• 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

一种能够抑制同源补体介导的膜攻击的新型膜糖蛋白。

A novel membrane glycoprotein capable of inhibiting membrane attack by homologous complement.

作者信息

Okada N, Harada R, Fujita T, Okada H

机构信息

Department of Microbiology, Fukuoka University School of Medicine, Japan.

出版信息

Int Immunol. 1989;1(2):205-8. doi: 10.1093/intimm/1.2.205.

DOI:10.1093/intimm/1.2.205
PMID:2487685
Abstract

Neuraminidase-treated human erythrocytes become sensitive to haemolysis by heterologous serum via activation of the alternative complement pathway (ACP), while remaining insensitive to homologous serum because of the presence of inhibitors on the cell membrane. We obtained a monoclonal antibody which renders the neuraminidase-treated erythrocytes sensitive to haemolysis by homologous human serum via the ACP. This antibody reacts with a 20 KDa membrane glycoprotein which interferes with the terminal stage of complement action on cell membranes. The 20 KDa protein is anchored to the membrane via phosphatidylinositol.

摘要

经神经氨酸酶处理的人红细胞通过替代补体途径(ACP)的激活而对异种血清溶血敏感,而由于细胞膜上存在抑制剂,对同种血清仍不敏感。我们获得了一种单克隆抗体,它使经神经氨酸酶处理的红细胞通过ACP对人同种血清溶血敏感。该抗体与一种20 kDa的膜糖蛋白反应,该蛋白干扰补体在细胞膜上作用的终末阶段。20 kDa蛋白通过磷脂酰肌醇锚定在膜上。

相似文献

1
A novel membrane glycoprotein capable of inhibiting membrane attack by homologous complement.一种能够抑制同源补体介导的膜攻击的新型膜糖蛋白。
Int Immunol. 1989;1(2):205-8. doi: 10.1093/intimm/1.2.205.
2
Monoclonal antibodies capable of causing hemolysis of neuraminidase-treated human erythrocytes by homologous complement.能够通过同源补体引起神经氨酸酶处理的人红细胞溶血的单克隆抗体。
J Immunol. 1989 Oct 1;143(7):2262-6.
3
Prevention of complement activation on the homologous cell membrane of nucleated cells as well as erythrocytes.防止补体在有核细胞以及红细胞的同源细胞膜上激活。
Eur J Immunol. 1983 Apr;13(4):340-4. doi: 10.1002/eji.1830130413.
4
Erythrocytes of patients with paroxysmal nocturnal haemoglobinuria acquire resistance to complement attack by purified 20-kD homologous restriction factor.阵发性夜间血红蛋白尿患者的红细胞通过纯化的20-kD同源限制因子获得对补体攻击的抗性。
Clin Exp Immunol. 1990 Apr;80(1):109-13. doi: 10.1111/j.1365-2249.1990.tb06449.x.
5
Purification of 1F5 antigen that prevents complement attack on homologous cell membranes.
J Immunol. 1990 Mar 1;144(5):1823-8.
6
Ability to activate the alternative complement pathway acquired by human and guinea-pig erythrocytes after contact with influenza virus.人类和豚鼠红细胞与流感病毒接触后获得的激活替代补体途径的能力。
Ann Immunol (Paris). 1980 Mar-Apr;131C(2):213-21.
7
Human protectin (CD59), an 18,000-20,000 MW complement lysis restricting factor, inhibits C5b-8 catalysed insertion of C9 into lipid bilayers.人保护素(CD59)是一种分子量为18,000 - 20,000的补体溶解限制因子,可抑制C5b - 8催化C9插入脂质双层。
Immunology. 1990 Sep;71(1):1-9.
8
Human protectin (CD59), an 18-20-kD homologous complement restriction factor, does not restrict perforin-mediated lysis.人反应蛋白(CD59)是一种18 - 20千道尔顿的同源补体限制因子,它并不限制穿孔素介导的细胞溶解。
J Exp Med. 1990 Jul 1;172(1):367-70. doi: 10.1084/jem.172.1.367.
9
Analysis of the effects of activation of the alternative pathway of complement on erythrocytes with an isolated deficiency of decay accelerating factor.对补体替代途径激活对衰变加速因子单独缺乏的红细胞的影响的分析。
J Immunol. 1992 Jan 15;148(2):498-502.
10
A monoclonal antibody that blocks the complement regulatory activity of guinea pig erythrocytes and characterization of the antigen involved as guinea pig decay-accelerating factor.一种阻断豚鼠红细胞补体调节活性的单克隆抗体以及所涉及抗原作为豚鼠衰变加速因子的特性鉴定
J Immunol. 1995 Jun 1;154(11):6103-11.

