Essential regulation of cell bioenergetics by constitutive InsP3 receptor Ca2+ transfer to mitochondria.

By Cé Sar, C. rdenas, Russell A. Miller, Ian Smith, Thi V Bui, J. Molgó, Marioly Mü, H. Vais, K. Cheung, Jun Yang and 5 more. Cell, 2010

1,018 citations recorded by the source corpus.

Subfields: Epidemiology, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/d252766c54257e88ccd3232cd1ebe220a44e64f2

How researchers see this paper

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In Epidemiology

1. Beth Levine
2. Guido Kroemer
3. D. Klionsky
4. N. Mizushima
5. I. Slaninová
6. Douglas R. Green
7. V. Deretic
8. L. Galluzzi

In Molecular Biology

1. Guido Kroemer
2. Beth Levine
3. D. Klionsky
4. Douglas R. Green
5. L. Galluzzi
6. Guillermo Mariño
7. Eric H. Baehrecke
8. V. Deretic

In Physiology

1. Guido Kroemer
2. Beth Levine
3. Katherine R Parzych
4. D. Klionsky
5. Alec C. Kimmelman
6. L. Galluzzi
7. M. Jäättelä
8. Douglas R. Green

Citations in the corpus

• MICU1 is an Essential Gatekeeper for MCU-Mediated Mitochondrial Ca2+ Uptake That Regulates Cell Survival (2012, positive): “Lack of this delivery, as shown here in response to knockdown of MCU, causes bioenergetic stress (Cardenas et al., 2010).”
• Metabolic control of cell death (2014, background): “The release of Ca ions from reticular stores provides an important control on mitochondrial Ca concentrations, which regulate a number of enzymes involved in the TCA cycle and in the electron transport chain (148).”
• Guidelines for the use and interpretation of assays for monitoring autophagy (2012, background): “One example is the chicken lymphoma DT40 cells (see Chicken B-lymphoid DT40 cells below) and their knockout variant for all three inositol 1,4,5-trisphosphate receptor isoforms.(241,772,773) In these cells, no differences in basal levels of LC3-II can be observed up to 4 h after addition of fresh me”
• Role of Mitochondrial Ca2+ in the Regulation of Cellular Energetics (2012, background): “In several cell lines, Cardenas et al showed that inability to release Ca2+ from the endoplasmic reticulum via inositol trisphosphate receptor Ca2+ release channel revealed a phenotype characteristic of an overall compromised mitochondrial function(14).”
• Mitochondrial reactive oxygen species promote production of proinflammatory cytokines and are elevated in TNFR1-associated periodic syndrome (TRAPS) (2011, background): “The endoplasmic reticulum, where mutant TNFR1 resides, can provide signals to activate mitochondrial respiration, including a calcium signal transduced by mitochondrial InsP3 receptors (Cárdenas et al., 2010).”
• Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition) (2012, neutral): “cancer cells in response to this treatment, which leads to cell death.(1244) This effect is tumor specific and different”