Neuronal survival induced by neurotrophins requires calmodulin
Egea Navarro, Joaquim
Dolcet Roca, Xavier
Yuste Mateos, Víctor J. (Víctor José)
Iglesias Durán, Montserrat
Rocamora Ibars, Nativitat
Comella i Carnicé, Joan Xavier
MetadataShow full item record
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.
Is part ofJournal of Cell Biology, 2001, vol. 154, núm. 3, p. 585–597
Showing items related by title, author, creator and subject.
Activation of Phosphatidylinositol 3-Kinase, but Not Extracellular-Regulated Kinases, Is Necessary to Mediate BrainDerived Neurotrophic Factor-Induced Motoneuron Survival Dolcet Roca, Xavier; Egea Navarro, Joaquim; Soler i Tatché, Rosa Ma.; Martin-Zanca, Dionisio; Comella i Carnicé, Joan Xavier (Wiley, 1999)Chick embryo spinal cord motoneurons develop a trophic response to some neurotrophins when they are maintained in culture in the presence of muscle extract. Thus, after 2 days in culture, brain-derived neurotrophic factor ...
Analysis of Ret knockin mice reveals a critical role for IKKs, but not PI 3-K, in neurotrophic factor-induced survival of sympathetic neurons. Encinas Martín, Mario; Rozen, Esteban Javier; Dolcet Roca, Xavier; Jain, Sanjay; Comella i Carnicé, Joan Xavier; Milbrandt, Jeffrey; Johnson, Eugene M. (Nature Publishing Group, 2008)We analyzed the survival responses and downstream signaling elicited by GDNF on sympathetic neurons from different Ret knockin mice. Lack of tyrosine 1062, a multidocking site in Ret, completely prevented GDNF-mediated ...
The death receptor antagonist FLIP-L interacts with Trk and is necessary for neurite outgrowth induced by neurotrophins Moubarak, Rana S.; Solé Serra, Carme; Pascual, Marta; Gutierrez, Humberto; Llovera i Tomàs, Marta; Pérez García, María José; Gozzelino, Raffaella; Segura Ginard, Miguel Francisco; Iglesias Guimarais, Victoria; Reix, Stéphanie; Soler i Tatché, Rosa Ma.; Davies, Alun M.; Soriano, Eduardo; Yuste Mateos, Víctor J. (Víctor José); Comella i Carnicé, Joan Xavier (Society for Neuroscience, 2010)FLICE-inhibitory protein (FLIP) is an endogenous inhibitor of the signaling pathway triggered by the activation of death receptors. Here, we reveal a novel biological function for the long form of FLIP (FLIP-L) in neuronal ...