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Roles of the 15-kDa Selenoprotein (Sep15) in Redox Homeostasis and Cataract Development Revealed by the Analysis of Sep 15 Knockout Miceстатья
Статья опубликована в высокорейтинговом журнале
Информация о цитировании статьи получена из
Web of Science,
Scopus
Статья опубликована в журнале из списка Web of Science и/или Scopus
Дата последнего поиска статьи во внешних источниках: 10 августа 2018 г.
- Авторы: Kasaikina Marina V., Fomenko Dmitri E., Labunskyy Vyacheslav M., Lachke Salil A., Qiu Wenya, Moncaster Juliet A., Zhang Jie, Wojnarowicz Mark W., Natarajan Sathish Kumar, Malinouski Mikalai, Schweizer Ulrich, Tsuji Petra A., Carlson Bradley A., Maas Richard L., Lou Marjorie F., Goldstein Lee E., Hatfield Dolph L., Gladyshev Vadim N.
- Журнал: Journal of Biological Chemistry
- Том: 286
- Номер: 38
- Год издания: 2011
- Издательство: American Society for Biochemistry and Molecular Biology Inc.
- Местоположение издательства: United States
- Первая страница: 33203
- Последняя страница: 33212
- DOI: 10.1074/jbc.m111.259218
- Аннотация: The 15-kDa selenoprotein (Sep15) is a thioredoxin-like, endoplasmic reticulum-resident protein involved in the quality control of glycoprotein folding through its interaction with UDP-glucose:glycoprotein glucosyltransferase. Expression of Sep15 is regulated by dietary selenium and the unfolded protein response, but its specific function is not known. In this study, we developed and characterized Sep15 KO mice by targeted removal of exon 2 of the Sep15 gene coding for the cysteine-rich UDP-glucose:glycoprotein glucosyltransferase-binding domain. These KO mice synthesized a mutant mRNA, but the shortened protein product could be detected neither in tissues nor in Sep15 KO embryonic fibroblasts. Sep15 KO mice were viable and fertile, showed normal brain morphology, and did not activate endoplasmic reticulum stress pathways. However, parameters of oxidative stress were elevated in the livers of these mice. We found that Sep15 mRNA was enriched during lens development. Further phenotypic characterization of Sep15 KO mice revealed a prominent nuclear cataract that developed at an early age. These cataracts did not appear to be associated with severe oxidative stress or glucose dysregulation. We suggest that the cataracts resulted from an improper folding status of lens proteins caused by Sep15 deficiency.
- Добавил в систему: Гладышев Вадим Николаевич