Steady-state levels of calcium ions in endoplasmic reticulum reflect a balance between active inward transport, mediated by MgATP-dependent Ca2+ pumps, and passive backflux of the ions, through putative "leak channels". We have investigated the efflux of Ca2+ from rat liver microsomal vesicles, passively pre-equilibrated in the presence radiolabelled Ca. Similarly, we have also evaluated the efflux of a low-Mwt uncharged compound, i.e., sucrose. The results show that two major passive Ca2+ efflux pathways exist. One appeared to involve the translocon pore, since it was stimulated by the translocon opener puromycin, and also allowed the passage of sucrose. Putative channels likely mediated the other one, since it required counter ion influx and was inhibited by Gd3+ and La3+. The latter pathway did not appear to involve inactive Ca2+ pumps, Bcl2 proteins, or known channels, such as the InsP3 and ryanodine receptors. While sucrose efflux was highly represented in a rough microsomal subfraction-enriched in the translocon component Sec61 alpha--the efflux of Ca2+ was represented both in smooth and in rough microsomes. We conclude that the passive efflux of Ca2+ from the (liver) ER could be mediated by both the translocon pore and putative Ca2+ leak channels. However, the relative role of these Ca2+ efflux pathways in the intact cell as well as the molecular nature of the Ca2+ leak channel(s) remain to be clarified.

Giunti, R., Gamberucci, A., Fulceri, R., Banhegyi, G., Benedetti, A. (2007). Both translocon and a cation channel are involved in the passive Ca2+ leak from the endoplasmic reticulum: a mechanistic study on rat liver microsomes. ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS, 462(1), 115-121 [10.1016/j.abb.2007.03.039].

Both translocon and a cation channel are involved in the passive Ca2+ leak from the endoplasmic reticulum: a mechanistic study on rat liver microsomes

GIUNTI, R.;GAMBERUCCI, A.;FULCERI, R.;BENEDETTI, A.
2007-01-01

Abstract

Steady-state levels of calcium ions in endoplasmic reticulum reflect a balance between active inward transport, mediated by MgATP-dependent Ca2+ pumps, and passive backflux of the ions, through putative "leak channels". We have investigated the efflux of Ca2+ from rat liver microsomal vesicles, passively pre-equilibrated in the presence radiolabelled Ca. Similarly, we have also evaluated the efflux of a low-Mwt uncharged compound, i.e., sucrose. The results show that two major passive Ca2+ efflux pathways exist. One appeared to involve the translocon pore, since it was stimulated by the translocon opener puromycin, and also allowed the passage of sucrose. Putative channels likely mediated the other one, since it required counter ion influx and was inhibited by Gd3+ and La3+. The latter pathway did not appear to involve inactive Ca2+ pumps, Bcl2 proteins, or known channels, such as the InsP3 and ryanodine receptors. While sucrose efflux was highly represented in a rough microsomal subfraction-enriched in the translocon component Sec61 alpha--the efflux of Ca2+ was represented both in smooth and in rough microsomes. We conclude that the passive efflux of Ca2+ from the (liver) ER could be mediated by both the translocon pore and putative Ca2+ leak channels. However, the relative role of these Ca2+ efflux pathways in the intact cell as well as the molecular nature of the Ca2+ leak channel(s) remain to be clarified.
Giunti, R., Gamberucci, A., Fulceri, R., Banhegyi, G., Benedetti, A. (2007). Both translocon and a cation channel are involved in the passive Ca2+ leak from the endoplasmic reticulum: a mechanistic study on rat liver microsomes. ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS, 462(1), 115-121 [10.1016/j.abb.2007.03.039].
File in questo prodotto:
File Dimensione Formato  
ABB-'07.pdf

non disponibili

Tipologia: Post-print
Licenza: NON PUBBLICO - Accesso privato/ristretto
Dimensione 365.91 kB
Formato Adobe PDF
365.91 kB Adobe PDF   Visualizza/Apri   Richiedi una copia

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11365/20227
 Attenzione

Attenzione! I dati visualizzati non sono stati sottoposti a validazione da parte dell'ateneo