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- W1567984469 abstract "Sustained neuroinflammation is recognized as a key pathophysiological contributor to many neurodegenerative diseases, including Parkinson’s disease (PD). Resident brain microglia mediate chronic neuroinflammation through the production of proinflammatory cytokines and chemokines. Identifying the key molecular signaling events perpetuating microglial activation could unravel novel mechanisms underlying glial-neuronal interactions that contribute to persistent inflammation and progressive neurodegeneration in PD. In the present study, we examined the role that Fyn, a non-receptor tyrosine kinase, plays in microglial activation in cell culture and animal models of PD. First, we show that the known inflammogen LPS (lipopolysaccharide) rapidly activated Fyn kinase, as measured by Fyn-Y416 phosphorylation and Fyn kinase assays in the BV2 microglial cell line as well as in primary microglia. Notably, immunocytochemical studies revealed that activated Fyn is preferentially localized to the microglial membrane per..." @default.
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- W1567984469 date "2014-04-01" @default.
- W1567984469 modified "2023-10-11" @default.
- W1567984469 title "Fyn kinase regulates microglial neuroinflammatory responses in cell culture and animal models of Parkinson’s disease (1055.7)" @default.
- W1567984469 doi "https://doi.org/10.1096/fasebj.28.1_supplement.1055.7" @default.
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