货号 |
bs-15197R-1 |
品牌 |
|
浓度 |
|
货期 |
现货 |
英文名称 |
Rabbit Anti-C5 antibody |
中文名称 |
Rabbit Anti-C5 antibody |
研究领域 |
细胞生物,免疫学,新陈代谢, |
英文别名 |
Anaphylatoxin C5a analog; C3 and PZP-like alpha-2-macroglobulin domain-containing protein 4; C5; C5a; CO5_HUMAN; Complement C5 alpha'' chain; Complement C5; Complement component C5; CPAMD4. |
反应物种(已验证) |
Human |
反应物种(预测) |
Mouse,Rat |
产品应用(已验证) |
WB,FCM |
产品应用(可推荐) |
ELISA |
推荐稀释比例 |
WB=1:500-2000,Elisa=1:5000-10000,Flow Cyt=2ug/Test, |
克隆类型 |
多克隆 |
抗体来源 |
Rabbit |
理论分子量 |
104/112 |
细胞定位 |
分泌型蛋白 |
性状 |
Liquid |
免疫原 |
KLH conjugated synthetic peptide derived from human C5 |
抗原表位 |
951-1100/1676 |
亚型 |
IgG |
纯化方法 |
affinity purified by Protein A |
SUBCELLULAR |
Secreted. |
SIMILARITY |
Contains 1 anaphylatoxin-like domain.
Contains 1 NTR domain. |
SUBUNIT |
C5 precursor is first processed by the removal of 4 basic residues, forming two chains, beta and alpha, linked by a disulfide bond. C5 convertase activates C5 by cleaving the alpha chain, releasing C5a anaphylatoxin and generating C5b (beta chain + alpha' |
Function |
Activation of C5 by a C5 convertase initiates the spontaneous assembly of the late complement components, C5-C9, into the membrane attack complex. C5b has a transient binding site for C6. The C5b-C6 complex is the foundation upon which the lytic complex i |
DISEASE |
Defects in C5 are the cause of complement component 5 deficiency (C5D) [MIM:609536]. A rare defect of the complement classical pathway associated with susceptibility to severe recurrent infections, predominantly by Neisseria gonorrhoeae or Neisseria menin |
SWISS |
P02748 |
Gene ID |
727 |
保存条件 |
Shipped at 4℃. Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. |
Important Note |
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. |
英文介绍 |
The complement component proteins: C2, C3, C4 and C5 are potent anaphyl-atoxins that are released during complement activation. Binding of these proteins to their respective G protein-coupled receptors, C3aR, C1R and C5aR, induces proinflammatory events, such as cellular degranulation, smooth muscle contraction, arachidonic acid metabolism, cytokine release, leukocyte activation and cellular chemotaxis. Activation of the complement system leads to the formation of C5b-9 terminal complex, and while C5b-9 can promote cell lysis, the sublytic assembly of C5b-9 on plasma membranes causes an opposite result and induces cell cycle activation and survival. C5b-9 can rescue oligodendrocytes from FAS-mediated apoptosis by regulating caspase-8 processing via PI 3-K signaling. C5b-9 may play a pro-inflammatory role in the acute phase of multiple sclerosis, but may also be neuroprotective during the chronic phase of the disease. Complement C5 precursor contains C5a anaphylatoxin. C3a and C5a secretion correlates with pathophysiological phenotypes such as asthma and bacterial meningitis. |