出典: meddic

C3aアナフィラトキシン C3a anaphylatoxin


活性はC5aの約1/200 (SMB.35)

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出典(authority):フリー百科事典『ウィキペディア(Wikipedia)』「2013/01/19 13:10:53」(JST)

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  • G protein coupled receptor specificity for C3a and compound 48/80-induced degranulation in human mast cells: Roles of Mas-related genes MrgX1 and MrgX2.
  • Kashem SW, Subramanian H, Collington SJ, Magotti P, Lambris JD, Ali H.AbstractAlthough human mast cells express G protein coupled receptors for the anaphylatoxin C3a, previous studies indicated that C3a causes mast cell degranulation, at least in part, via a C3a receptor-independent mechanism similar to that proposed for polycationic molecules such as compound 48/80. The purpose of the present study was to delineate the receptor specificity of C3a-induced degranulation in human mast cells. We found that C3a, a C3a receptor "superagonist" (E7) and compound 48/80 induced Ca(2+) mobilization and degranulation in a differentiated human mast cell line, LAD2. However, C3a and E7 caused Ca(2+) mobilization in an immature mast cell line, HMC-1 but compound 48/80 did not. We have previously shown that LAD2 cells express MrgX1 and MrgX2 but HMC-1 cells do not. To delineate the receptor specificity for C3a and compound 48/80 further, we generated stable transfectants expressing MrgX1 and MrgX2 in a rodent mast cell line, RBL-2H3 cells. We found that compound 48/80 caused degranulation in RBL-2H3 cells expressing MrgX1 and MrgX2 but C3a did not. By contrast, E7 activated RBL-2H3 cells expressing MrgX2 but not MrgX1. These findings demonstrate that in contrast to previous reports, C3a and compound 48/80 do not use a shared mechanism for mast cell degranulation. It shows that while compound 48/80 utilizes MrgX1 and MrgX2 for mast cell degranulation C3a does not. It further reveals the novel finding that the previously characterized synthetic peptide, C3a receptor "superagonist" E7 activates human mast cells via two mechanisms; one involving the C3a receptor and the other MrgX2.
  • European journal of pharmacology.Eur J Pharmacol.2011 Oct 1;668(1-2):299-304. Epub 2011 Jul 3.
  • Although human mast cells express G protein coupled receptors for the anaphylatoxin C3a, previous studies indicated that C3a causes mast cell degranulation, at least in part, via a C3a receptor-independent mechanism similar to that proposed for polycationic molecules such as compound 48/80. The purp
  • PMID 21741965
  • Cellular glutathione in fatty liver in vitro models.
  • Garcia MC, Amankwa-Sakyi M, Flynn TJ.SourceFDA, Center for Food Safety and Applied Nutrition, Division of Toxicology, Laurel, MD 20708, United States.
  • Toxicology in vitro : an international journal published in association with BIBRA.Toxicol In Vitro.2011 Oct;25(7):1501-6. Epub 2011 May 17.
  • The range of non-alcoholic fatty liver disease (NAFLD) includes simple hepatic steatosis, the inflammatory non-alcoholic steatohepatitis (NASH), fibrosis and cirrhosis. The accumulation of specific lipids in hepatocytes has been associated with oxidative stress and progression of the disease. Elevat
  • PMID 21620948


  • 被粉砕性の異なる石灰石微粉末を混和したC3A相高含有セメントの流動性
  • 荻野 正貴,新 大軌,丸屋 英二 [他]
  • セッコウ・石灰・セメント・地球環境の科学 18(351), 70-74, 2011-03
  • NAID 40018733585
  • Synthetic Studies on (+)-Biotin, Part 15: A Chiral Squaramide-Mediated Enantioselective Alcoholysis Approach toward the Total Synthesis of (+)-Biotin
  • Chen Xu-Xiang,Xiong Fei,Fu Han,Liu Zhi-Qian,Chen Fen-Er
  • An efficient stereocontrolled total synthesis of (+)-biotin (1) has been achieved via the intermediacy of Roches lactone 5 starting from cis-1,3-dibenzyl-2-imidazole-4,5-dicarboxylic acid (2). The bif …
  • NAID 130000648970


C3a is a one of the proteins formed by the cleavage of complement component 3; the other is C3b. It stimulates mast cell degranulation, thus triggering an immune response. C3a plays an important role in chemotaxis, though not as important a ...


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拡張検索C3a complement



アレキシン alexin

  • 図:IMM.63
pathway start first step
classical pathway antigen-antibody complex C1q, C1r, C1s, C4, C2
lectin pathway mannose-binding lectin or ficolin binds carbohydrate on pathogen surface MBL/ficolin, MASP-2, C4, C2
alternative pathway pathogen surface C3, B, D

補体の相互作用 IMM.62

  • C1qがカスケードの最初となる。3つの方法で補体カスケードがはじまる。
  • (1)多価陰イオン表面(例えば、グラム陰性細菌のリポテイコ酸)
  • (2)バクテリアの多糖のホスホコリンに結合(例えば肺炎球菌のC蛋白質)
  • (3)抗原抗体複合体に結合して自然免疫と獲得免疫のエフェクター機構を結びつける。
  • 炭化水素鎖を認識するレクチンがカスケードの最初となる。
  • C3からはじまる。血漿中のC3が病原体の表面で自発的に活性化されることで補体反応がはじまる。
3つの経路は共通してC3 convertaseを生成。C3 convertaseはC3→C3a+C3b
C3a: C3a is a peptide mediator of local inflammation
C3b: C3b binds covalently to the bacterial cell membrane and opsonizes the bacteria
C5 convertaseはC3bにC3 convertaseが結合してできる
C5 converaseはC5→C5a+C5b
C5a: powerful peptide mediator of inflammation
C5b: C5b,C6,C7,C8,C9: membrane-attack complex


  • C5a,C3a,C4a: smooth muscle contraction.(IMM.75)
  • C5a,C3a: act on the endo thelial cells lining blood vessels to induce adhesion molecules.(IMM.75)
  • C5a>C3a>C4a: increase in blood flow, increase vascular permeability, increase binding of phagocytes to exdothielial cells.(IMM.76)
  • C5a: activates mast cells to release mediators, such as histamine and TNF-α. that contribute the inflammatory response(IMM.76).
  • C5a: acts directly on neutrophils and monocytes and attracting neutrophils and monocytes(IMM.75)
  • C3a: contributes to the pypotension and edema seen in endotoxic shock
  • C5a: activated by endotoxin, funcions in neutrophil chemotaxis



  • 増加:



factor D, D
第二経路C3, C3b, B, C3bBb, C3a

C3a complement」



complement C3a



WordNet   license wordnet

「the 3rd letter of the Roman alphabet」

WordNet   license wordnet

「(music) the keynote of the scale of C major」

WordNet   license wordnet

「a general-purpose programing language closely associated with the UNIX operating system」

PrepTutorEJDIC   license prepejdic




補体第三成分 third component of complement
補体C3a, C3b
  • 補体の一つ
  • C3は血清中に最も多く存在する
  • C3 convertaseによってC3aC3bを生じる
  • C3 convertase活性を持つのは2つ
1. C4bC2a (古典的経路)
2. C3bBbP (別経路)

"http://meddic.jp/C3a" より作成