Membrane attack by complement: the assembly and biology of terminal complement complexes.
Membrane attack by complement: the assembly and biology of terminal complement complexes.
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DOI：
10.1007/s12026-011-8239-5
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发表时间：
2011-10
影响因子：
4.4
通讯作者：
Rus, Horea
中科院分区：
文献类型：
--
作者：
Tegla, Cosmin A.;Cudrici, Cornelia;Patel, Snehal;Trippe, Richard, III;Rus, Violeta;Niculescu, Florin;Rus, Horea
关键词：
补体系统激活在先天免疫和获得性免疫中都起着重要作用。补体的激活和随后在细胞膜上形成的C5b-9通道（膜攻击复合物）导致细胞死亡。然而，当有核细胞表面聚集的通道数量有限时，亚裂解C5b-9可通过激活信号转导通路和转录因子，抑制细胞凋亡，从而诱导细胞周期进程。C5b-9的这种诱导依赖于磷脂酰肌醇3-激酶/Akt/ fox01和ERK1通路的激活，以Gi蛋白依赖的方式。C5b-9诱导CDK4和CDK2的顺序激活，使G1/ s期转变和细胞增殖成为可能。此外，它还诱导了RGC-32，这是一种通过与Akt和cyclin B1-CDC2复合物相互作用在细胞周期激活中起作用的新基因。C5b-9还通过诱导Bad磷酸化和阻断FLIP、caspase-8和Bid切割的激活来抑制细胞凋亡。因此，亚裂解C5b-9在细胞活化、增殖和分化中起着重要作用，从而有助于维持细胞和组织的稳态。
Complement system activation plays an important role in both innate and acquired immunity. Activation of complement and the subsequent formation of C5b-9 channels (the membrane attack complex) on cell membranes lead to cell death. However, when the number of channels assembled on the surface of nucleated cells is limited, sublytic C5b-9 can induce cell cycle progression by activating signal transduction pathways and transcription factors and inhibiting apoptosis. This induction by C5b-9 is dependent upon the activation of the phosphatidylinositol 3-kinase/Akt/FOXO1 and ERK1 pathways in a Gi protein-dependent manner. C5b-9 induces sequential activation of CDK4 and CDK2, enabling the G1/S-phase transition and cellular proliferation. In addition, it induces RGC-32, a novel gene that plays a role in cell cycle activation by interacting with Akt and the cyclin B1-CDC2 complex. C5b-9 also inhibits apoptosis by inducing the phosphorylation of Bad and blocking the activation of FLIP, caspase-8, and Bid cleavage. Thus, sublytic C5b-9 plays an important role in cell activation, proliferation, and differentiation, thereby contributing to the maintenance of cell and tissue homeostasis.
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DOI：
10.1152/ajprenal.00100.2003
发表时间：
2003-10-01
影响因子：
4.2
作者：
Aoudjit, L;Stanciu, M;Takano, T
通讯作者：
Takano, T
影响因子：
15.3
作者：
BIESECKER, G;KATZ, S;KOFFLER, D
通讯作者：
KOFFLER, D
影响因子：
158.5
作者：
BIESECKER, G;LAVIN, L;KOFFLER, D
通讯作者：
KOFFLER, D
影响因子：
11.2
作者：
Breij, Esther C. W.;Brink, Bianca P.;Boe, Lars
通讯作者：
Boe, Lars
影响因子：
4.7
作者：
Dashiell, SM;Koski, CL
通讯作者：
Koski, CL