Anti-C3d antibody [7C10] (ab17453)
Key features and details
- Mouse monoclonal [7C10] to C3d
- Suitable for: IHC
- Reacts with: Human
- Isotype: IgG1
Overview
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Product name
Anti-C3d antibody [7C10]
See all C3d primary antibodies -
Description
Mouse monoclonal [7C10] to C3d -
Host species
Mouse -
Specificity
This product is specific to C3d, but also C3b and iC3b, since C3d is a product from C3b.
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Tested applications
Suitable for: IHCmore details -
Species reactivity
Reacts with: Human -
Immunogen
Full length native protein (purified) corresponding to Human C3d.
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Epitope
Epitope specificity differs from that of ab17455. -
Positive control
- IHC-P: Human kidney tissue.
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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
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Form
Liquid -
Storage instructions
Shipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C. Avoid freeze / thaw cycle. -
Storage buffer
pH: 7.40
Preservative: 0.098% Sodium azide
Constituents: PBS, 2.9% Sodium chloride -
Concentration information loading...
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Purity
Protein A purified -
Clonality
Monoclonal -
Clone number
7C10 -
Myeloma
x63-Ag8.653 -
Isotype
IgG1 -
Light chain type
kappa -
Research areas
Associated products
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Alternative Versions
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Compatible Secondaries
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Conjugation kits
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Isotype control
Applications
The Abpromise guarantee
Our Abpromise guarantee covers the use of ab17453 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 |
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IF |
1/10.
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IHC |
1/10.
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Notes |
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IF
1/10. |
IHC
1/10. |
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: 718 Human
- Omim: 120700 Human
- SwissProt: P01024 Human
- Unigene: 529053 Human
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Alternative names
- Acylation stimulating protein cleavage product antibody
- AHUS5 antibody
- ARMD9 antibody
see all
Images
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Immunohistochemical analysis of human kidney labelling C3d with ab17453 at a dilution of 1/10. Plasma of veins were stained strongly.
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Immunofluorescent analysis of human kidney labelling C3d with ab17453 at a dilution of 1/10. Plasma of veins were stained strongly.
Datasheets and documents
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SDS download
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Datasheet download
References (11)
ab17453 has been referenced in 11 publications.
- Werneburg S et al. Targeted Complement Inhibition at Synapses Prevents Microglial Synaptic Engulfment and Synapse Loss in Demyelinating Disease. Immunity 52:167-182.e7 (2020). PubMed: 31883839
- Petrosyan A et al. A glomerulus-on-a-chip to recapitulate the human glomerular filtration barrier. Nat Commun 10:3656 (2019). PubMed: 31409793
- Battin C et al. Neuropilin-1 Acts as a Receptor for Complement Split Products. Front Immunol 10:2209 (2019). PubMed: 31572401
- Pathak A et al. Factor H binding proteins protect division septa on encapsulated Streptococcus pneumoniae against complement C3b deposition and amplification. Nat Commun 9:3398 (2018). PubMed: 30139996
- Hu C et al. Complement Inhibitor CRIg/FH Ameliorates Renal Ischemia Reperfusion Injury via Activation of PI3K/AKT Signaling. J Immunol 201:3717-3730 (2018). PubMed: 30429287