C3b Mouse
Description
Overview of Mouse C3b
Mouse C3b is a 175 kDa protein fragment derived from the cleavage of complement component C3, a central molecule in the innate immune system. It plays critical roles in opsonization, complement activation, and immune cell signaling. Derived from mouse serum or plasma, C3b is produced via proteolytic cleavage by C3 convertases (e.g., alternative pathway convertase) and retains a reactive thioester bond for covalent attachment to pathogens or damaged cells .
Functional Roles in Immune Response
C3b is pivotal in three core processes:
Opsonization and Phagocytosis
C3b binds pathogens, apoptotic cells, and immune complexes via covalent ester/amide bonds, marking them for destruction. It interacts with receptors like CR1 (CD35) and CR3 (CD11b/CD18) on phagocytes, enhancing engulfment . In liver injury models, C3b deposition facilitates rapid clearance of damaged hepatocytes, as seen in wild-type mice versus C3-deficient mice with delayed tissue removal .
Complement Amplification
Surface-bound C3b forms C5 convertase (C3bBb or C4b2a) with factor B and C2, respectively, driving C5 cleavage into C5a (anaphylatoxin) and C5b (membrane attack complex precursor). This amplifies inflammation and pathogen lysis .
Immune Regulation
C3b breakdown products (iC3b, C3d) modulate B-cell and T-cell responses by binding receptors on antigen-presenting cells (APCs), promoting adaptive immunity .
Functional Assays
Mouse C3b is used to study:
Inactivated C3b
A modified form of C3b (e.g., PRO-2813) lacks binding sites for factor B, preventing convertase formation while retaining properdin and CR3 receptor interactions. This variant is used to study C3b’s non-complement roles, such as receptor-mediated signaling .
Diagnostic Tools
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Monoclonal Antibodies: mAb 3/26 targets neo-epitopes on C3b/iC3b/C3c, enabling detection of acute complement activation (e.g., in liver injury models) .
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ELISA Kits: Quantify C3b/iC3b/C3c in plasma/serum to assess inflammatory responses .
Case Study 1: Liver Regeneration
In CCl4-induced liver injury, wild-type mice showed rapid C3b deposition in damaged tissue, correlating with hepatocyte proliferation. C3-deficient mice exhibited delayed tissue clearance and reduced regeneration, underscoring C3b’s role in phagocytosis and repair .
Challenges and Considerations
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Strain Variability: Complement activity levels differ among mouse strains, necessitating strain-specific optimization in assays .
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Sample Handling: Plasma/serum collection and processing (e.g., EDTA anticoagulation) critically affect C3b detection .
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Chronic vs. Acute Inflammation: C3b/iC3b is abundant in acute inflammation but minimal in chronic states, where C3dg predominates .
Product Specs
C3b, a key component of the complement system, is generated when native C3 is cleaved by the alternative pathway C3 convertase. This cleavage releases C3a, an anaphylatoxin. C3b plays a critical role in all three complement pathways (classical, lectin, and alternative). Upon activation, each pathway forms C3 convertases, enzyme complexes that bind to target surfaces and cleave C3, generating C3b and C3a. The majority of C3b generated during complement activation binds to target surfaces. Surface-bound C3b is vital for the activation of C5, leading to the formation of C5b-9 complexes, also known as the membrane attack complex (MAC). The MAC forms pores in target cell membranes, causing lysis. Furthermore, surface-bound C3b, as well as its breakdown products iC3b and C3d, are recognized by receptors on immune cells like lymphocytes and phagocytes. This interaction facilitates antigen presentation, a crucial process in adaptive immunity, and stimulates the proliferation of antigen-specific B and T cells.
Mouse Complement C3b, with a molecular weight of 175kDa, is produced in a mouse plasma environment.
The product is a sterile-filtered solution.
The C3b solution is prepared in a phosphate-buffered saline (PBS) solution at a pH of 7.2.
For optimal stability and product integrity, the following storage guidelines are recommended:
- Short-term storage (2-4 weeks): Refrigerate at 4°C. Ensure the entire vial contents are used within this period.
- Long-term storage: Freeze at temperatures below -20°C. For extended storage, adding a carrier protein such as 0.1% HSA or BSA is advised.
Important: Repeated freezing and thawing of the product should be avoided to prevent degradation.
The purity level of the product is greater than 95%, as determined by SDS-PAGE analysis.
Complement C3, C3 and PZP-like alpha-2-macroglobulin domain-containing protein 1, C3, CPAMD1.
Mouse Plasma.
Product Science Overview
Complement C3b is derived from the cleavage of complement component C3. The cleavage is typically mediated by C3 convertases, which are enzyme complexes generated during the activation of the complement pathways. There are three pathways of complement activation: the classical pathway, the lectin pathway, and the alternative pathway. All three pathways converge at the activation of C3, leading to the generation of C3b .
Upon cleavage of C3, a small fragment called C3a is released, and the larger fragment, C3b, becomes covalently attached to the surface of pathogens or cells. This process is known as opsonization, which tags the pathogens for destruction by phagocytes .
C3b has several critical functions in the immune response:
- Opsonization: C3b binds to the surface of pathogens, marking them for phagocytosis by immune cells such as macrophages and neutrophils.
- Formation of C5 Convertase: C3b associates with other complement components to form C5 convertase, which cleaves C5 into C5a and C5b. This step is essential for the formation of the membrane attack complex (MAC), which can lyse pathogens.
- Immune Complex Clearance: C3b helps in the clearance of immune complexes from the bloodstream, preventing their deposition in tissues and subsequent inflammation .
Mouse models are extensively used to study the complement system, including C3b. These models help in understanding the role of complement in various diseases, such as autoimmune disorders, infections, and inflammatory conditions. For instance, mouse models expressing human complement receptors CR1 and CR2 have been developed to study the human complement system’s regulation and its implications in diseases .
