Anti-C3 / C3b抗体[2B10B9B2] (ab106108)

概述

  • 产品名称Anti-C3 / C3b抗体[2B10B9B2]
    参阅全部 C3 / C3b 一抗
  • 描述
    小鼠单克隆抗体[2B10B9B2] to C3 / C3b
  • 特异性ab106108 reacts with an epitope on C3b. It reacts both with intact C3 and C3b.
  • 经测试应用适用于: WB, ELISAmore details
    不适用于: IP
  • 种属反应性
    与反应: Rat
  • 免疫原

    Rat C3/ C3b

性能

应用

Our Abpromise guarantee covers the use of ab106108 in the following tested applications.

The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.

应用 Ab评论 说明
WB 1/50. Predicted molecular weight: 187 kDa.
ELISA 1/50.
  • 应用说明Is unsuitable for IP.
  • 靶标

    • 功能C3 plays a central role in the activation of the complement system. Its processing by C3 convertase is the central reaction in both classical and alternative complement pathways. After activation C3b can bind covalently, via its reactive thioester, to cell surface carbohydrates or immune aggregates.
      Derived from proteolytic degradation of complement C3, C3a anaphylatoxin is a mediator of local inflammatory process. It induces the contraction of smooth muscle, increases vascular permeability and causes histamine release from mast cells and basophilic leukocytes.
    • 组织特异性Plasma.
    • 疾病相关Defects in C3 are the cause of complement component 3 deficiency (C3D) [MIM:613779]. A rare defect of the complement classical pathway. Patients develop recurrent, severe, pyogenic infections because of ineffective opsonization of pathogens. Some patients may also develop autoimmune disorders, such as arthralgia and vasculitic rashes, lupus-like syndrome and membranoproliferative glomerulonephritis.
      Genetic variation in C3 is associated with susceptibility to age-related macular degeneration type 9 (ARMD9) [MIM:611378]. ARMD is a multifactorial eye disease and the most common cause of irreversible vision loss in the developed world. In most patients, the disease is manifest as ophthalmoscopically visible yellowish accumulations of protein and lipid that lie beneath the retinal pigment epithelium and within an elastin-containing structure known as Bruch membrane.
      Defects in C3 are a cause of susceptibility to hemolytic uremic syndrome atypical type 5 (AHUS5) [MIM:612925]. An atypical form of hemolytic uremic syndrome. It is a complex genetic disease characterized by microangiopathic hemolytic anemia, thrombocytopenia, renal failure and absence of episodes of enterocolitis and diarrhea. In contrast to typical hemolytic uremic syndrome, atypical forms have a poorer prognosis, with higher death rates and frequent progression to end-stage renal disease. Note=Susceptibility to the development of atypical hemolytic uremic syndrome can be conferred by mutations in various components of or regulatory factors in the complement cascade system. Other genes may play a role in modifying the phenotype.
    • 序列相似性Contains 1 anaphylatoxin-like domain.
      Contains 1 NTR domain.
    • 翻译后修饰C3b is rapidly split in two positions by factor I and a cofactor to form iC3b (inactivated C3b) and C3f which is released. Then iC3b is slowly cleaved (possibly by factor I) to form C3c (beta chain + alpha' chain fragment 1 + alpha' chain fragment 2), C3dg and C3f. Other proteases produce other fragments such as C3d or C3g.
      Phosphorylation sites are present in the extracelllular medium.
    • 细胞定位Secreted.
    • Information by UniProt
    • 数据库链接
    • 别名
      • Acylation-stimulating protein cleavage product antibody
      • AHUS5 antibody
      • ARMD9 antibody
      • ASP antibody
      • C3 and PZP-like alpha-2-macroglobulin domain-containing protein 1 antibody
      • C3 antibody
      • CO3_HUMAN antibody
      • Complement C3 antibody
      • Complement C3 beta chain antibody
      • Complement C3c alpha' chain fragment 2 antibody
      • Complement component 3 antibody
      • Complement component C3 antibody
      • Complement factor 3 antibody
      • CPAMD1 antibody
      • Plp antibody
      see all

    Anti-C3 / C3b antibody [2B10B9B2] (ab106108)参考文献

    ab106108 has not yet been referenced specifically in any publications.

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