The publication detail shows the title, authors (with indicators showing other profiled authors), information on the publishing organization, abstract and a link to the article in PubMed. This abstract is what is used to create the fingerprint of the publication. If any grants are referenced by the publication, they will be listed here as well.
The role of G-protein-coupled receptor kinase 5 in pathogenesis of sporadic Parkinson's disease.
Shigeki Arawaka; Manabu Wada; Saori Goto; Hiroki Karube; Masahiro Sakamoto; Chang-Hong Ren; Shingo Koyama; Hikaru Nagasawa; Hideki Kimura; Toru Kawanami; et al. (Profiled Author: Iwatsubo, Takeshi)
Department of Neurology, Hematology, Metabolism, Endocrinology and Diabetology, Faculty of Medicine, Yamagata University, Yamagata 990-9585, Japan.
The Journal of neuroscience : the official journal of the Society for Neuroscience 2006;26(36):9227-38.
Sporadic Parkinson's disease (sPD) is a common neurodegenerative disorder, characterized by selective degeneration of dopaminergic neurons in the substantia nigra. Although the pathogenesis of the disease remains undetermined, phosphorylation of alpha-synuclein and its oligomer formation seem to play a key role. However, the protein kinase(s) involved in the phosphorylation in the pathogenesis of sPD has not been identified. Here, we found that G-protein-coupled receptor kinase 5 (GRK5) accumulated in Lewy bodies and colocalized with alpha-synuclein in the pathological structures of the brains of sPD patients. In cotransfected cells, GRK5 phosphorylated Ser-129 of alpha-synuclein at the plasma membrane and induced translocation of phosphorylated alpha-synuclein to the perikaryal area. GRK5-catalyzed phosphorylation also promoted the formation of soluble oligomers and aggregates of alpha-synuclein. Genetic association study revealed haplotypic association of the GRK5 gene with susceptibility to sPD. The haplotype contained two functional single-nucleotide polymorphisms, m22.1 and m24, in introns of the GRK5 gene, which bound to YY1 (Yin Yang-1) and CREB-1 (cAMP response element-binding protein 1), respectively, and increased transcriptional activity of the reporter gene. The results suggest that phosphorylation of alpha-synuclein by GRK5 plays a crucial role in the pathogenesis of sPD.
This section shows information related to the publication - computed using the fingerprint of the publication - including related publications, related experts and related grants with fingerprints representing significant amounts of overlap between their fingerprint and this publication. The red dots indicate whether those experts or terms appear within the publication, thereby showing potential and actual connections.
Trojanowski, John Q
15 May 1997 - 30 April 2010
NATIONAL INSTITUTE ON AGING
Total Funding: $ 24,601,856
Dickson, Dennis William
30 September 1999 - 31 August 2009
NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE
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Total Funding: $ 1,918,101
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A Takeda; M Hashimoto; M Mallory; M Sundsumo; L Hansen; A Sisk; E MasliahLaboratory investigation; a journal of technical methods and pathology 1998;78(9):1169-77.
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