FITC Anti-C4d antibody [LP69] (ab187930)
Key features and details
- FITC Mouse monoclonal [LP69] to C4d
- Reacts with: Human
- Conjugation: FITC. Ex: 493nm, Em: 528nm
- Isotype: IgG1
Overview
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Product name
FITC Anti-C4d antibody [LP69]
See all C4d primary antibodies -
Description
FITC Mouse monoclonal [LP69] to C4d -
Host species
Mouse -
Conjugation
FITC. Ex: 493nm, Em: 528nm -
Specificity
ab187930 recognises the C4d fragment of complement component C4. -
Species reactivity
Reacts with: Human -
Immunogen
Full length native protein (purified) corresponding to Human C4d. Complement C4d from normal Human plasma.
Database link: P0C0L4 -
General notes
Reproducibility is key to advancing scientific discovery and accelerating scientists’ next breakthrough.
Abcam is leading the way with our range of recombinant antibodies, knockout-validated antibodies and knockout cell lines, all of which support improved reproducibility.
We are also planning to innovate the way in which we present recommended applications and species on our product datasheets, so that only applications & species that have been tested in our own labs, our suppliers or by selected trusted collaborators are covered by our Abpromise™ guarantee.
In preparation for this, we have started to update the applications & species that this product is Abpromise guaranteed for.
We are also updating the applications & species that this product has been “predicted to work with,” however this information is not covered by our Abpromise guarantee.
Applications & species from publications and Abreviews that have not been tested in our own labs or in those of our suppliers are not covered by the Abpromise guarantee.
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Properties
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Form
Liquid -
Storage instructions
Shipped at 4°C. Store at +4°C. Store In the Dark. -
Storage buffer
Preservative: 0.09% Sodium azide
Constituent: 99% PBS -
Concentration information loading... -
Purity
Protein G purified -
Purification notes
Purified from tissue culture supernatant. -
Clonality
Monoclonal -
Clone number
LP69 -
Isotype
IgG1 -
Research areas
Associated products
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Alternative Versions
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Isotype control
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Recombinant Protein
Target
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Function
C4 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 disease
Defects 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. -
Sequence similarities
Contains 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 localization
Secreted. - 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
see all
References (0)
ab187930 has not yet been referenced specifically in any publications.
