Rabbit Anti-C4A Recombinant Antibody (CBXC-2768) (CBMAB-C3326-CQ)

Name: Rabbit Anti-C4A Recombinant Antibody (CBXC-2768)
SKU: CBMAB-C3326-CQ
Rating: 5 (1 reviews)

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Datasheet

SDS

Request for COA

Datasheet Target References Q & As Review & reward Protocols Associated Products

Basic Information

Host Animal

Rabbit

Clone

CBXC-2768

Application

FC, IH, WB

Immunogen

A synthesized peptide derived from human C4A.

Host Species

Rabbit

Specificity

Human

Antibody Isotype

IgG

Clonality

Monoclonal

Application Notes

The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Application	Note
WB	1:500-1:2,000
IHC	1:50-1:200
FC	1:50

Formulations & Storage [For reference only, actual COA shall prevail!]

Format

Liquid

Buffer

PBS, pH 7.4, 0.4-0.5mg/ml BSA, 50% glycerol

Preservative

0.02% sodium azide

Concentration

Batch dependent

Storage

Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

More Infomation

Target

Full Name

Complement C4A

Introduction

This gene encodes the acidic form of complement factor 4, part of the classical activation pathway. The protein is expressed as a single chain precursor which is proteolytically cleaved into a trimer of alpha, beta, and gamma chains prior to secretion. The trimer provides a surface for interaction between the antigen-antibody complex and other complement components. The alpha chain is cleaved to release C4 anaphylatoxin, an antimicrobial peptide and a mediator of local inflammation. Deficiency of this protein is associated with systemic lupus erythematosus and type I diabetes mellitus. This gene localizes to the major histocompatibility complex (MHC) class III region on chromosome 6. Varying haplotypes of this gene cluster exist, such that individuals may have 1, 2, or 3 copies of this gene. Two transcript variants encoding different isoforms have been found for this gene.

Entrez Gene ID

720

UniProt ID

P0C0L4

Alternative Names

C42; C4A3; C4A4; C4A6; C4AD; C4S; CO4; CPAMD2; RG; C4A

Function

Non-enzymatic component of C3 and C5 convertases and thus essential for the propagation of the classical complement pathway. Covalently binds to immunoglobulins and immune complexes and enhances the solubilization of immune aggregates and the clearance of IC through CR1 on erythrocytes. C4A isotype is responsible for effective binding to form amide bonds with immune aggregates or protein antigens, while C4B isotype catalyzes the transacylation of the thioester carbonyl group to form ester bonds with carbohydrate antigens.
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.

Biological Process

Cellular protein metabolic process Source: Reactome
Complement activation Source: BHF-UCL
Complement activation, classical pathway Source: UniProtKB-KW
Inflammatory response Source: UniProtKB-KW
Innate immune response Source: UniProtKB-KW
Positive regulation of apoptotic cell clearance Source: BHF-UCL
Post-translational protein modification Source: Reactome
Regulation of complement activation Source: Reactome

Cellular Location

Secreted; Synapse; Axon; Dendrite

Involvement in disease

Complement component 4A deficiency (C4AD): A rare defect of the complement classical pathway associated with the development of autoimmune disorders, mainly systemic lupus with or without associated glomerulonephritis.
Systemic lupus erythematosus (SLE): Disease susceptibility is associated with variants affecting the gene represented in this entry. Interindividual copy-number variation (CNV) of complement component C4 and associated polymorphisms result in different susceptibilities to SLE. The risk of SLE susceptibility has been shown to be significantly increased among subjects with only two copies of total C4. A high copy number is a protective factor against SLE. A chronic, relapsing, inflammatory, and often febrile multisystemic disorder of connective tissue, characterized principally by involvement of the skin, joints, kidneys and serosal membranes. It is of unknown etiology, but is thought to represent a failure of the regulatory mechanisms of the autoimmune system. The disease is marked by a wide range of system dysfunctions, an elevated erythrocyte sedimentation rate, and the formation of LE cells in the blood or bone marrow.

PTM

Prior to secretion, the single-chain precursor is enzymatically cleaved to yield 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. The proteolytic cleavages often are incomplete so that many structural forms can be found in plasma.
N- and O-glycosylated. O-glycosylated with a core 1 or possibly core 8 glycan.

Yilmaz, M., Yalcin, E., Presumey, J., Aw, E., Ma, M., Whelan, C. W., ... & Carroll, M. C. (2021). Overexpression of schizophrenia susceptibility factor human complement C4A promotes excessive synaptic loss and behavioral changes in mice. Nature neuroscience, 24(2), 214-224.

Han, X., de la Fuente, M., & Nieman, M. T. (2021). Complement factor C4a does not activate protease‐activated receptor 1 (PAR1) or PAR4 on human platelets. Research and Practice in Thrombosis and Haemostasis, 5(1), 104-110.

Simoni, L., Presumey, J., van der Poel, C. E., Castrillon, C., Chang, S. E., Utz, P. J., & Carroll, M. C. (2020). Complement C4A regulates autoreactive B cells in murine lupus. Cell reports, 33(5), 108330.

Morales, R., Zhang, L., Wu, Y., Wilcox, J., Engelman, T., Ni, Y., ... & Tang, W. W. (2020). C3a, C4a, and C5a Complement Anaphylatoxins Are Paradoxically Decreased in Acute and Chronic Heart Failure. Journal of Cardiac Failure, 26(10), S19-S20.

Jüptner, M., Flachsbart, F., Caliebe, A., Lieb, W., Schreiber, S., Zeuner, R., ... & Schröder, J. O. (2018). Low copy numbers of complement C4 and homozygous deficiency of C4A may predispose to severe disease and earlier disease onset in patients with systemic lupus erythematosus. Lupus, 27(4), 600-609.

Liesmaa, I., Paakkanen, R., Järvinen, A., Valtonen, V., & Lokki, M. L. (2018). Clinical features of patients with homozygous complement C4A or C4B deficiency. PloS one, 13(6), e0199305.

Wang, H., Ricklin, D., & Lambris, J. D. (2017). Complement-activation fragment C4a mediates effector functions by binding as untethered agonist to protease-activated receptors 1 and 4. Proceedings of the National Academy of Sciences, 114(41), 10948-10953.

Zorzetto, M., Datturi, F., Divizia, L., Pistono, C., Campo, I., Silvestri, A. D., ... & Ricevuti, G. (2017). Complement C4A and C4B gene copy number study in Alzheimer's disease patients. Current Alzheimer Research, 14(3), 303-308.

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Please try the standard protocols which include: protocols, troubleshooting and guide.

Enzyme-linked Immunosorbent Assay (ELISA)
Flow Cytometry
Immunofluorescence (IF)
Immunohistochemistry (IHC)
Immunoprecipitation (IP)
Western Blot (WB)
Enzyme-Linked Immunospot (ELISpot)
Proteogenomics
Other Protocols

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Isotype control

For research use only. Not intended for any clinical use.

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