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Polo-like kinase 2 (PLK2) phosphorylates alpha-synuclein at serine 129 in central nervous system. 2009
Kelly J Inglis, and
David Chereau, and
Elizabeth F Brigham, and
San-San Chiou, and
Susanne Schöbel, and
Normand L Frigon, and
Mei Yu, and
Russell J Caccavello, and
Seth Nelson, and
Ruth Motter, and
Sarah Wright, and
David Chian, and
Pamela Santiago, and
Ferdie Soriano, and
Carla Ramos, and
Kyle Powell, and
Jason M Goldstein, and
Michael Babcock, and
Ted Yednock, and
Frederique Bard, and
Guriqbal S Basi, and
Hing Sham, and
Tamie J Chilcote, and
Lisa McConlogue, and
Irene Griswold-Prenner, and
John P Anderson
Elan Pharmaceuticals, South San Francisco, California 94080.
Several neurological diseases, including Parkinson disease and dementia with Lewy bodies, are characterized by the accumulation of alpha-synuclein phosphorylated at Ser-129 (p-Ser-129). The kinase or kinases responsible for this phosphorylation have been the subject of intense investigation. Here we submit evidence that polo-like kinase 2 (PLK2, also known as serum-inducible kinase or SNK) is a principle contributor to alpha-synuclein phosphorylation at Ser-129 in neurons. PLK2 directly phosphorylates alpha-synuclein at Ser-129 in an in vitro biochemical assay. Inhibitors of PLK kinases inhibited alpha-synuclein phosphorylation both in primary cortical cell cultures and in mouse brain in vivo. Finally, specific knockdown of PLK2 expression by transduction with short hairpin RNA constructs or by knock-out of the plk2 gene reduced p-Ser-129 levels. These results indicate that PLK2 plays a critical role in alpha-synuclein phosphorylation in central nervous system.
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Sarah Wright, and
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Pamela Santiago, and
Ferdie Soriano, and
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Seth Nelson, and
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Sarah Wright, and
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Pamela Santiago, and
Ferdie Soriano, and
Carla Ramos, and
Kyle Powell, and
Jason M Goldstein, and
Michael Babcock, and
Ted Yednock, and
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Seth Nelson, and
Ruth Motter, and
Sarah Wright, and
David Chian, and
Pamela Santiago, and
Ferdie Soriano, and
Carla Ramos, and
Kyle Powell, and
Jason M Goldstein, and
Michael Babcock, and
Ted Yednock, and
Frederique Bard, and
Guriqbal S Basi, and
Hing Sham, and
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