JCB logo
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents
Published online 19 April 2004. doi:10.1083/jcb.200311061
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 165, Number 2, 223-232
This Article
Right arrow Full Text
Right arrow Full Text (PDF, 1332K)
Right arrow PPT slides of all figures
Right arrow Alert me when this article is cited
Right arrow Citation Map
Services
Right arrow Email this article
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new content in the JCB
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Pinton, P.
Right arrow Articles by Rizzuto, R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Pinton, P.
Right arrow Articles by Rizzuto, R.
Related Collections
Right arrowRelated Article
Social Bookmarking
Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Facebook   Add to Reddit   Add to Technorati   Add to Twitter  
What's this?

Article

Long-term modulation of mitochondrial Ca2+ signals by protein kinase C isozymes



Paolo Pinton1, Sara Leo1, Mariusz R. Wieckowski1, Giulietta Di Benedetto2, and Rosario Rizzuto1

1 Section of General Pathology, Department of Experimental and Diagnostic Medicine, Telethon Center for Cell Imaging and Interdisciplinary Center for the Study of Inflammation, University of Ferrara, 44100 Ferrara, Italy
2 Venetian Institute of Molecular Medicine, 35129 Padova, Italy

Address correspondence to R. Rizzuto, Section of General Pathology, Department of Experimental and Diagnostic Medicine, Via Borsari 46, 44100 Ferrara, Italy. Tel.: 39 0532 291361. Fax: 39 0532 247278. email: r.rizzuto{at}unife.it

The modulation of Ca2+ signaling patterns during repetitive stimulations represents an important mechanism for integrating through time the inputs received by a cell. By either overexpressing the isoforms of protein kinase C (PKC) or inhibiting them with specific blockers, we investigated the role of this family of proteins in regulating the dynamic interplay of the intracellular Ca2+ pools. The effects of the different isoforms spanned from the reduction of ER Ca2+ release (PKC{alpha}) to the increase or reduction of mitochondrial Ca2+ uptake (PKC{zeta} and PKCß/PKC{delta}, respectively). This PKC-dependent regulatory mechanism underlies the process of mitochondrial Ca2+ desensitization, which in turn modulates cellular responses (e.g., insulin secretion). These results demonstrate that organelle Ca2+ homeostasis (and in particular mitochondrial processing of Ca2+ signals) is tuned through the wide molecular repertoire of intracellular Ca2+ transducers.

Key Words: organelle; aequorin; calcium; kinases; signal transduction

Abbreviations used in this paper: {Delta}{Psi}m, mitochondrial membrane potential; AEQ, aequorin; IP3, inositol 1,4,5 trisphosphate; ROS, reactive oxygen species.


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Facebook Facebook   Add to Reddit Reddit   Add to Technorati Technorati   Add to Twitter Twitter    What's this?

Related Article

PKCs pick through Ca2+
Nicole LeBrasseur
J. Cell Biol. 2004 165: 163. [Full Text] [PDF]



This article has been cited by other articles:



  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents