FITC Anti-C3c antibody (ab182890) | Abcam (2024)

Overview

• Product name

  FITC Anti-C3c antibody
  See all C3c primary antibodies

• Description

  FITC Goat polyclonal to C3c

  See Also

  Anti-Complement C3 Antibodies | InvitrogenC3 Goat Polyclonal Antibody – AP21439FC-NLife Science & Diagnostic Research Tools | MP Biomedicals | 安倍医疗器械贸易（上海）有限公司官网

• Host species

  Goat

• Conjugation

  FITC. Ex: 493nm, Em: 528nm

• Specificity

  Fluorescein isothiocyanate-conjugated IgG fraction of polyclonal Goat antiSerum to C3c fragment of Rat complement factor C3.

  The antiSerum does not cross-react with any other component of Rat plasma. Inter-species cross-reactivity is a normal feature of antibodies to plasma proteins since they frequently share antigenic determinants. Cross-reactivity of this antiSerum has not been tested in detail

• Tested applications

  Suitable for: ELISA, IHC-Fr, ICC, ICC/IFmore details

• Species reactivity

  Reacts with: Rat
  

• Immunogen

  Full length native protein (purified) corresponding to Rat C3c. C3c is isolated and purified from pooled normal rat serum.
  Database link: P01026

• General notes

  The Life Science industry has been in the grips of a reproducibility crisis for a number of years. Abcam is leading the way in addressing this with our range of recombinant monoclonal antibodies and knockout edited cell lines for gold-standard validation. Please check that this product meets your needs before purchasing.

  If you have any questions, special requirements or concerns, please send us an inquiry and/or contact our Support team ahead of purchase. Recommended alternatives for this product can be found below, along with publications, customer reviews and Q&As

Properties

• Form

  Lyophilized:Add 1 ml sterile distilled water.Concentration is reconstitution Dependent. If reconstituted to 1 ml as instructed, final concentration will be 10.3 mg/ml.

• Storage instructions

  Shipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C or -80°C. Avoid freeze / thaw cycle. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour. Store In the Dark.

• Storage buffer

  pH: 7.20
  Constituent: 100% PBS

• Concentration information loading...

• Purity

  IgG fraction

• Clonality

  Polyclonal

• Isotype

  IgG

• Research areas

  • Immunology
  • Innate Immunity
  • Complement
  • Classical Pathway

  • Immunology
  • Innate Immunity
  • Complement
  • Alternative Pathway

Associated products

• Isotype control

  • FITC Goat IgG - Isotype control (ab37374)

Applications

Target

• Function

  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.

• Tissue specificity

  Plasma.

• Involvement in disease

  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.

• Sequence similarities

  Contains 1 anaphylatoxin-like domain.
  Contains 1 NTR domain.

• Post-translational
  modifications

  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.

• Cellular localization

  Secreted.

• Information by UniProt

• Database links

  • Entrez Gene: 24232 Rat
  • SwissProt: P01026 Rat
  • Unigene: 11378 Rat

• Form

  Cleaved into the following 10 chains:1) Complement C3 beta chain 2) Complement C3 alpha chain 3) C3a anaphylatoxin 4) Complement C3b alpha' chain 5) Complement C3c alpha' chain fragment 1 6) Complement C3dg fragment 7) Complement C3g fragment 8) Complement C3d fragment 9) Complement C3f fragment 10) Complement C3c alpha' chain fragment 2

• Alternative names

  • acylation-stimulating protein cleavage product antibody
  • AHUS5 antibody
  • ARMD9 antibody

  see all

Protocols

Datasheets and documents

References (0)