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1.

001-es BibID:BIBFORM049809
Első szerző:Csernoch László (élettanász)
Cím:Elementary calcium release events (ECRE) in the presence of the scorpion toxin maurocalcine / L. Csernoch, H. Szappanos, J. Cseri, M. Gönczi, J. Sabatier, X. Altafaj, M. DeWaard, M. Ronjat
Dátum:2004
Tárgyszavak:Orvostudományok Elméleti orvostudományok idézhető absztrakt
Megjelenés:Biophysical Journal. - 86 (2004), p. 579a. -
További szerzők:Szappanos Henrietta (1976-) (biológus, élettanász) Cseri Julianna (1949-2022) (laboratóriumi diagnosztika szakorvos) Gönczi Mónika (1974-) (élettanász) Sabatier, Jean Marc Altafaj, Xavier DeWaard, M. Ronjat, Michel
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2.

001-es BibID:BIBFORM049404
Első szerző:Csernoch László (élettanász)
Cím:Surface charge distribution commands the maurocacline effect on the ryanodine receptor / L. Csernoch, M. Ronjat, J. M. Sabatier, Cs. Szegedi, I. Jóna
Dátum:2004
Megjegyzések:Maurocalcine (MCa) ? isolated from the venom of the Scorpio Maurus Palmatus ? has been described as an extremely potent modulator of the sarcoplasmic reticulum calcium release channel (CRC/RyR). Using single channel bilayer electrophysiology and confocal laser scanning microscopy we have shown that MCa is capable of altering the open probability and the gating characteristics of CRC/RyR by inducing long lasting subconductance states (LLSS). LLSS can last for several seconds. In parallel MCa induces complex event of calcium release in line-scan images. Using mutants of MCa we have demonstrated that the surface charge and/or charge distribution is the most important single parameter of the MCa effect. Altering even a single amino acid which destroys the positively charged area overwhelmingly influences the effect of the toxin on CRC/RyR. The effectiveness of the mutants is roughly proportionally with the real distance from the critical 24 residue. Their effects on the isolated channel and on the calcium release events were between those of the wild type and the ineffective Arg24Ala mutant.
Tárgyszavak:Természettudományok Biológiai tudományok idézhető absztrakt
calcium release
Megjelenés:Journal of Muscle Research and Cell Motility. - 25 (2004), p. 257. -
További szerzők:Ronjat, Michel Sabatier, Jean Marc Szegedi Csaba Jóna István (1948-) (élettanász, fizikus)
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3.

001-es BibID:BIBFORM049814
Első szerző:Pouvreau, Sandrine
Cím:Transient loss of voltage control of Ca2+ release in the presence of Maurocalcine in mouse skeletal muscle / S. Pouvreau, L. Csernoch, B. Allard, J. M. Sabatier, M. de Waard, M. Ronjat, V. Jacquemond
Dátum:2006
Tárgyszavak:Orvostudományok Elméleti orvostudományok idézhető absztrakt
Megjelenés:Biophysical Journal. - 90 (2006), p. 1280a. -
További szerzők:Csernoch László (1961-) (élettanász) Allard, Bruno Sabatier, Jean Marc DeWaard, M. Ronjat, Michel Jacquemond, Vincent
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4.

001-es BibID:BIBFORM020027
Első szerző:Pouvreau, Sandrine
Cím:Transient loss of voltage control of Ca2+ release in the presence of maurocalcine in skeletal muscle / Sandrine Pouvreau, Laszlo Csernoch, Bruno Allard, Jean Marc Sabatier, Michel De Waard, Michel Ronjat, Vincent Jacquemond
Dátum:2006
ISSN:0006-3495
Megjegyzések:In skeletal muscle, sarcoplasmic reticulum (SR) calcium release is controlled by the plasma membrane voltage through interactions between the voltage-sensing dihydropyridine receptor (DHPr) and the ryanodine receptor (RYr) calcium release channel. Maurocalcine (MCa), a scorpion toxin peptide presenting some homology with a segment of a cytoplasmic loop of the DHPr, has been previously shown to strongly affect the activity of the isolated RYr. We injected MCa into mouse skeletal muscle fibers and measured intracellular calcium under voltage-clamp conditions. Voltage-activated calcium transients exhibited similar properties in control and in MCa-injected fibers during the depolarizing pulses, and the voltage dependence of calcium release was similar under the two conditions. However, MCa was responsible for a pronounced sustained phase of Ca2+ elevation that proceeded for seconds following membrane repolarization, with no concurrent alteration of the membrane current. The magnitude of the underlying uncontrolled extra phase of Ca2+ release correlated well with the peak calcium release during the pulse. Results suggest that MCa binds to RYr that open on membrane depolarization and that this interaction specifically alters the process of repolarization-induced closure of the channels.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Biophysical Journal. - 91 : 6 (2006), p. 2206-2215. -
További szerzők:Csernoch László (1961-) (élettanász) Allard, Bruno Sabatier, Jean Marc De Waard, Michel Ronjat, Michel Jacquemond, Vincent
Internet cím:DOI
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5.

001-es BibID:BIBFORM004142
Első szerző:Szappanos Henrietta (biológus, élettanász)
Cím:Differential effects of maurocalcine on Ca2+ release events and depolarisation-induced Ca2+ release in rat skeletal muscle / Szappanos H., Smida-Resgui S., Cseri J., Simut C., Sabatier J.M., De Waard M., Kovacs L., Csernoch L., Ronjat M.
Dátum:2005
Megjegyzések:Maurocalcine (MCa), a 33 amino acid toxin obtained from scorpion venom, has been shown to interact with the isolated skeletal-type ryanodine receptor (RyR1) and to strongly modify its calcium channel gating. In this study, we explored the effects of MCa on RyR1 in situ to establish whether the functional interaction of RyR1 with the voltage-sensing dihydropyridine receptor (DHPR) would modify the ability of MCa to interact with RyR1. In developing skeletal muscle cells the addition of MCa into the external medium induced a calcium transient resulting from RyR1 activation and strongly inhibited the effect of the RyR1 agonist chloro-m-cresol. In contrast, MCa failed to affect the depolarization-induced Ca2+ release. In intact adult fibres MCa did not induce any change in the cytosolic Ca2+ concentration. However, when the surface membrane was permeabilized and calcium release events were readily observable, MCa had a time-dependent dual effect: it first increased event frequency, from 0.060 ? 0.002 to 0.150 ? 0.007 sarcomere?1 s?1, and reduced the amplitude of individual events without modifying their spatial distribution. Later on it induced the appearance of long-lasting events resembling the embers observed in control conditions but having a substantially longer duration. We propose that the functional coupling of DHPRs and RyR1s within a Ca2+ release unit prevents MCa from either reaching its binding site or from being able to modify the gating not only of the RyR1s physically coupled to DHPRs but all RyR1s within the Ca2+ release unit.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:The Journal of Physiology (London). - 565 : (Pt3) (2005), p. 843-853. -
További szerzők:Smida-Resgui, Sophia Cseri Julianna (1949-2022) (laboratóriumi diagnosztika szakorvos) Simut, Cecilia Sabatier, Jean Marc De Waard, Michel Kovács László (1939-) (élettanász) Csernoch László (1961-) (élettanász) Ronjat, Michel
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