Laboratory Investigation on Protein 1/ Clara Cell 10 kDa Protein
Project/Area Number |
11672302
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Laboratory medicine
|
Research Institution | Asahikawa Medical College (2000-2001) Jichi Medical University (1999) |
Principal Investigator |
ITOH Yoshihisa Asahikawa Medical College, Department of Medicine, Professor, 医学部, 教授 (20129026)
|
Project Period (FY) |
1999 – 2001
|
Project Status |
Completed (Fiscal Year 2001)
|
Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2001: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2000: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1999: ¥1,800,000 (Direct Cost: ¥1,800,000)
|
Keywords | Protein 1 / Clara cell 10 kDa Protein / Uteroglobin / SNPs / Platelet / プロテイン1 / クララ細胞蛋白 / β2-マイクログロブリン / カテプシンD / サルコイドーシス / SNP / モノクローナル抗体 / エピトープ / β_2-マイクログロブリン / 酵素免疫測定法 / 気管支喘息 |
Research Abstract |
Protein 1, also called as clara cell 10 kDa protein or uteroglobin, is nonglycoprotein with a molecular weight of 14 kDa playing anti-inflammatory function. In the present term the following research work was successfully performed: 1. β2-microglobulin (β2-m) is unstable in acidic urine, but not protein 1. We could identify cathepsin D responsible for the degradation ofβ2-m. Stability of protein 1 can be explained by no cleavage sites present on its molecule. We will need the revaluation of the stability of all the urinary proteins for proper clinical use. 2. The G38A gene polymorphism on uteroglobin/P1 was investigated in normal individuals and patients with IgA nephropathy. The frequency of G38AA is 24 %, being 2 times higher in the diseases than normal. Furthermore we found decrease of the uteroglobin value in the patients' sera indicating that G38AA may be a predisposing factor for the diseases as a result of relative decrease of anti-inflammatory effects. We have newly discovered SNPs on P1 gene. 3. We recently found that pi exert an inhibitory effect on platelet aggregation by blocking influx of Ca. Further precise study is in progress to elucidate precise mechanisms.
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Report
(4 results)
Research Products
(18 results)