引用本文的文献

1
Molecules That Have Rarely Been Studied in Lymphatic Endothelial Cells.鲜有研究的淋巴管内皮细胞分子。
Int J Mol Sci. 2024 Nov 14;25(22):12226. doi: 10.3390/ijms252212226.
2
Complement system in Anti-CD20 mAb therapy for cancer: A mini-review.补体系统在抗 CD20 mAb 治疗癌症中的作用:小型综述。
Int J Immunopathol Pharmacol. 2023 Jan-Dec;37:3946320231181464. doi: 10.1177/03946320231181464.
3
(Patho)Physiology of Glycosylphosphatidylinositol-Anchored Proteins I: Localization at Plasma Membranes and Extracellular Compartments.
糖基磷脂酰肌醇锚定蛋白的病理生理学 I:在质膜和细胞外隔室中的定位。
Biomolecules. 2023 May 18;13(5):855. doi: 10.3390/biom13050855.
4
Molecular pathogenesis of human CD59 deficiency.人类CD59缺乏症的分子发病机制。
Neurol Genet. 2018 Oct 26;4(6):e280. doi: 10.1212/NXG.0000000000000280. eCollection 2018 Dec.
5
New Insights on Complement Inhibitor CD59 in Mouse Laser-Induced Choroidal Neovascularization: Mislocalization After Injury and Targeted Delivery for Protein Replacement.补体抑制剂CD59在小鼠激光诱导脉络膜新生血管形成中的新见解:损伤后的定位错误及蛋白质替代的靶向递送
J Ocul Pharmacol Ther. 2017 Jun;33(5):400-411. doi: 10.1089/jop.2016.0101. Epub 2017 Mar 23.
6
Mouse ficolin B has an ability to form complexes with mannose-binding lectin-associated serine proteases and activate complement through the lectin pathway.小鼠纤维胶凝蛋白B具有与甘露糖结合凝集素相关丝氨酸蛋白酶形成复合物并通过凝集素途径激活补体的能力。
J Biomed Biotechnol. 2012;2012:105891. doi: 10.1155/2012/105891. Epub 2012 Feb 29.
7
Complement-mediated injury and protection of endothelium: lessons from atypical haemolytic uraemic syndrome.补体介导的内皮损伤与保护:非典型溶血尿毒综合征的启示。
Immunobiology. 2012 Feb;217(2):195-203. doi: 10.1016/j.imbio.2011.07.028. Epub 2011 Jul 30.
8
CD59 but not DAF deficiency accelerates atherosclerosis in female ApoE knockout mice.CD59而非衰变加速因子(DAF)的缺乏会加速雌性载脂蛋白E基因敲除小鼠的动脉粥样硬化进程。
Mol Immunol. 2009 May;46(8-9):1702-9. doi: 10.1016/j.molimm.2009.02.009. Epub 2009 Mar 17.
9
Effect of IL-4 on altered expression of complement activation regulators in rat pancreatic cells during severe acute pancreatitis.白细胞介素-4对重症急性胰腺炎大鼠胰腺细胞中补体激活调节因子表达改变的影响。
World J Gastroenterol. 2005 Nov 21;11(43):6770-4. doi: 10.3748/wjg.v11.i43.6770.
10
Decay-accelerating factor induction by tumour necrosis factor-alpha, through a phosphatidylinositol-3 kinase and protein kinase C-dependent pathway, protects murine vascular endothelial cells against complement deposition.肿瘤坏死因子-α通过磷脂酰肌醇-3激酶和蛋白激酶C依赖性途径诱导衰变加速因子,可保护小鼠血管内皮细胞免受补体沉积。
Immunology. 2003 Oct;110(2):258-68. doi: 10.1046/j.1365-2567.2003.01733.x.