The dynamic interactions of the main pathways for active Ca2+ transport have been analysed in living cells by altering the expression of their components. The plasma membrane (PMCA) and the endoplasmic reticulum (ER) (SERCA) Ca2+ pumps were transiently overexpressed in CHO cells, and the Ca2+ homeostasis in the subcellular compartments was investigated using specifically targeted chimaeras of the Ca2+-sensitive photoprotein aequorin, In resting cells, overexpression of the PMCA and SERCA pumps caused a reduction and an increase in ER [Ca2+] levels, respectively; while no significant differences were detected in cytosolic and mitochondrial [Ca2+]. Upon stimulation with an inositol 1,4,5-trisphosphate (IP3)-generating agonist, the amplitude of the mitochondrial and cytosolic Ca2+ rises correlated,vith the ER [Ca2+] only up to a threshold value, above which the feedback inhibition of the IP3 channel by Ca2+ appeared to be limiting.

Effects of PMCA and SERCA pumps overexpression on the kinetics of cell Ca2+ signalling

BRINI, MARISA;MANNI, SABRINA;RIZZUTO, ROSARIO;
2000

Abstract

The dynamic interactions of the main pathways for active Ca2+ transport have been analysed in living cells by altering the expression of their components. The plasma membrane (PMCA) and the endoplasmic reticulum (ER) (SERCA) Ca2+ pumps were transiently overexpressed in CHO cells, and the Ca2+ homeostasis in the subcellular compartments was investigated using specifically targeted chimaeras of the Ca2+-sensitive photoprotein aequorin, In resting cells, overexpression of the PMCA and SERCA pumps caused a reduction and an increase in ER [Ca2+] levels, respectively; while no significant differences were detected in cytosolic and mitochondrial [Ca2+]. Upon stimulation with an inositol 1,4,5-trisphosphate (IP3)-generating agonist, the amplitude of the mitochondrial and cytosolic Ca2+ rises correlated,vith the ER [Ca2+] only up to a threshold value, above which the feedback inhibition of the IP3 channel by Ca2+ appeared to be limiting.
2000
File in questo prodotto:
Non ci sono file associati a questo prodotto.
Pubblicazioni consigliate

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/11577/2463658
Citazioni
  • ???jsp.display-item.citation.pmc??? ND
  • Scopus 108
  • ???jsp.display-item.citation.isi??? 104
social impact