Results 261 to 270 of about 667,052 (292)

Dependence of Na+Ca2+ exchange and Ca2+Ca2+ exchange on monovalent cations

Biochimica et Biophysica Acta (BBA) - Biomembranes, 1983
Two mechanisms of passive Ca2+ transport, Na+-Ca2+ exchange and Ca2+-Ca2+ exchange, were studied using highly-purified dog heart sarcolemmal vesicles. About 80% of the Ca2+ accumulated by Na+-Ca2+ exchange or Ca2+-Ca2+ exchange could be released as free Ca2+, while up to 20% was probably bound.
R F, Ledvora, C, Hegyvary
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Ca2+ Signaling and Intracellular Ca2+ Binding Proteins

Journal of Biochemistry, 1996
Changes in cytosolic Ca2+ concentrations evoke a wide range of cellular responses and intracellular Ca(2+)-binding proteins are the key molecules to transduce Ca2+ signaling via enzymatic reactions or modulation of protein/protein interations (Fig.1).
I, Niki, H, Yokokura, T, Sudo, M, Kato, H, Hidaka   +4 more
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Inhibition of erythrocyte Ca2+-PUMP BY Ca2+ antagonists

Biochemical Pharmacology, 1990
Inside-out vesicularized membrane fragments from human erythrocytes were prepared to study the effects of various Ca2+ channel entry blockers of plasma membrane Ca2+ transport and (Ca2+ + Mg2+)-ATPase activity concomitantly. Verapamil and diltiazem (0.01 to 5 mM) inhibited both (Ca2+ + Mg2+)-ATPase activity and initial rates of 45Ca2+ net uptake ...
B U, Raess, D M, Record
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L-type Ca2+ channels in Ca2+ channelopathies

Biochemical and Biophysical Research Communications, 2004
Voltage-gated L-type Ca2+ channels (LTCCs) mediate depolarization-induced Ca2+ entry in electrically excitable cells, including muscle cells, neurons, and endocrine and sensory cells. In this review we summarize the role of LTCCs for human diseases caused by genetic Ca2+ channel defects (channelopathies).
Jörg, Striessnig, Jean-Charles, Hoda, Alexandra, Koschak, Francesca, Zaghetto, Carmen, Müllner, Martina J, Sinnegger-Brauns, Claudia, Wild, Katrin, Watschinger, Alexander, Trockenbacher, Gilda, Pelster   +9 more
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Ca2+ Pumps and Ca2+ Antiporters in Plant Development

2010
Calcium (Ca2+) efflux transporters remove Ca2+ from the cytosol of the cell either by transporting it out of the cell across the plasma membrane or into internal organelles. These transporters, which include Ca2+-ATPases and Ca2+/H+ antiporters, have a critical role in preventing Ca2+ toxicity, maintaining cytosolic Ca2+ at a low resting level, and ...
J. K. Pittman, M.C. Bonza, M.I. De Michelis   +2 more
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Ca2+-stimulated ATPase: inactivation by Ca2+ and mechanism

Molecular and Cellular Biochemistry, 1982
The preincubation of the rat blood cell membranes in the presence of low Ca2+ levels causes an irreversible inhibition of the Ca2+-stimulated ATPase activity. The inactivation is dependent on the Ca2+ concentration and the apparent Ki is identical to the Ca2+ concentration needed to reach the half-maximal activity of the enzyme.
C H, Pedemonte, H F, Balegno
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Ca2+ in the heart

Journal of Molecular and Cellular Cardiology, 1987
Ca research in the heart was historically surveyed. First, reference was made to the development of the concept involving Ca2+ in the contraction of skeletal muscle. This was followed by an overview of studies on Ca regulation in cardiac muscle. Emphasis was laid on the fact that the "Ca era" today originated from Ca research in muscle initiated by ...
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Regulation of Ca2+ fluxes in rat liver mitochondria by Ca2+. Effects on Ca2+ distribution

Journal of Bioenergetics and Biomembranes, 1990
Rat liver mitochondria are able to temporarily lower the steady-state concentration of external Ca2+ after having accumulated a pulse of added Ca2+. This has been attributed to inhibition of a putative delta psi-modulated efflux pathway [Bernardi, P. (1984) Biochim. Biophys. Acta 766, 277-282].
N E, Saris, H, Kröner
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