Casein kinase 2 interacts with and phosphorylates ataxin-3 / 神经科学通报·英文版
Neuroscience Bulletin
; (6): 271-277, 2008.
Article
ي En
| WPRIM
| ID: wpr-264667
المكتبة المسؤولة:
WPRO
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>
النص الكامل:
1
الفهرس:
WPRIM
الموضوع الرئيسي:
Phosphorylation
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Repressor Proteins
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Cell Line, Transformed
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Nuclear Proteins
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Transfection
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Casein Kinase II
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Immunoprecipitation
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Ataxin-3
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Glutathione Transferase
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Metabolism
نوع الدراسة:
Prognostic_studies
المحددات:
Humans
اللغة:
En
مجلة:
Neuroscience Bulletin
السنة:
2008
نوع:
Article