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Sci. STKE, 13 January 2004
Vol. 2004, Issue 215, p. re1
[DOI: 10.1126/stke.2152004re1]
REVIEWS
Flirting in Little Space: The ER/Mitochondria Ca2+ Liaison
Rosario Rizzuto1,
Michael R. Duchen2, and
Tullio Pozzan3,4*
1Department of Experimental and Diagnostic Medicine, Section of General Pathology, University of Ferrara, Italy. 2Department of Physiology, University College London, UK. 3Department of Biomedical Sciences and CNR Institute of Neurosciences, University of Padua, Italy. 4Venetian Institute of Molecular Medicine, Padua, Italy.
Gloss: This STKE Review, with 3 figures and 96 references, concerns the relation between mitochondria and intracellular Ca2+ signals. It has become increasingly apparent that a reciprocal relation exists between the mitochondria and the endoplasmic reticulum (ER) with regard to Ca2+ signaling. Physiological Ca2+ signals may affect mitochondrial function by stimulating key metabolic enzymes and, under some conditions, may lead to programmed cell death (apoptosis) following the release of mitochondrial proteins. Mitochondria in turn may affect Ca2+ release from the ER, thereby shaping the intracellular Ca2+ signal. Interactions between mitochondria and the ER are critically dependent on the localization of mitochondria within the cell and appear to involve the juxtaposition of mitochondria to "hotspots," microdomains of elevated Ca2+ concentration around the mouths of ER Ca2+ release sites. The molecular mechanisms that define the organization of mitochondria with regard to the ER, and the extent to which mitochondrial function varies among different cell types, are open questions whose answers remain to be determined.
Rapid Procoagulant Phosphatidylserine Exposure Relies on High Cytosolic Calcium Rather Than on Mitochondrial Depolarization.
A. Arachiche, D. Kerbiriou-Nabias, I. Garcin, T. Letellier, and J. Dachary-Prigent (2009)
Arterioscler Thromb Vasc Biol
29, 1883-1889
|Abstract »|Full Text »|PDF »
Mitochondrial degeneration and not apoptosis is the primary cause of embryonic lethality in ceramide transfer protein mutant mice.
X. Wang, R. P. Rao, T. Kosakowska-Cholody, M. A. Masood, E. Southon, H. Zhang, C. Berthet, K. Nagashim, T. K. Veenstra, L. Tessarollo, et al. (2009)
J. Cell Biol.
184, 143-158
|Abstract »|Full Text »|PDF »
Purinergic Control of T Cell Activation by ATP Released Through Pannexin-1 Hemichannels.
U. Schenk, A. M. Westendorf, E. Radaelli, A. Casati, M. Ferro, M. Fumagalli, C. Verderio, J. Buer, E. Scanziani, and F. Grassi (2008)
Science Signaling
1, ra6
|Abstract »|Full Text »|PDF »
Phosphorylation of inositol 1,4,5-trisphosphate receptors by protein kinase B/Akt inhibits Ca2+ release and apoptosis.
T. Szado, V. Vanderheyden, J. B. Parys, H. De Smedt, K. Rietdorf, L. Kotelevets, E. Chastre, F. Khan, U. Landegren, O. Soderberg, et al. (2008)
PNAS
105, 2427-2432
|Abstract »|Full Text »|PDF »
The Inositol 1,4,5-Trisphosphate Receptor Is Required to Signal Autophagic Cell Death.
D. Lam, A. Kosta, M.-F. Luciani, and P. Golstein (2008)
Mol. Biol. Cell
19, 691-700
|Abstract »|Full Text »|PDF »
Endoplasmic reticulum remains continuous and undergoes sheet-to-tubule transformation during cell division in mammalian cells.
M. Puhka, H. Vihinen, M. Joensuu, and E. Jokitalo (2007)
J. Cell Biol.
179, 895-909
|Abstract »|Full Text »|PDF »
D. Poburko, C.-H. Liao, V. S. Lemos, E. Lin, Y. Maruyama, W. C. Cole, and C. van Breemen (2007)
Circ. Res.
101, 1030-1038
|Abstract »|Full Text »|PDF »
Endothelial Mitochondria: Contributing to Vascular Function and Disease.
Mitochondrial reactive oxygen species and Ca2+ signaling.
C. Camello-Almaraz, P. J. Gomez-Pinilla, M. J. Pozo, and P. J. Camello (2006)
Am J Physiol Cell Physiol
291, C1082-C1088
|Abstract »|Full Text »|PDF »
Mitochondria at the Synapse.
C. V. Ly and P. Verstreken (2006)
Neuroscientist
12, 291-299
|Abstract »|PDF »
Mitochondrial Buffering of Calcium in the Heart: Potential Mechanism for Linking Cyclic Energetic Cost With Energy Supply?.
P. G. Sullivan, C. W. Balke, and K. A. Esser (2006)
Circ. Res.
99, 109-110
|Full Text »|PDF »
Elevated Cytosolic Na+ Decreases Mitochondrial Ca2+ Uptake During Excitation-Contraction Coupling and Impairs Energetic Adaptation in Cardiac Myocytes.
C. Maack, S. Cortassa, M. A. Aon, A. N. Ganesan, T. Liu, and B. O'Rourke (2006)
Circ. Res.
99, 172-182
|Abstract »|Full Text »|PDF »
An intimate collaboration between peroxisomes and lipid bodies.
D. Binns, T. Januszewski, Y. Chen, J. Hill, V. S. Markin, Y. Zhao, C. Gilpin, K. D. Chapman, R. G.W. Anderson, and J. M. Goodman (2006)
J. Cell Biol.
173, 719-731
|Abstract »|Full Text »|PDF »
Plasma Membrane Localization of Ras Requires Class C Vps Proteins and Functional Mitochondria in Saccharomyces cerevisiae.
