Isolation and properties of Ca2+-transporting glycoprotein and peptide from beef heart mitochondria

Mironova, Galina D.; Sirota, T. V.; Pronevich, L.A.; Trofimenko, Natalia V.; Mironov, Gennadi P.; Grigorjev, Pavel A.; Кондрашова, М. Н.

doi:10.1007/bf00751016

Cited by 34 publications

(9 citation statements)

References 20 publications

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“…Despite the wealth of pharmacologic and electrophysiological data describing the MCU, the molecular identity of the channel is still unknown. Attempts to identify the MCU have led to the isolation of a number of soluble Ca 2+ binding glycoproteins from ox and rat liver and beef heart mitochondria (30–32). Depletion of a 34–40 kDa glycoprotein from the mitochondria IM space reduced Ca 2+ transport that was partially restored upon re-addition of the glycoprotein faction.…”

Section: Mitochondrial Ca2+ Dynamicsmentioning

confidence: 99%

Crosstalk signaling between mitochondrial Ca2+ and ROS

Feissner

Skalska²,

Gaum³

et al. 2009

Front Biosci

375

280

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Mitochondria are central to energy metabolism as the source of much of the cell’s ATP, as well as being a hub for cellular Ca2+ signaling. Mitochondrial Ca2+ is a positive effector of ATP synthesis, yet Ca2+ overload can lead to mitochondrial dysfunction and cell death. Moreover, Ca2+ uptake by mitochondria is involved in shaping cellular Ca2+ dynamics by regulating the concentrations of Ca2+ within microdomains between mitochondria and sarco/endoplasmic reticulum and plasma membrane Ca2+ transporters. Reactive oxygen species (ROS) generated as a consequence of ATP production in the mitochondria are important for cellular signaling, yet contribute to oxidative stress and cellular damage. ROS regulate the activity of redox sensitive enzymes and ion channels within the cell, including Ca2+ channels. For both Ca2+ and ROS, a delicate balance exists between the beneficial and detrimental effects on mitochondria. In this review we bring together current data on mitochondrial Ca2+ uptake, ROS generation, and redox modulation of Ca2+ transport proteins. We present a model for crosstalk between Ca2+ and ROS signaling pathways within mitochondrial microdomains.

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Section: Mitochondrial Ca2+ Dynamicsmentioning

confidence: 99%

Crosstalk signaling between mitochondrial Ca2+ and ROS

Feissner

Skalska²,

Gaum³

et al. 2009

Front Biosci

375

280

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“…Several groups reported the reconstitution of mitochondrial Ca 2+ uptake activity in in vitro systems, yet were unsuccessful in identifying the underlying proteins16,17,18. Since we lack specific, cell-permeant small molecules with which to interrogate these uptake pathways, it is difficult to rigorously evaluate how mitochondrial calcium uptake impacts development and disease15,19 .…”

mentioning

confidence: 99%

MICU1 encodes a mitochondrial EF hand protein required for Ca2+ uptake

Perocchi

Gohil

Girgis

et al. 2010

Nature

797

740

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Mitochondrial calcium uptake plays a central role in cell physiology by stimulating ATP production, shaping cytosolic calcium transients, and regulating cell death. The biophysical properties of mitochondrial calcium uptake have been studied in detail, but the underlying proteins remain elusive. Here, we utilize an integrative strategy to predict human genes involved in mitochondrial calcium entry based on clues from comparative physiology, evolutionary genomics, and organelle proteomics. RNA interference against 13 top candidates highlighted one gene that we now call mitochondrial calcium uptake 1 (MICU1). Silencing MICU1 does not disrupt mitochondrial respiration or membrane potential but abolishes mitochondrial calcium entry in intact and permeabilized cells, and attenuates the metabolic coupling between cytosolic calcium transients and activation of matrix dehydrogenases. MICU1 is associated with the organelle’s inner membrane and has two canonical EF hands that are essential for its activity, suggesting a role in calcium sensing. MICU1 represents the founding member of a set of proteins required for high capacity mitochondrial calcium entry. Its discovery may lead to the complete molecular characterization of mitochondrial calcium uptake pathways, and offers genetic strategies for understanding their contribution to normal physiology and disease.

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“…A protein of 13 14 kD having an isoelectric point of 3.4 was eventu ally purified from the glycoprotein preparation and called calvectin [61]. In 1982, Mironova et al also isolated a Ca binding glycoprotein with a molecular mass of 40 kD from beef heart mitochondria and obtained from it a small hydrophobic peptide that formed ruthenium red sensitive Ca channels when reconstituted in phospholipid black lipid membranes [62]. Saris tested antibodies against the preparation, obtaining in this case only one precipitation band.…”

Section: Mitochondrial Calcium Handlingmentioning

confidence: 99%

A historical review of cellular calcium handling, with emphasis on mitochondria

Saris

Carafoli

2005

Biochemistry (Moscow)

125

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Calcium ions are of central importance in cellular physiology, as they carry the signal activating cells to perform their programmed function. Ca(2+) is particularly suitable for this role because of its chemical properties and because its free concentration gradient between the extra-cellular and the cytosolic concentrations is very high, about four orders of magnitude. The cytosolic concentration of Ca(2+) is regulated by binding and chelation by various substances and by transport across plasma and intracellular membranes. Various channels, transport ATPases, uniporters, and antiporters in the plasma membrane, endoplasmic and sarcoplasmic reticulum, and mitochondria are responsible for the transport of Ca(2+). The regulation of these transport systems is the subject of an increasing number of studies. In this short review, we focus on the mitochondrial transporters, i.e. the calcium uniporter used for Ca(2+) uptake, and the antiporters used for the efflux, i.e. the Ca(2+)/Na(+) antiporter in mitochondria and the plasma membrane of excitable cells, and the Ca(2+)/nH(+) antiporter in liver and some other mitochondrial types. Mitochondria are of special interest in that Ca(2+) stimulates respiration and oxidative phosphorylation to meet the energy needs of activated cells. The studies on Ca(2+) and mitochondria began in the fifties, but interest in mitochondrial Ca(2+) handling faded in the late seventies since it had become apparent that mitochondria in resting cells contain very low Ca(2+). Interest increased again in the nineties also because it was discovered that mitochondria and Ca(2+) had a central role in apoptosis and necrosis. This is of special interest in calcium overload and oxidative stress conditions, when the opening of the mitochondrial permeability transition pore is stimulated.

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Isolation and properties of Ca2+-transporting glycoprotein and peptide from beef heart mitochondria

Cited by 34 publications

References 20 publications

Crosstalk signaling between mitochondrial Ca2+ and ROS

Crosstalk signaling between mitochondrial Ca2+ and ROS

MICU1 encodes a mitochondrial EF hand protein required for Ca2+ uptake

A historical review of cellular calcium handling, with emphasis on mitochondria

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