Polyenzymatic activation of cellular hydrolases induced by interferon; its role in cell lysis and other interferon--related phenomena.

D Zagury, J C Mazière, D A Morgan, M Fouchard, P Hosli
{"title":"Polyenzymatic activation of cellular hydrolases induced by interferon; its role in cell lysis and other interferon--related phenomena.","authors":"D Zagury,&nbsp;J C Mazière,&nbsp;D A Morgan,&nbsp;M Fouchard,&nbsp;P Hosli","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>Treatment of human cultured T cells by interferon (IFN), which enhances cell-mediated cytotoxicity directed against human K562 cell targets (NK-like activity) induces an activation of cell hydrolases. Treatment of mouse cultured L929 cells by IFN and double strand RNA enhancing cell autolysis induces first an activation of tested hydrolases (hexosaminidase, beta-glucuronidase, acid and alkaline phosphatases). Polyenzymatic activation of hydrolases induced by IFN is similar to coordinate enzymatic induction described by Hosli which occurs by lack of specific enzyme when non-digestible substrates are absorbed by cells. It is hypothesized that the polyenzymatic activation which accounts for cell lysis is a general defense mechanism which might also explain other actions related to IFN such as antiviral effect, inhibition of cell division, diminution of protein synthesis and cell surface alteration.</p>","PeriodicalId":9217,"journal":{"name":"Biomedicine / [publiee pour l'A.A.I.C.I.G.]","volume":"34 2","pages":"82-8"},"PeriodicalIF":0.0000,"publicationDate":"1981-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Biomedicine / [publiee pour l'A.A.I.C.I.G.]","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

Treatment of human cultured T cells by interferon (IFN), which enhances cell-mediated cytotoxicity directed against human K562 cell targets (NK-like activity) induces an activation of cell hydrolases. Treatment of mouse cultured L929 cells by IFN and double strand RNA enhancing cell autolysis induces first an activation of tested hydrolases (hexosaminidase, beta-glucuronidase, acid and alkaline phosphatases). Polyenzymatic activation of hydrolases induced by IFN is similar to coordinate enzymatic induction described by Hosli which occurs by lack of specific enzyme when non-digestible substrates are absorbed by cells. It is hypothesized that the polyenzymatic activation which accounts for cell lysis is a general defense mechanism which might also explain other actions related to IFN such as antiviral effect, inhibition of cell division, diminution of protein synthesis and cell surface alteration.

分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
干扰素诱导细胞水解酶的多酶活化它在细胞裂解和其他干扰素相关现象中的作用。
干扰素(IFN)可增强针对人K562细胞靶标(nk样活性)的细胞介导的细胞毒性,通过干扰素(IFN)处理人培养的T细胞可诱导细胞水解酶的激活。用IFN和双链RNA处理小鼠培养的L929细胞,增强细胞自溶,首先诱导所测水解酶(己糖氨酸酶、β -葡萄糖醛酸酶、酸性和碱性磷酸酶)的激活。IFN诱导水解酶的多酶活化类似于Hosli描述的协调酶诱导,即当细胞吸收不可消化的底物时,由于缺乏特定的酶而发生。据推测,导致细胞裂解的多酶激活是一种普遍的防御机制,它也可以解释与IFN相关的其他作用,如抗病毒作用、抑制细胞分裂、减少蛋白质合成和细胞表面改变。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
自引率
0.00%
发文量
0
期刊最新文献
Localisation of alphafetoprotein (AFP) in murine teratocarcinoma. lack of suppressor cell activity for natural killer cells in infant, aged and a low responder strain of mice. Prospective study of Epstein Barr virus (EBV) infection during pregnancy. Alcohol-induced Cushingoid syndrome. Tricyclic antidepressants induce sphingomyelinase deficiency in fibroblast and neuroblastoma cell cultures.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1