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Activation of the alternative complement pathway: recognition of surface structures on activators by bound C3b.

作者信息

Pangburn M K, Morrison D C, Schreiber R D, Müller-Eberhard H J

出版信息

J Immunol. 1980 Feb;124(2):977-82.

PMID:7356723
Abstract
摘要

相似文献

1
Activation of the alternative complement pathway: recognition of surface structures on activators by bound C3b.替代补体途径的激活:结合的C3b识别激活物上的表面结构。
J Immunol. 1980 Feb;124(2):977-82.
2
Functional discrimination by human monocytes between their C3b receptors and their recognition units for particulate activators of the alternative complement pathway.人类单核细胞对其C3b受体与其替代补体途径颗粒激活剂识别单位之间的功能区分。
J Immunol. 1980 Jul;125(1):124-8.
3
Effect of gangliosides on activation of the alternative pathway of human complement.神经节苷脂对人补体替代途径激活的影响。
J Immunol. 1988 Mar 1;140(5):1581-7.
4
Capsular sialic acid prevents activation of the alternative complement pathway by type III, group B streptococci.荚膜唾液酸可防止B族Ⅲ型链球菌激活替代补体途径。
J Immunol. 1982 Mar;128(3):1278-83.
5
Development and application of an enzyme-linked immunosorbent assay for the quantitation of alternative complement pathway activation in human serum.一种用于定量检测人血清中替代补体途径激活的酶联免疫吸附测定法的开发与应用。
J Clin Invest. 1984 Jan;73(1):160-70. doi: 10.1172/JCI111187.
6
Induction of granulocyte histaminase release by particle-bound complement C3 cleavage products (C3b, C3bi) and IgG.颗粒结合的补体C3裂解产物(C3b、C3bi)和IgG诱导粒细胞组胺酶释放。
J Immunol. 1983 Jul;131(1):439-44.
7
Human alternative complement pathway: membrane-associated sialic acid regulates the competition between B and beta1 H for cell-bound C3b.人类替代补体途径:膜相关唾液酸调节B因子和β1H因子对细胞结合C3b的竞争。
J Immunol. 1979 Jan;122(1):75-81.
8
[Progress in the knowledge of complement. I. Structure, activation and control of the complement system].[补体知识的进展。I. 补体系统的结构、激活与调控]
Nouv Presse Med. 1979 Jun 30;8(29):2385-7.
9
Erythrocyte-bound complement components in health and disease.健康与疾病状态下红细胞结合的补体成分
Prog Clin Biol Res. 1980;43:133-55.
10
Guinea pig erythrocytes, after their contact with influenza virus, acquire the ability to activate the human alternative complement pathway through virus-induced desialation of the cells.豚鼠红细胞在与流感病毒接触后,通过病毒诱导的细胞去唾液酸化作用,获得激活人类替代补体途径的能力。
J Immunol. 1982 Feb;128(2):629-34.

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Front Plant Sci. 2019 Mar 20;10:260. doi: 10.3389/fpls.2019.00260. eCollection 2019.
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The properdin pathway: an "alternative activation pathway" or a "critical amplification loop" for C3 and C5 activation?备解素途径:C3 和 C5 激活的“替代激活途径”还是“关键扩增环”?
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C5a induces caspase-dependent apoptosis in brain vascular endothelial cells in experimental lupus.
在实验性狼疮中,C5a可诱导脑血管内皮细胞发生半胱天冬酶依赖性凋亡。
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Mouse Cd59b but not Cd59a is upregulated to protect cells from complement attack in response to inflammatory stimulation.小鼠的Cd59b而非Cd59a会在炎症刺激下上调,以保护细胞免受补体攻击。
Genes Immun. 2015 Oct;16(7):437-45. doi: 10.1038/gene.2015.29. Epub 2015 Jul 23.
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Identification of a novel mode of complement activation on stimulated platelets mediated by properdin and C3(H2O).鉴定补体在受刺激血小板上通过备解素和 C3(H2O)介导的新型激活方式。
J Immunol. 2013 Jun 15;190(12):6457-67. doi: 10.4049/jimmunol.1300610. Epub 2013 May 15.
6
Local release of properdin in the cellular microenvironment: role in pattern recognition and amplification of the alternative pathway of complement.局部固有因子在细胞微环境中的释放:在补体替代途径的模式识别和放大中的作用。
Front Immunol. 2013 Jan 17;3:412. doi: 10.3389/fimmu.2012.00412. eCollection 2012.
7
Translational mini-review series on complement factor H: renal diseases associated with complement factor H: novel insights from humans and animals.补体因子H相关的转化性小型综述系列:与补体因子H相关的肾脏疾病——来自人类和动物的新见解
Clin Exp Immunol. 2008 Feb;151(2):210-30. doi: 10.1111/j.1365-2249.2007.03574.x.
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Disruption of the C5a receptor gene increases resistance to acute Gram-negative bacteremia and endotoxic shock: opposing roles of C3a and C5a.C5a受体基因的破坏增加了对急性革兰氏阴性菌血症和内毒素休克的抵抗力:C3a和C5a的相反作用。
Mol Immunol. 2008 Apr;45(7):1907-15. doi: 10.1016/j.molimm.2007.10.037. Epub 2007 Dec 11.
9
Hypercomplementemia in adult patients with IgA nephropathy.成年IgA肾病患者的补体血症过高
J Clin Lab Anal. 2007;21(2):77-84. doi: 10.1002/jcla.20154.
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Binding of complement factor H to endothelial cells is mediated by the carboxy-terminal glycosaminoglycan binding site.补体因子H与内皮细胞的结合是由羧基末端糖胺聚糖结合位点介导的。
Am J Pathol. 2005 Oct;167(4):1173-81. doi: 10.1016/S0002-9440(10)61205-9.