Casein kinase 2 interacts with and phosphorylates ataxin-3 / 神经科学通报·英文版
Neuroscience Bulletin
;
(6): 271-277, 2008.
Artigo
em Inglês
| WPRIM
| ID: wpr-264667
ABSTRACT
<p><b>OBJECTIVE</b>Machado-Joseph disease (MJD)/Spinocerebellar ataxia type 3 (SCA3) is an autosomal dominant neurodegenerative disorder caused by an expansion of polyglutamine tract near the C-terminus of the MJD1 gene product, ataxin-3. The precise mechanism of the MJD/SCA3 pathogenesis remains unclear. A growing body of evidence demonstrates that phosphorylation plays an important role in the pathogenesis of many neurodegenerative diseases. However, few kinases are known to phosphorylate ataxin-3. The present study is to explore whether ataxin-3 is a substrate of casein kinase 2 (CK2).</p><p><b>METHODS</b>The interaction between ataxin-3 and CK2 was identified by glutathione S-transferase (GST) pull-down assay and co-immunoprecipition assay. The phosphorylation of ataxin-3 by CK2 was measured by in vitro phosphorylation assays. Results (1) Both wild type and expanded ataxin-3 interacted with CK2alpha and CK2beta in vitro. (2) In 293 cells, both wild type and expanded ataxin-3 interacted with CK2beta, but not CK2alpha. (3) CK2 phosphorylated wild type and expanded ataxin-3.</p><p><b>CONCLUSION</b>Ataxin-3 is a substrate of protein kinase CK2.</p>
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Fosforilação
/
Proteínas Repressoras
/
Linhagem Celular Transformada
/
Proteínas Nucleares
/
Transfecção
/
Caseína Quinase II
/
Imunoprecipitação
/
Ataxina-3
/
Glutationa Transferase
/
Metabolismo
Tipo de estudo:
Estudo prognóstico
Limite:
Humanos
Idioma:
Inglês
Revista:
Neuroscience Bulletin
Ano de publicação:
2008
Tipo de documento:
Artigo
Similares
MEDLINE
...
LILACS
LIS