FITC Anti-C3c antibody (ab4212)
Key features and details
- FITC Rabbit polyclonal to C3c
- Suitable for: ICC/IF
- Reacts with: Human
- Conjugation: FITC. Ex: 493nm, Em: 528nm
- Isotype: IgG
Overview
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Product name
FITC Anti-C3c antibody
See all C3c primary antibodies -
Description
FITC Rabbit polyclonal to C3c -
Host species
Rabbit -
Conjugation
FITC. Ex: 493nm, Em: 528nm -
Specificity
This antibody reacts with human C3c complement and with the C3c part of C3 and C3b. -
Tested applications
Suitable for: ICC/IFmore details -
Species reactivity
Reacts with: Human
Predicted to work with: Mouse, Rat, Sheep, Goat, Guinea pig, Cow, Cat, Dog, Pig, Kangaroo, Mink
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Immunogen
C3c complement isolated from complement activated human serum.
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General notes
Fluorescein isothiocyanate (FITC) isomer 1.
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Properties
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Form
Liquid -
Storage instructions
Shipped at 4°C. Store at +4°C. -
Storage buffer
Preservative: 0.05% Sodium azide
Constituent: 1% BSA -
Concentration information loading... -
Purity
IgG fraction -
Purification notes
Traces of contaminating antibodies have been removed by solid phase absorption with human plasma proteins. -
Clonality
Polyclonal -
Isotype
IgG -
Research areas
Associated products
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Isotype control
Applications
The Abpromise guarantee
Our Abpromise guarantee covers the use of ab4212 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
| Application | Abreviews | Notes |
|---|---|---|
| ICC/IF |
Use a concentration of 1 µg/ml.
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| Notes |
|---|
|
ICC/IF
Use a concentration of 1 µg/ml. |
Target
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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
modificationsC3b 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
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Database links
- Entrez Gene: 476728 Dog
- Entrez Gene: 718 Human
- Entrez Gene: 12266 Mouse
- Entrez Gene: 397072 Pig
- Entrez Gene: 24232 Rat
- Omim: 120700 Human
- SwissProt: P01024 Human
- SwissProt: P01027 Mouse
see all -
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
Images
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Immunocytochemistry/ Immunofluorescence - FITC Anti-C3c antibody (ab4212)
ICC/IF image of ab4212 stained HepG2 cells. The cells were 4% formaldehyde fixed (10 min) and then incubated in 1%BSA / 10% normal goat serum / 0.3M glycine in 0.1% PBS-Tween for 1h to permeabilise the cells and block non-specific protein-protein interactions. The cells were then incubated with the antibody (ab4212, 1µg/ml) overnight at +4°C. Alexa Fluor® 594 WGA was used to label plasma membranes (red) at a 1/200 dilution for 1h. DAPI was used to stain the cell nuclei (blue) at a concentration of 1.43µM.
Protocols
Datasheets and documents
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SDS download
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Datasheet download
References (6)
ab4212 has been referenced in 6 publications.
- Pan T et al. Circulating Heme Oxygenase-1 and Complement Activation in Transplant-Associated Thrombotic Microangiopathy. Biol Blood Marrow Transplant N/A:N/A (2019). PubMed: 30871975
- Ispasanie E et al. Spontaneous point mutations in the capsule synthesis locus leading to structural and functional changes of the capsule in serogroup A meningococcal populations. Virulence 9:1138-1149 (2018). PubMed: 30067453
- Noone DG et al. Von Willebrand factor regulates complement on endothelial cells. Kidney Int 90:123-34 (2016). PubMed: 27236750
- Bahia El Idrissi N et al. Complement activation at the motor end-plates in amyotrophic lateral sclerosis. J Neuroinflammation 13:72 (2016). PubMed: 27056040
- Zhang Y et al. Effect of the glycosyltransferases on the capsular polysaccharide synthesis of Streptococcus suis serotype 2. Microbiol Res 185:45-54 (2016). PubMed: 26946377
- Kim SJ et al. Intravitreal human complement factor H in a rat model of laser-induced choroidal neovascularisation. Br J Ophthalmol 97:367-70 (2013). Rat . PubMed: 23258212