Anti-C4d antibody [LP69] (ab167093)
- Datasheet
- References (2)
- Protocols
Overview
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Product nameAnti-C4d antibody [LP69]
See all C4d primary antibodies -
DescriptionMouse monoclonal [LP69] to C4d
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Host speciesMouse
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Specificityab167093 reacts with an antigenic determinant in the C4d domain of C4.
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Tested applicationsSuitable for: IHC-Fr, IHC-Pmore details
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Species reactivityReacts with: Human
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Immunogen
Complement C4d from normal Human plasma.
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Positive control
- Kidney transplant rejection tissue.
Properties
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FormLiquid
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Storage instructionsShipped at 4°C. Upon delivery aliquot and store at -20°C or -80°C. Avoid repeated freeze / thaw cycles.
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Storage bufferPreservative: 0.065% Sodium azide
Constituent: 99% PBS -
Concentration information loading...
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PurityProtein G purified
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ClonalityMonoclonal
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Clone numberLP69
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IsotypeIgG1
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Research areas
Associated products
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Alternative Versions
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Compatible Secondaries
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Isotype control
Applications
Our Abpromise guarantee covers the use of ab167093 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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IHC-Fr | Use at an assay dependent concentration. | |
IHC-P | 1/25. |
Target
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FunctionC4 plays a central role in the activation of the classical pathway of the complement system. It is processed by activated C1 which removes from the alpha chain the C4a anaphylatoxin. The remaining alpha chain fragment C4b is the major activation product and is an essential subunit of the C3 convertase (C4b2a) and the C5 convertase (C3bC4b2a) enzymes of the classical complement pathway.
Derived from proteolytic degradation of complement C4, C4a 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. -
Involvement in diseaseDefects in C4A are the cause of complement component 4A deficiency (C4AD) [MIM:120810]. A rare defect of the complement classical pathway associated with the development of autoimmune disorders, mainly systemic lupus with or without associated glomerulonephritis.
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Sequence similaritiesContains 1 anaphylatoxin-like domain.
Contains 1 NTR domain. -
Post-translational
modificationsPrior to secretion, the single-chain precursor is enzymatically cleaved to yield the non-identical chains (alpha, beta and gamma). During activation, the alpha chain is cleaved by C1 into C4a and C4b, and C4b stays linked to the beta and gamma chains. Further degradation of C4b by C1 into the inactive fragments C4c and C4d blocks the generation of C3 convertase.
N- and O-glycosylated. O-glycosylated with a core 1 or possibly core 8 glycan. -
Cellular localizationSecreted.
- Information by UniProt
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Database links
- Entrez Gene: 100293534 Human
- Entrez Gene: 100507685 Human
- Entrez Gene: 720 Human
- Entrez Gene: 721 Human
- Omim: 120810 Human
- Omim: 120820 Human
- SwissProt: P0C0L4 Human
- SwissProt: P0C0L5 Human
see all -
Alternative names
- acidic C4 antibody
- Acidic complement C4 antibody
- basic C4 antibody
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Images
Protocols
References
This product has been referenced in:
- Blom AM et al. Testing the Activity of Complement Convertases in Serum/Plasma for Diagnosis of C4NeF-Mediated C3 Glomerulonephritis. J Clin Immunol 36:517-27 (2016). Read more (PubMed: 27146825) »
- Atkinson C et al. Donor brain death exacerbates complement-dependent ischemia/reperfusion injury in transplanted hearts. Circulation 127:1290-9 (2013). IHC ; Human . Read more (PubMed: 23443736) »