View : 13 Download: 0

PINK1 gene knockdown leads to increased binding of parkin with actin filament

Title
PINK1 gene knockdown leads to increased binding of parkin with actin filament
Authors
Kim K.-H.Son J.H.
Ewha Authors
손형진
SCOPUS Author ID
손형진scopus
Issue Date
2010
Journal Title
Neuroscience Letters
ISSN
0304-3940JCR Link
Citation
vol. 468, no. 3, pp. 272 - 276
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
Mutations in the PINK1 gene are known to cause early onset familial Parkinson's disease (PD). Genetic fruit fly model studies and rescue experiments with parkin overexpression suggest that PINK1 and parkin are associated via an unidentified mechanism. To gain additional insight into this interaction, we have investigated the impact of PINK1 deficiency on the biological function of parkin using actin filament dynamics. Actin is known to be associated with parkin and is a key regulator of eukaryotic cell death. PINK1 gene knockdown (KD) significantly increased actin aggregation and its binding with parkin. Known PD-related pathological conditions, such as oxidative stress and mitochondrial dysfunction, also increased actin aggregation and parkin binding. PINK1 KD resulted in the increased phosphorylation of cofilin, a protein important for the remodeling of actin filament and neurodegeneration. These results suggest that altered actin dynamics and increased association of parkin with actin filament might underlie the pathological conditions resulting from PINK1 deficiency. © 2009 Elsevier Ireland Ltd. All rights reserved.
DOI
10.1016/j.neulet.2009.11.011
Appears in Collections:
약학대학 > 약학과 > Journal papers
Files in This Item:
There are no files associated with this item.
Export
RIS (EndNote)
XLS (Excel)
XML


qrcode

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

BROWSE