C3 Antibody (Polyclonal)

A goat antiserum raised against human C3 protein.


Product Specifications

Citations 10
Clonality

Polyclonal

Immunogen Highly purified human C3 protein
Applications See citations and technical data sheet for application info.
Concentration > 40 mg/mL
Conjugate Unconjugated
Cross Reactivity

Human, Baboon, Horse, Hamster, Rabbit, Guinea Pig, Rat, Mouse, Rhesus macaque

Ordering Information

For Research Use Only in the United States. Not for use in diagnostic procedures.
Catalog Number A304
Catalog Number (CE) N/A
Size 2.0 mL
Price (USD) $200.00
Price (EURO) 170,00 €

Contact us

US Phone+1 (858) 552 1100
EU Phone+353 (91) 412 474
US Emailcontact-us@quidelortho.com
EU Emailcontact-emea@quidelortho.com

Specifications

Description

A goat antiserum raised against human C3 protein.

Size 2.0 mL
Concentration

> 40 mg/mL

Applications See citations and technical data sheet for application info.
Form Liquid. Whole Antiserum. ≤ 0.1% Sodium Azide
Clonality Polyclonal
Immunogen Highly purified human C3 protein
Conjugate Unconjugated
Cross Reactivity Human, Baboon, Horse, Hamster, Rabbit, Guinea Pig, Rat, Mouse, Rhesus macaque
Isotype Goat IgG
Purity N/A
Source

Goat

Specificity The Anti-Human C3 Polyclonal Antisera was tested against normal human plasma by double immunodiffusion, one-dimensional immunoelectrophoresis, quantitative radial immunodifussion, and quantitative rocket immunoelectrophoresis. The antiserum was determined to be monospecific for C3 at varying concentrations.
Storage

Short term (30 days) 4˚C. Long term at or below –20˚C.

Background

C3 plays a central role for the classical, alternative, and lectin pathways of the complement system. The circulating form of C3 is naturally glycosylated and contains two disulfide-bonded chains that weigh approximately 110 kD and 75 kD, respectively. The average concentration of circulating C3 in human serum/plasma is 1.25 mg/mL. Activation of any of the three complement pathways results in the cleavage of C3 into C3a and C3b fragments. C3a is one of the three complement-derived anaphylatoxins. The C3a polypeptide also exhibits immunoregulatory activity. This activity is dependent on the physical binding of C3a to helper T lymphocytes, which results in the inhibition of helper T cell function. C3a also suppresses the production, in vitro, of lymphokines by PHA or Con A simulated human PBL. This suppression is dependent on the presence of the carboxyl terminal arg-77, due to the inactivity of C3a-des-arg. Upon complement activation, the C3b fragment’s reactive site (a thioester bond) becomes accessible to nucleophilic attack by target cell acceptor molecules or non-complement proteolytic enzymes. Such an attack results in a covalent ester bond between the C3b fragment and the target cell surface. This attachment provides the binding site for C5, initiating membrane attack complex assembly. The ability of C3b to continue cleaving C5 is lost upon cleavage into iC3b and C3f by naturally occurring plasma regulator proteins, Factor H and Factor I. iC3b remains bound to the cell surface and can continue to mediate the opsonization of complement-coated target cells by binding CR3 receptors, or in the presence of CR1, iC3b can further be hydrolyzed by a variety of proteolytic enzymes, trypsin, elastase, plasmin or Factor I, into C3c and C3d,g.

Citations

Title Year Applications Sample Species Sample Sample Details

Selective Binding of Heparin/Heparan Sulfate Oligosaccharides to Factor H and Factor H-Related Proteins: Therapeutic Potential for C3 Glomerulopathies

2021

FC

Cell Culture

ciGEnCs Cells

Selective Binding of Heparin/Heparan Sulfate Oligosaccharides to Factor H and Factor H-Related Proteins: Therapeutic Potential for C3 Glomerulopathies

2021

FC

Cell Culture

HUVEC Cells

The Plasmodium falciparum blood stages acquire factor H family proteins to evade destruction by human complement

2016

IF, WB

Cell Culture

Plasmodium falciparum culture

Variability and action mechanism of a family of anticomplement proteins in Ixodes ricinus

2008

ELISA

Human

Serum

Ixodes ricinus incubated

Binding of vitronectin by the Moraxella catarrhalis UspA2 protein interferes with late stages of the complement cascade

2006

FC, WB

Human

Serum

Moraxella catarrhalis

Multiple-Organ Complement Deposition on Vascular Endothelium in COVID-19 Patients.

2021

IF

Human

Kidney Tissue

COVID-19

Multiple-Organ Complement Deposition on Vascular Endothelium in COVID-19 Patients.

2021

IF

Human

Liver Tissue

COVID-19

Multiple-Organ Complement Deposition on Vascular Endothelium in COVID-19 Patients.

2021

IF

Human

Lung Tissue

COVID-19

The Plasmodium falciparum blood stages acquire factor H family proteins to evade destruction by human complement

2016

IF, WB

Human

Red Blood Cells

Plasmodium falciparum incubated

Decidual endothelial cells express surface-bound C1q as a molecular bridge between endovascular trophoblast and decidual endothelium

2008

IHC

Human

Decidual Endothelial Cells