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Reciprocal signals between microglia and neurons regulate α-synuclein secretion by exophagy through a neuronal cJUN-N-terminal kinase-signaling axis.

J Neuroinflammation.. 2016-03; 
Christensen DP, Ejlerskov P, Rasmussen I, Vilhardt F.
Products/Services Used Details Operation
... 2592, Epitomics, San Francisco, CA); mouse monoclonal anti-β-actin (A-1978, Sigma-Aldrich, St Louis, MO); rabbit polyclonal anti-p25α antibody (Enzo Life Sciences, Farmingdale, NY); mouse monoclonal anti-FLAG tag antibody (#A00187-200, Genscript, Aachen, Germany ...

摘要

BACKGROUND:Secretion of proteopathic α-synuclein (α-SNC) species from neurons is a suspected driving force in the propagation of Parkinson's disease (PD). We have previously implicated exophagy, the exocytosis of autophagosomes, as a dominant mechanism of α-SNC secretion in differentiated PC12 or SH-SY5Y nerve cells. Here we have examined the regulation of exophagy associated with different forms of nerve cell stress relevant to PD. RESULTS:We identify cJUN-N-terminal kinase (JNK) activity as pivotal in the secretory fate of autophagosomes containing α-SNC. Pharmacological inhibition or genetic (shRNA) knockdown of JNK2 or JNK3 decreases α-SNC secretion in differentiated PC12 and SH-SY5Y cells, respectivel... More

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