2003 Fiscal Year Final Research Report Summary
Functional and dynamic gene expression profiling of polyglutamine
| Project/Area Number |
14370213
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Neurology
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| Research Institution | Tokyo Medical and Dental University (2003)
Tokyo Metropolitan Organization for Medical Research (2002) |
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Principal Investigator |
OKAZAWA Hitoshi Tokyo Medical and Dental University, Medical Research institute, Professor, 難治疾患研究所, 教授 (50261996)
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| Co-Investigator(Kenkyū-buntansha) |
KANAZAWA Ichiro National Center for Psychiatry and neurology, DEAN, 総長 (30110498)
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| Project Period (FY) |
2002 – 2003
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| Keywords | POLYGLUTAMINE DISEASES / MEURODEGENTATION / PQBP-1 / TRANSCRIPTION / NUCLEARFUNCTION / RNA POLYMERASE II |
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| Research Abstract |
Polyglutamine diseases are caused by abnormal proteins containing an elongated polyglutamine tract sequence. It is generally believed that aggregation of the mutant proteins is essential for the pathology. However, molecular events induced by abnormal proteins during aggregation process are not fully elucidated. In this project, we applied genomics and proteomics to this question and investigated which genes and proteins are affected in expression. In brief, we found that different disease genes cause different gene and protein expression changes in a neuron type-specific manner. During the process, we found novel modifier genes of polyglutamine disease pathology, which could be used for the future development of molecular therapeutics.
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Research Products
(12 results)
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[Publications] Okazawa H., Rich T., Chang A., Lin X., Waragai M., Kajikawa M., Enokido Y, Komuo A., Kato S.Shibata M., Hatanaka H., Mouradian M.M., Sudol M., Kanazawa I.: "Interaction between mutant ataxin-1 and PQBP-1 affects transcription and cell death."Neuron. 34. 701-703 (2002)
Description
「研究成果報告書概要(欧文)」より
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