1992 Fiscal Year Final Research Report Summary
Molecular genetic analysis of muirne senile amyloidosis.
| Project/Area Number |
03670171
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Experimental pathology
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| Research Institution | KYOTO UNIVERSITY |
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Principal Investigator |
HIGUCHI Keiichi Department of Senescence Biology, Chest Disease Research Institute, Lecturer, 胸部疾患研究所, 講師 (20173156)
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| Co-Investigator(Kenkyū-buntansha) |
HOSOKAWA Masanori Dept. Senescence Biology, Chest Dis. Res. Inst. Associate Professor, 胸部疾患研究所, 助教授 (00127135)
TAKEDA Tosio Dept. Senescence Biology, Chest Dis. Res. Inst. Professor, 胸部疾患研究所, 教授 (00027088)
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| Project Period (FY) |
1991 – 1992
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| Keywords | Senile amyloidosis / Mouse / Genetic Analysis / Congenic mice / apoA-II / Genome mapping / mRNA / Senescence Accelerated Mouse (SAM) |
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| Research Abstract |
From the two-year investigation entitled "Molecular genetic analysis of mouse senile amyloidosis", we found the followings,
1. The presence of a genetic element other than molecular type of amyloid precursor protein apoA-II which modifies the development of mouse senile amyloidosis was deduced from the genetic analysis using F1, F2, and back-crossed mice between the A/J and SAM-P/1 strains of mice.
2. The progress of senescence may accelerate the development of mouse senile amyloidosis.
3. A genome mapping system using endogenous leukemia proviruses as a DNA marker has been developed for genetic analysis and positional cloning of genetic elements modifying amyloidosis.
4. Congenic strains of mice carrying amyloidogenic apoA-II (Apoa2^c) on the genetic background of SAM-R/1 with normal aging process and amyloid-resistant apoA-II (Apoa2^b) on the genetic background of SAM-P/1 with accelerated aging process were developed.
5. Using congenic strains of mice, it was revealed that (1), Apoa2^c reduced the concentration and particle size of serum high density lipoprotein, (2) Apoa2^c accelerates the development of mouse senile amyloidosis.
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