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001-es BibID:	BIBFORM049390
Első szerző:	Jóna István (élettanász, fizikus)
Cím:	Effect of maurocalcine on RyR1 and RyR2 is substantially different / Istvan Jona, Janos Almassy, Michel Ronjat, Balazs Lukacs
Dátum:	2007
ISSN:	0006-3495
Megjegyzések:	Effect of a scorpion toxin (maurocalcine, MCa) on the RyR was studied using Müller-Rudin type bilayer. Canine cardiac SR calcium channel (RyR2) was isolated, solubilized and incorporated into lipid bilayer. Channel parameters were determined under voltage clamp conditions, using charge carrier of 250 mM KCl while ionized calcium buffered to 274 nM and 50 microM. It is shown that MCa evokes long lasting subconductance state (LLSS) events if the current is opposite of the physiological calcium movement - similarly to RyR1 (as prviously reported), but these events in case of RyR2 are more frequent [63.5 ? 5.7 versus 17.3 ? 2.7 in a minute] and about 10 times shorter [12 ? 0.9 sec versus 193 ? 14 ms] than in case of RyR1. During these LLSS events, the channel frequently goes into the close state - for a short period - end returns to the subconductance state. These intra-LLSS closings are longer for the RyR2-MCa interaction than for the RyR1-MCa interaction. The open probability (Po) - determined between the LLSS events - is also effected. In case of physiological current MCa does not evoke LLSS at all, however there is a slight increase of the open probability. Similarly to the RyR1, the effect of the toxin on RyR2 is voltage independent and its concentration dependence indicates one binding site. The MCa effect is calcium independent. These findings indicate that the region of the RyR2 which interacts with the 2-3 loop of the DHPR is different from that of the RyR1.
Tárgyszavak:	Természettudományok Biológiai tudományok idézhető absztrakt calcium release
Megjelenés:	Biophysical Journal. - 91 : Suppl. (2007), p. 87a. -
További szerzők:	Almássy János (1981-) (élettanász, biológus, angol-magyar szakfordító) Ronjat, Michel Lukács Balázs (1978-) (élettanász)
Internet cím:	Szerző által megadott URL Intézményi repozitóriumban (DEA) tárolt változat
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