Abstract:
:Increasing evidence suggests that dynein has an important role in the clearance of misfolded proteins by autophagy. Here we show that treatment of cells with 1-methyl-4-phenylpyridinium (MPP) cause alpha-synuclein overexpression and aggregation, leading to the accumulation of autophagic vacuoles and the recruitment of LC3-II to these vacuoles in the cytoplasm. After MPP treatment, dynein expression decreased and was mainly aggregated at the periphery of cytoplasm and lost its colocalization with alpha-synuclein and lamp1, indicating that dynein lost its function in the aggresome formation and failed to return autophagosome and lysosomes to the center of the cell for degradation. We consider that dynein plays an important role in the autophagic clearance of aggregate-prone proteins.
journal_name
Neuroreportjournal_title
Neuroreportauthors
Cai ZL,Shi JJ,Yang YP,Cao BY,Wang F,Huang JZ,Yang F,Zhang P,Liu CFdoi
10.1097/WNR.0b013e32832986c4subject
Has Abstractpub_date
2009-04-22 00:00:00pages
569-73issue
6eissn
0959-4965issn
1473-558Xjournal_volume
20pub_type
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