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1
The recovery of human polymorphonuclear leucocytes from sublytic complement attack is mediated by changes in intracellular free calcium.人多形核白细胞从亚溶细胞性补体攻击中的恢复是由细胞内游离钙的变化介导的。
Biochem J. 1985 Oct 1;231(1):205-8. doi: 10.1042/bj2310205.
2
Measurement of intracellular calcium ions and oxygen radicals in polymorphonuclear leucocyte-erythrocyte 'ghost' hybrids.多形核白细胞-红细胞“空壳”杂交体中细胞内钙离子和氧自由基的测量。
J Physiol. 1983 May;338:537-50. doi: 10.1113/jphysiol.1983.sp014688.
3
Direct measurement of the increase in intracellular free calcium ion concentration in response to the action of complement.直接测量细胞内游离钙离子浓度因补体作用而增加的情况。
Biochem J. 1981 Feb 15;194(2):551-60. doi: 10.1042/bj1940551.
4
Intracellular Ca2+ and cell injury: a paradoxical role of Ca2+ in complement membrane attack.细胞内钙离子与细胞损伤:钙离子在补体膜攻击中的矛盾作用。
Cell Calcium. 1986 Dec;7(5-6):399-411. doi: 10.1016/0143-4160(86)90042-4.
5
Complement membrane attack complex, perforin, and bacterial exotoxins induce in K562 cells calcium-dependent cross-protection from lysis.补体膜攻击复合物、穿孔素和细菌外毒素可诱导K562细胞产生对裂解的钙依赖性交叉保护作用。
J Immunol. 1995 Aug 15;155(4):2203-10.
6
Transient changes in erythrocyte membrane permeability are induced by sublytic amounts of the complement membrane attack complex (C5b-9).补体膜攻击复合物(C5b-9)的亚溶解量可诱导红细胞膜通透性的短暂变化。
Blood. 1993 Jan 1;81(1):200-5.
7
Elimination of terminal complement complexes in the plasma membrane of nucleated cells: influence of extracellular Ca2+ and association with cellular Ca2+.有核细胞质膜中末端补体复合物的清除:细胞外Ca2+的影响及其与细胞内Ca2+的关联
J Immunol. 1986 Jul 1;137(1):263-70.
8
Is intracellular Ca2+ the trigger for oxygen radical production by polymorphonuclear leucocytes?细胞内钙离子是多形核白细胞产生氧自由基的触发因素吗?
Cell Calcium. 1984 Feb;5(1):1-19. doi: 10.1016/0143-4160(84)90150-7.
9
Formation of the Ca2+-activated photoprotein obelin from apo-obelin and mRNA inside human neutrophils.在人类中性粒细胞内由脱辅基腔肠素荧光蛋白和信使核糖核酸形成钙离子激活的腔肠素荧光蛋白。
Biochem J. 1988 May 15;252(1):143-9. doi: 10.1042/bj2520143.
10
Sendai virus causes a rise in intracellular free Ca2+ before cell fusion.仙台病毒在细胞融合前会导致细胞内游离钙离子浓度升高。
Biochem J. 1982 Sep 15;206(3):671-4. doi: 10.1042/bj2060671.

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1
Terminal complement complex deposition on chondrocytes promotes premature senescence in age- and trauma-related osteoarthritis.终末补体复合物在软骨细胞上的沉积会促进与年龄和创伤相关的骨关节炎中的细胞早衰。
Front Immunol. 2025 Jan 14;15:1470907. doi: 10.3389/fimmu.2024.1470907. eCollection 2024.
2
Citrullination of C1-inhibitor as a mechanism of impaired complement regulation in rheumatoid arthritis.瓜氨酸化 C1 抑制剂作为类风湿关节炎中补体调节受损的机制。
Front Immunol. 2023 Jun 22;14:1203506. doi: 10.3389/fimmu.2023.1203506. eCollection 2023.
3
Increased plasma level of terminal complement complex in AMD patients: potential functional consequences for RPE cells.AMD 患者血浆末端补体复合物水平升高:对 RPE 细胞的潜在功能影响。
Front Immunol. 2023 Jun 8;14:1200725. doi: 10.3389/fimmu.2023.1200725. eCollection 2023.
4
The neoepitope of the complement C5b-9 Membrane Attack Complex is formed by proximity of adjacent ancillary regions of C9.补体 C5b-9 膜攻击复合物的新表位是由相邻 C9 辅助区域的邻近形成的。
Commun Biol. 2023 Jan 13;6(1):42. doi: 10.1038/s42003-023-04431-y.
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Complement membrane attack complex is an immunometabolic regulator of NLRP3 activation and IL-18 secretion in human macrophages.补体膜攻击复合物是人类巨噬细胞中 NLRP3 活化和 IL-18 分泌的免疫代谢调节剂。
Front Immunol. 2022 Sep 27;13:918551. doi: 10.3389/fimmu.2022.918551. eCollection 2022.
6
Accommodation in allogeneic and xenogeneic organ transplantation: Prevalence, impact, and implications for monitoring and for therapeutics.同种异体和异种器官移植中的适应现象:发生率、影响以及对监测和治疗的意义。
Hum Immunol. 2023 Jan;84(1):5-17. doi: 10.1016/j.humimm.2022.08.001. Epub 2022 Oct 14.
7
Evaluation of pH and calcium ion release at the simulated external root resorption cavities of teeth obturated with bioceramic sealer.评价用生物陶瓷封闭剂封闭的牙齿模拟外部根管吸收腔的 pH 值和钙离子释放情况。
Clin Exp Dent Res. 2022 Aug;8(4):900-905. doi: 10.1002/cre2.573. Epub 2022 Apr 6.
8
COVID-19, Pre-Eclampsia, and Complement System.COVID-19、子痫前期与补体系统
Front Immunol. 2021 Nov 17;12:775168. doi: 10.3389/fimmu.2021.775168. eCollection 2021.
9
Therapeutic Targeting of the Complement System: From Rare Diseases to Pandemics.补体系统的治疗靶向:从罕见病到流行病。
Pharmacol Rev. 2021 Apr;73(2):792-827. doi: 10.1124/pharmrev.120.000072.
10
Rheumatoid arthritis and citrullination.类风湿关节炎与瓜氨酸化。
Curr Opin Rheumatol. 2018 Jan;30(1):72-78. doi: 10.1097/BOR.0000000000000452.

