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Phosphoinositide 3-kinase gamma mediates microglial phagocytosis via lipid kinase-independent control of cAMP

Schmidt, C. and Schneble, N. and Muller, J. P. and Bauer, R. and Perino, A. and Marone, R. and Rybalkin, S. D. and Wymann, M. P. and Hirsch, E. and Wetzker, R.. (2013) Phosphoinositide 3-kinase gamma mediates microglial phagocytosis via lipid kinase-independent control of cAMP. Neuroscience, Vol. 233. pp. 44-53.

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Official URL: http://edoc.unibas.ch/dok/A6338020

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Abstract

Microglial phagocytosis plays a key role in neuroprotective and neurodegenerative responses of the innate immune system in the brain. Here we investigated the regulatory function of phosphoinositide 3-kinase gamma (PI3Kgamma) in phagocytosis of bacteria and Zymosan particles by mouse brain microglia in vitro and in vivo. Using genetic and pharmacological approaches our data revealed PI3Kgamma as an essential mediator of microglial phagocytosis. Unexpectedly, microglia expressing lipid kinase deficient mutant PI3Kgamma exhibited similar phagocytosis as wild-type cells. These data suggest kinase-independent stimulation of cAMP phosphodiesterase activity by PI3Kgamma as a crucial mediator of phagocytosis. In sum our findings indicate PI3Kgamma-dependent suppression of cAMP signaling as a critical regulatory element of microglial phagocytosis.
Faculties and Departments:03 Faculty of Medicine > Departement Biomedizin > Division of Biochemistry and Genetics > Cancer- and Immunobiology (Wymann)
UniBasel Contributors:Wymann, Matthias P.
Item Type:Article, refereed
Article Subtype:Research Article
Bibsysno:Link to catalogue
Publisher:Elsevier
ISSN:0306-4522
Note:Publication type according to Uni Basel Research Database: Journal article
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Last Modified:06 Mar 2015 07:44
Deposited On:06 Mar 2015 07:44

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