| Project/Area Number |
12670805
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Dermatology
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| Research Institution | AKITA UNIVERSITY |
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Principal Investigator |
YONEDA Kozo Akita University School of Medicine, Lecturer, 医学部, 講師 (60260626)
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| Co-Investigator(Kenkyū-buntansha) |
MANABE Motomu Akita University School of Medicine Professor, 医学部, 教授 (30138309)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 2001: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2000: ¥2,000,000 (Direct Cost: ¥2,000,000)
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| Keywords | Keratin / Filaggrin / Keratin Disease / Ubiqutin / 角化細胞 / ユビチキン / 26Sプロテアソーム |
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| Research Abstract |
Recently, mutations in keratin genes have been identified in many hereditary skin diseases. These skin disorders are now termed as keratin diseases. However, there are lots of unsolved problems in the pathophysiology of these keratin diseases. For example, we do not know why acanthosis of epidermis is induced following the keratin gene mutation yet. The reasonable rationale to the hyperkeratosis of some keratin disorders has not been obatined. In order to acquire the clue to solve these unanswered questions, we try to make keratin disease keratincyte model. At first, we introduced the mutation into keratin 14 cDNA (Arg-125→Cys) by PCR.
Next, this mutated keratin 14 is subcloned to pIND/V5-His vector which has heat shock promoter and ecdysone/glucocorticod response element. When double transfection of pIND/V5-His K14 (Arg-125→Cys) and pVgRXR was conducted, keratin aggregates were observed in the transfected cells. When transfected cells were stained with anti-ubiquitin antibody, the keratin aggregates were revealed to be ubiquitinated These results indicated that the ubiquitinproteasome pathway may play an important role in the pathophysiology of keratin diseases.
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