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AlF4-对大鼠组蛋白H1核苷酸及DNA体外结合的干扰。对阿尔茨海默病发病机制的启示。

Interference of AlF4- with nucleotide and DNA binding of rat histone H1 in vitro. Implications for the pathogenesis of Alzheimer's disease.

作者信息

Oikarinen J, Mannermaa R M, Tarkka T, Yli-Mäyry N, Majamaa K

机构信息

Collagen Research Unit, University of Oulu, Finland.

出版信息

Neurosci Lett. 1991 Nov 11;132(2):171-4. doi: 10.1016/0304-3940(91)90294-4.

DOI:10.1016/0304-3940(91)90294-4
PMID:1784417
Abstract

We demonstrate here that the H2PO4- analogue AlF4- binds to the nucleotide-binding site of rat liver histone H1 in vitro, and interferes with nucleotide recognition and H1 DNA binding. AlF4- may thus compromise the genetically determined pattern of protein synthesis through binding to H1, the general repressor. The present findings are of interest as a number of studies have implicated aluminium as a factor in the pathogenesis of Alzheimer's disease.

摘要

我们在此证明,H2PO4-类似物AlF4-在体外与大鼠肝脏组蛋白H1的核苷酸结合位点结合,并干扰核苷酸识别和H1与DNA的结合。因此,AlF4-可能通过与通用阻遏物H1结合而损害蛋白质合成的遗传决定模式。由于许多研究表明铝是阿尔茨海默病发病机制中的一个因素,所以目前的研究结果很有意义。

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