxia (2006, methodology): “To avoid the use of pharmacological agents that might have non-specific effects on the cell, we utilized cells that had been depleted of their mitochondrial DNA (ρ cells; Chandel et al. 1998; Chandel & Schumacker, 1999; Guzy et al. 2005; Mansfield et al. 2005).”
HIF-1 mediates adaptation to hypoxia by actively downregulating mitochondrial oxygen consumption. (2006, background): “Several reports have also suggested a link between altered mitochondrial function in hypoxia and HIF activation (Brunelle et al., 2005; Guzy et al., 2005; Mansfield et al., 2005).”
Reactive Oxygen Species in Inflammation and Tissue Injury (2014, positive): “In p47phox - / - mice, TNFa-induced NF-jB activation and ICAM-1 expression were significantly attenuated as compared with the wild-type mice (117, 432).”
Mitochondrial reactive oxygen species and cancer (2014, background): “Importantly, cells depleted of RISP are incapable of stabilizing HIFα under hypoxia, whereas cells depleted of cytochrome b retain their ability to stabilize HIFα [51-54].”
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].”