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阿尔茨海默病淀粉样蛋白前体中的金属蛋白酶抑制剂结构域。

A metalloproteinase inhibitor domain in Alzheimer amyloid protein precursor.

作者信息

Miyazaki K, Hasegawa M, Funahashi K, Umeda M

机构信息

Division of Cell Biology, Kihara Institute for Biological Research, Yokohama City University, Japan.

出版信息

Nature. 1993 Apr 29;362(6423):839-41. doi: 10.1038/362839a0.

Abstract

Extracellular deposition of amyloid beta-protein (beta-AP), or A4 protein (M(r) 4,000), is associated with Alzheimer's disease and with Down's syndrome (trisomy for chromosome 21). The large membrane-bound precursor protein (APP) of beta-AP is normally cleaved within the beta-AP region by a putative proteinase (APP secretase) to release its extracellular portion; beta-AP is produced by an alternative proteolytic processing. Here we demonstrate that APP contains a proteinase inhibitor domain for the matrix metalloproteinase gelatinase A, which is located in the C-terminal glycosylated region of the secretory forms of APP. In addition, we show that the gelatinase has an APP secretase-like activity, which hydrolyses the Lys16-Leu17 bond in the beta-AP sequence. Our results indicate that the proteinase inhibitor domain of APP and gelatinase A may be involved in the formation of beta-AP.

摘要

β-淀粉样蛋白(β-AP)或A4蛋白(分子量4000)的细胞外沉积与阿尔茨海默病以及唐氏综合征(21号染色体三体)有关。β-AP的大型膜结合前体蛋白(APP)通常在β-AP区域内被一种假定的蛋白酶(APP分泌酶)切割,以释放其细胞外部分;β-AP是通过另一种蛋白水解加工过程产生的。在此我们证明,APP含有一个针对基质金属蛋白酶明胶酶A的蛋白酶抑制剂结构域,该结构域位于APP分泌形式的C末端糖基化区域。此外,我们表明明胶酶具有类似APP分泌酶的活性,可水解β-AP序列中的Lys16-Leu17键。我们的结果表明,APP的蛋白酶抑制剂结构域和明胶酶A可能参与了β-AP的形成。

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