Universitat de Lleida
    • English
    • català
    • español
  • English 
    • English
    • català
    • español
  • Login
Repositori Obert UdL
View Item 
  •   Home
  • Recerca
  • Ciències Mèdiques Bàsiques
  • Articles publicats (Ciències Mèdiques Bàsiques)
  • View Item
  •   Home
  • Recerca
  • Ciències Mèdiques Bàsiques
  • Articles publicats (Ciències Mèdiques Bàsiques)
  • View Item
JavaScript is disabled for your browser. Some features of this site may not work without it.

Neuronal survival induced by neurotrophins requires calmodulin

Thumbnail
View/Open
005715.pdf (590.2Kb)
Issue date
2001
Author
Egea Navarro, Joaquim
Espinet Mestre, Carme
Soler i Tatché, Rosa Ma.
Dolcet Roca, Xavier
Yuste Mateos, Víctor J. (Víctor José)
Encinas Martín, Mario
Iglesias Durán, Montserrat
Rocamora Ibars, Nativitat
Comella i Carnicé, Joan Xavier
Suggested citation
Egea Navarro, Joaquim; Espinet Mestre, Carme; Soler i Tatché, Rosa Ma.; Dolcet Roca, Xavier; Yuste Mateos, Víctor J. (Víctor José); Encinas Martín, Mario; ... Comella i Carnicé, Joan Xavier. (2001) . Neuronal survival induced by neurotrophins requires calmodulin. Journal of Cell Biology, 2001, vol. 154, núm. 3, p. 585–597. https://doi.org/10.1083/jcb.200101023.
Impact


Web of Science logo    citations in Web of Science

Scopus logo    citations in Scopus

Google Scholar logo  Google Scholar
Share
Export to Mendeley
Metadata
Show full item record
Abstract
It has been reported that phosphoinositide 3-kinase (PI 3-kinase) and its downstream target, protein kinase B (PKB), play a central role in the signaling of cell survival triggered by neurotrophins (NTs). In this report, we have analyzed the involvement of Ca2+ and calmodulin (CaM) in the activation of the PKB induced by NTs. We have found that reduction of intracellular Ca2+ concentration or functional blockade of CaM abolished NGF-induced activation of PKB in PC12 cells. Similar results were obtained in cultures of chicken spinal cord motoneurons treated with brain-derived neurotrophic factor (BDNF). Moreover, CaM inhibition prevented the cell survival triggered by NGF or BDNF. This effect was counteracted by the transient expression of constitutive active forms of the PKB, indicating that CaM regulates NT-induced cell survival through the activation of the PKB. We have investigated the mechanisms whereby CaM regulates the activation of the PKB, and we have found that CaM was necessary for the proper generation and/or accumulation of the products of the PI 3-kinase in intact cells.
URI
http://hdl.handle.net/10459.1/46380
DOI
https://doi.org/10.1083/jcb.200101023
Is part of
Journal of Cell Biology, 2001, vol. 154, núm. 3, p. 585–597
European research projects
Collections
  • Articles publicats (Ciències Mèdiques Bàsiques) [559]

Contact Us | Send Feedback | Legal Notice
© 2022 BiD. Universitat de Lleida
Metadata subjected to 
 

 

Browse

All of the repositoryCommunities & CollectionsBy Issue DateAuthorsTitlesSubjectsThis CollectionBy Issue DateAuthorsTitlesSubjects

Statistics

View Usage Statistics

D'interès

Política institucional d'accés obertDiposita les teves publicacionsDiposita dades de recercaSuport a la recerca

Contact Us | Send Feedback | Legal Notice
© 2022 BiD. Universitat de Lleida
Metadata subjected to