本文引用的文献

1
Studies on the fibrinogen, dextran and phytohemagglutinin methods of isolating leukocytes.关于纤维蛋白原、右旋糖酐和植物血凝素分离白细胞方法的研究。
Blood. 1956 May;11(5):436-54.
2
Release of arachidonic acid: a new function of the late complement components.花生四烯酸的释放:补体晚期成分的一项新功能。
Immunobiology. 1984 May;166(4-5):473-83. doi: 10.1016/S0171-2985(84)80024-8.
3
Consequences of cell membrane attack by complement: release of arachidonate and formation of inflammatory derivatives.补体对细胞膜攻击的后果:花生四烯酸的释放及炎症衍生物的形成。
Proc Natl Acad Sci U S A. 1983 Nov;80(21):6647-51. doi: 10.1073/pnas.80.21.6647.
4
Measurement of intracellular calcium ions and oxygen radicals in polymorphonuclear leucocyte-erythrocyte 'ghost' hybrids.多形核白细胞-红细胞“空壳”杂交体中细胞内钙离子和氧自由基的测量。
J Physiol. 1983 May;338:537-50. doi: 10.1113/jphysiol.1983.sp014688.
5
Immunolocalization of complement component C9 on necrotic and non-necrotic muscle fibres in myositis using monoclonal antibodies: a primary role of complement in autoimmune cell damage.利用单克隆抗体对肌炎中坏死和非坏死肌纤维上补体成分C9进行免疫定位:补体在自身免疫性细胞损伤中的主要作用
Immunology. 1984 May;52(1):181-8.
6
Direct measurement of the increase in intracellular free calcium ion concentration in response to the action of complement.直接测量细胞内游离钙离子浓度因补体作用而增加的情况。
Biochem J. 1981 Feb 15;194(2):551-60. doi: 10.1042/bj1940551.
7
Immunoaffinity purification of human complement component C9 using monoclonal antibodies.使用单克隆抗体对人补体成分C9进行免疫亲和纯化。
J Immunol Methods. 1983 Nov 25;64(3):269-81. doi: 10.1016/0022-1759(83)90434-9.
8
Humoral immune killing of nucleated cells: mechanisms of complement-mediated attack and target cell defense.
Crit Rev Immunol. 1981 Jan;1(3):165-209.
9
Inositol trisphosphate, a novel second messenger in cellular signal transduction.肌醇三磷酸,细胞信号转导中的一种新型第二信使。
Nature. 1984;312(5992):315-21. doi: 10.1038/312315a0.
10
2-Chloroadenosine inhibits complement-induced reactive oxygen metabolite production and recovery of human polymorphonuclear leucocytes attacked by complement.2-氯腺苷抑制补体诱导的活性氧代谢产物的产生,并促进受到补体攻击的人多形核白细胞的恢复。
Biochem Biophys Res Commun. 1985 Jan 31;126(2):692-7. doi: 10.1016/0006-291x(85)90240-2.

人多形核白细胞从亚溶细胞性补体攻击中的恢复是由细胞内游离钙的变化介导的。

The recovery of human polymorphonuclear leucocytes from sublytic complement attack is mediated by changes in intracellular free calcium.

作者信息

Morgan B P, Campbell A K

出版信息

Biochem J. 1985 Oct 1;231(1):205-8. doi: 10.1042/bj2310205.

DOI:10.1042/bj2310205
PMID:4062885
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1152725/
Abstract

Using polymorphonuclear leucocyte-erythrocyte ghost hybrids entrapping the calcium-activated photoprotein obelin, we have demonstrated that sublytic amounts of the complement membrane attack complex induce a rapid but transient increase in intracellular free calcium ion concentration ([Ca2+]i). This increase in [Ca2+]i occurs prior to, and is required for, rapid removal of membrane attack complexes from the cell surface. The increase in [Ca2+]i is not only due to increased influx from outside the cell, but also results from mobilization of intracellular stores. The possible mechanism of mobilization of calcium, and the importance of an increase in [Ca2+]i as a mediator of recovery processes in nucleated cells, are discussed.

摘要

利用包裹钙激活光蛋白水母发光蛋白的多形核白细胞-红细胞幽灵杂种,我们已经证明,亚溶破量的补体膜攻击复合物会导致细胞内游离钙离子浓度([Ca2+]i)迅速但短暂地升高。[Ca2+]i的这种升高发生在膜攻击复合物从细胞表面快速清除之前,并且是其必要条件。[Ca2+]i的升高不仅是由于细胞外流入增加,还源于细胞内储存的动员。文中讨论了钙动员的可能机制,以及[Ca2+]i升高作为有核细胞恢复过程介质的重要性。