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| HIDALGO,CECILIA; BULL,RICARDO; MARENGO,JUAN J; PÉREZ,CLAUDIO F; DONOSO,PAULINA. |
| The effects of redox reagents on the activity of the intracellular calcium release channels (ryanodine receptors) of skeletal and cardiac muscle, or brain cortex neurons, was examined. In lipid bilayer experiments, oxidizing agents (2,2'-dithiodipyridine or thimerosal) modified the calcium dependence of all single channels studied. After controlled oxidation channels became active at sub µM calcium concentrations and were not inhibited by increasing the calcium concentration to 0.5 mM. Subsequent reduction reversed these effects. Channels purified from amphibian skeletal muscle exhibited the same behavior, indicating that the SH groups responsible for modifying the calcium dependence belong to the channel protein. Parallel experiments that... |
| Tipo: Journal article |
Palavras-chave: Calcium dependence; Neurons; Redox state; Ryanodine receptors; Sarcoplasmic reticulum; Skeletal and cardiac muscle. |
| Ano: 2000 |
URL: http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602000000200011 |
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| HIDALGO,CECILIA; ARACENA,PAULA; SANCHEZ,GINA; DONOSO,PAULINA. |
| In skeletal and cardiac muscle cells, specific isoforms of the Ryanodine receptor channels mediate Ca2+ release from the sarcoplasmic reticulum. These channels are highly susceptible to redox modifications, which regulate channel activity. In this work, we studied the effects of Ca2+ (endogenous agonist) and Mg2+ (endogenous inhibitor) on the kinetics of Ca2+ release from sarcoplasmic reticulum vesicles isolated from skeletal or cardiac mammalian muscle. Native skeletal vesicles exhibited maximal stimulation of release kinetics by 10-20 µM [Ca2+], whereas in native cardiac vesicles, maximal stimulation of release required only 1 µM [Ca2+]. In 10 µM [Ca2+], free [Mg2+] < 0.1 mM produced marked inhibition of release from skeletal vesicles but free [Mg2+]... |
| Tipo: Journal article |
Palavras-chave: Redox state; Ryanodine receptors; Sarcoplasmic reticulum; Calcium release kinetics; Mg2+ inhibition; S-nitrosoglutathione. |
| Ano: 2002 |
URL: http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602002000200009 |
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| VERKHRATSKY,ALEXEI. |
| The endoplasmic reticulum (ER) is an important organelle involved in various types of signaling in nerve cells. The ER serves as a dynamic Ca2+ pool being thus involved in rapid signaling events associated with cell stimulation by either electrical (action potential) or chemical (neurotransmitters) signals. This function is supported by Ca2+ release channels (InsP3 and ryanodine receptors) and SERCA Ca2+ pumps residing in the endomembrane. In addition the ER provides a specific environment for the posttranslational protein processing and transport of various molecules towards their final destination. In parallel, the ER acts as a "calcium tunnel," which facilitates Ca2+ movements within the cell by avoiding cytoplasmic routes. Finally the ER appears as a... |
| Tipo: Journal article |
Palavras-chave: Calcium signaling; Endoplasmic reticulum; Ryanodine receptors; InsP3 receptors. |
| Ano: 2004 |
URL: http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602004000400027 |
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| FRIEL,DAVID. |
| In neurons, depolarizing stimuli open voltage-gated Ca2+ channels, leading to Ca2+ entry and a rise in the cytoplasmic free Ca2+ concentration ([Ca2+]i). While such [Ca2+]i elevations are initiated by Ca2+ entry, they are also influenced by Ca2+ transporting organelles such as mitochondria and the endoplasmic reticulum (ER). This review summarizes contributions from the ER to depolarization-evoked [Ca2+]i responses in sympathetic neurons. As in other neurons, ER Ca2+ uptake depends on SERCAs, while passive Ca2+ release depends on ryanodine receptors (RyRs). RyRs are Ca2+ permeable channels that open in response to increases in [Ca2+]i, thereby permitting [Ca2+]i elevations to trigger Ca2+ release through Ca2+-induced Ca2+ release (CICR). However, whether... |
| Tipo: Journal article |
Palavras-chave: Dynamics; Sympathetic neurons; Endoplasmic reticulum; Ryanodine receptors. |
| Ano: 2004 |
URL: http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602004000400024 |
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| FARRELL,EMILY F; ANTARAMIAN,ANAID; BENKUSKY,NANCY; ZHU,XINSHENG; RUEDA,ANGÉLICA; GÓMEZ,ANA M; VALDIVIA,HÉCTOR H. |
| Activation of Ca2+ release channels/ryanodine receptors (RyR) by the inward Ca2+ current (I Ca) gives rise to Ca2+-induced Ca2+ release (CICR), the amplifying Ca2+ signaling mechanism that triggers contraction of the heart. CICR, in theory, is a high-gain, self-regenerating process, but an unidentified mechanism stabilizes it in vivo. Sorcin, a 21.6 kDa Ca2+-binding protein, binds to cardiac RyRs with high affinity and completely inhibits channel activity. Sorcin significantly inhibits both the spontaneous activity of RyRs in quiescent cells (visualized as Ca2+ sparks) and the I Ca-triggered activity of RyRs that gives rise to [Ca2+]i transients. Since sorcin decreases the amplitude of the [Ca2+]i transient without affecting the amplitude of I Ca, the... |
| Tipo: Journal article |
Palavras-chave: Sorcin; Ryanodine receptors; CICR; Dihydropyridine receptor; Sarcoplasmic reticulum. |
| Ano: 2004 |
URL: http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602004000400015 |
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