| Project/Area Number |
14370256
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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 |
Dermatology
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| Research Institution | Asahikawa Medical College |
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Principal Investigator |
IIZUKA Hajime Asahikawa Medical College, Department of Dermatology, Professor, 医学部, 教授 (90113513)
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| Co-Investigator(Kenkyū-buntansha) |
ISHIDA Akemi (YAMAMOTO Akemi) Asahikawa Medical College, Department of Dermatology, Instructor, 医学部, 講師 (30241441)
TAKAHASHI Hidetoshi Asahikawa Medical College, Department of Dermatology, Instructor, 医学部, 講師 (00216748)
NAKAMURA Satoshi Asahikawa Medical College, Department of Dermatology, Assistant, 医学部, 助手 (20292112)
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| Project Period (FY) |
2002 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥8,500,000 (Direct Cost: ¥8,500,000)
Fiscal Year 2004: ¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 2003: ¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 2002: ¥3,900,000 (Direct Cost: ¥3,900,000)
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| Keywords | Darier disease / endoplasmic reticulum / calcium pump / keratinization |
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| Research Abstract |
The functional abnormalities in Darier disease-causing calcium ATPase (Serca2B) mutants were explored. Among 51mutants, 15 showed negligible expression of SERCA2b, 21 showed negative ATPase activities, and 8 showed functional uncoupling of ATPase and calcium pump activities in Cos1 cells. The remaining 3 showed unique characteristics. They exhibited nearly normal expression, high ATPase and coupled calcium transport activities that were essentially identical (L321F) or slightly lower (I274V and M719I) as compared with those of the wild type. M719I and L321F possess 2-3 fold reduced affinity for cytoplasmic calcium, whereas I274V possesses the normal high affinity. L321F exhibited also the remarkably reduced sensitivity to the feedback inhibition of the transport cycle by accumulated luminal calcium. Thus different abnormalities in Darier disease causing ATPase (SERCA2b) showed distinct types of altered calcium homeostasis in Cos1 cells.
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