• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

人红细胞膜含有一种新型的12 kDa肌醇磷酸结合蛋白,该蛋白是一种亲免素。

The human erythrocyte membrane contains a novel 12-kDa inositolphosphate-binding protein that is an immunophilin.

作者信息

Cunningham E B

机构信息

Department of Biochemistry and Molecular Biology, University of Medicine and Dentistry, New Jersey Medical School, Newark 07103-2714, USA.

出版信息

Biochem Biophys Res Commun. 1995 Oct 4;215(1):212-8. doi: 10.1006/bbrc.1995.2455.

DOI:10.1006/bbrc.1995.2455
PMID:7575593
Abstract

A 12-kDa inositolphosphate-binding protein has been identified as a component of the human erythrocyte membrane. Its robust peptidylprolyl cis-trans isomerase activity that is strongly inhibited by the immunosuppressant drugs FK506 and rapamycin indicates that it is an immunophilin belonging to the FKBP class. The finding that its peptidylprolyl cis-trans isomerase activity is also strongly inhibited by nanomolar concentrations of the second messengers inositol 1,4,5-trisphosphate (IP3) and inositol 1,3,4,5-tetrakisphosphate (IP4) suggests that IP3 and IP4 could be physiological ligands for this membrane-associated immunophilin.

摘要

一种12千道尔顿的肌醇磷酸结合蛋白已被鉴定为人红细胞膜的一个组成部分。其强大的肽基脯氨酰顺反异构酶活性受到免疫抑制剂FK506和雷帕霉素的强烈抑制,这表明它是一种属于FKBP类的亲免素。其肽基脯氨酰顺反异构酶活性也受到纳摩尔浓度的第二信使肌醇1,4,5-三磷酸(IP3)和肌醇1,3,4,5-四磷酸(IP4)的强烈抑制,这一发现表明IP3和IP4可能是这种膜相关亲免素的生理配体。

相似文献

1
The human erythrocyte membrane contains a novel 12-kDa inositolphosphate-binding protein that is an immunophilin.人红细胞膜含有一种新型的12 kDa肌醇磷酸结合蛋白,该蛋白是一种亲免素。
Biochem Biophys Res Commun. 1995 Oct 4;215(1):212-8. doi: 10.1006/bbrc.1995.2455.
2
Cyclosporin A, FK506, and rapamycin: binding to immunophilins and biological action.环孢素A、FK506和雷帕霉素:与亲免素的结合及生物学作用。
Chem Immunol. 1994;59:128-55.
3
Structure-function relationships in the FK506-binding protein (FKBP) family of peptidylprolyl cis-trans isomerases.肽基脯氨酰顺反异构酶FK506结合蛋白(FKBP)家族中的结构-功能关系。
Biochem J. 1996 Mar 1;314 ( Pt 2)(Pt 2):361-85.
4
A nonimmunosuppressive triene-modified rapamycin analog is a potent inhibitor of peptidyl prolyl cis-trans isomerase.
Biochem Biophys Res Commun. 1993 May 14;192(3):1340-6. doi: 10.1006/bbrc.1993.1563.
5
An inositolphosphate-binding immunophilin, IPBP12.一种肌醇磷酸结合免疫亲和素,IPBP12。
Blood. 1999 Oct 15;94(8):2778-89.
6
Time-dependent inhibition of peptidylprolyl cis-trans-isomerases by FK506 is probably due to cis-trans isomerization of the inhibitor's imide bond.FK506对肽基脯氨酰顺反异构酶的时间依赖性抑制可能是由于抑制剂的酰亚胺键发生顺反异构化所致。
Biochem J. 1995 Jan 1;305 ( Pt 1)(Pt 1):159-64. doi: 10.1042/bj3050159.
7
Immunity, microbial pathogenesis, and immunophilins: finding the keys, now where are the locks?
Infect Agents Dis. 1992 Jun;1(3):121-35.
8
A novel plant peptidyl-prolyl-cis-trans-isomerase (PPIase): cDNA cloning, structural analysis, enzymatic activity and expression.一种新型植物肽基脯氨酰顺反异构酶(PPIase):cDNA克隆、结构分析、酶活性及表达
Plant Mol Biol. 1996 Nov;32(3):493-504. doi: 10.1007/BF00019101.
9
FK506 as an agonist to induce inhibition of interleukin 2 production.
Transplantation. 1992 May;53(5):1150-3.
10
Structure-based design of novel, urea-containing FKBP12 inhibitors.基于结构的新型含尿素FKBP12抑制剂的设计。
J Med Chem. 1996 Apr 26;39(9):1872-84. doi: 10.1021/jm950798a.

引用本文的文献

1
The Arabidopsis thaliana immunophilin ROF1 directly interacts with PI(3)P and PI(3,5)P2 and affects germination under osmotic stress.拟南芥免疫素 ROF1 与 PI(3)P 和 PI(3,5)P2 直接相互作用,并影响渗透胁迫下的萌发。
PLoS One. 2012;7(11):e48241. doi: 10.1371/journal.pone.0048241. Epub 2012 Nov 2.
2
The 13-kD FK506 binding protein, FKBP13, interacts with a novel homologue of the erythrocyte membrane cytoskeletal protein 4.1.13千道尔顿的FK506结合蛋白FKBP13与红细胞膜细胞骨架蛋白4.1的一种新型同源物相互作用。
J Cell Biol. 1998 Apr 6;141(1):143-53. doi: 10.1083/jcb.141.1.143.