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Laboratory Investigation on Protein 1/ Clara Cell 10 kDa Protein

蛋白质 1/Clara 细胞 10 kDa 蛋白质的实验室研究

基本信息

批准号：
11672302
负责人：
ITOH Yoshihisa
金额：
$ 2.3万
依托单位：
Asahikawa Medical College (2000-2001)Jichi Medical University (1999)
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1999
资助国家：
日本
起止时间：
1999 至 2001
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-11672302/
关键词：
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

项目摘要

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.

蛋白1（Protein 1）又称克拉拉细胞10 kDa蛋白或子宫珠蛋白，是一种分子量为14 kDa的非糖蛋白，具有抗炎作用。β2-微球蛋白（β2-m）在酸性尿液中不稳定，但蛋白1不稳定。我们可以鉴定出降解β2-m的组织蛋白酶D。蛋白质1的稳定性可以通过其分子上不存在切割位点来解释。我们需要重新评估所有尿蛋白的稳定性，以便正确地用于临床。本文对正常人和伊加肾病患者子宫珠蛋白/P1基因G38 A多态性进行了研究。G38 AA的频率为24%，在疾病中是正常的2倍。此外，我们发现患者血清中子宫珠蛋白值降低，表明G38 AA可能是由于抗炎作用相对降低而导致疾病的易感因素。在P1基因上发现了新的SNPs.我们最近发现，pi通过阻断Ca内流而对血小板聚集产生抑制作用。正在进行进一步的精确研究，以阐明精确的机制。