Biosimilar Antibodies
C3a, Mouse, mAb 3/11, Hycult Biotech, HM1072
The monoclonal antibody 3/11 recognizes C3a, an activated fragment of the complement protein C3, a 190 kDa protein which is the most abundant complement protein in serum . C3 is the third component of the complement system and plays a central role in the complement cascade. The three pathways of compliment activation come together- at this key molecule. Cleavage of the pivotal complement component C3 results in the generation of a set of effector molecules which have diverse biological functions. The cleavage product C3b promotes complement acrtivation and the subsequent formation of the membrane attack complex. C3a, the small (ca. 10 kDa) cleavage product possesses anaphylatoxic as well as immunoregulatory- properties. It exerts its function through a specific receptor (C3aR), which belongs to the G-protein coupled receptor family. Expression of C3aR- has been reported in many cell types including myeloid and non-myeloid cells. Expression of C3aR on haematopoietic stem/progenitor cells has been shown to promote the trafficking/homing of these cells to the BM. Engagement of C3aR on DCs and T cells has been shown to up-regulate these cell functions. The monoclonal antibody 3/11 reacts specifically with the C3a anaphylatoxin, providing a tool for monitoring acute complement activation (C3a generation) in experimental mouse models.
Host
Mouse
Reactivity
Applications
Conjugation
C3aR, Human, mAb 17, Hycult Biotech, HM2195
The monoclonal antibody 17 reacts with the human receptor for C3a. The monoclonal antibody 17 is in the literature also referred to as clone hC3aRZ8. In the course of complement activation the C3a receptor functions as the cell surface receptor for the anaphylatoxin C3a, the C-terminal 77 amino acid cleavage product of the alpha chain of C3, but not for C3a-desArg. All cellular responses to C3a are specifically mediated by interactions with the membrane bound C3a receptor, a seven transmembrane GTP-binding-protein-coupled receptor that belongs to the rhodopsin supergene family. The 54 kDa C3a receptor is widely distributed in, myeloid cells, peripheral tissues and the central nervous system. Expression of C3aR has been demonstrated on neutrophils, monocytes, eosinophils, astrocytes, neurons and glial cells and is increased in inflammatory conditions. No C3aR expression was detectable on lymphocytes and on tonsillar B cells even after stimulation.
Host
Human
Reactivity
Applications
Conjugation
C3aR, Mouse, mAb 14D4, Hycult Biotech, HM1123
The monoclonal antibody 14D4 reacts with mouse C3aR, which is a member of the rhodopsin superfamily of 7-transmembrane G protein-coupled receptors, with a molecular weight of approximately 54 kDa. Expression of C3aR has been demonstrated on a wide variety of immune cells, including monocytes, macrophages, dendritic cells, neutrophils, basophils, eosinophils, mast cells, T lymphocytes and B lymphocytes. In addition, C3aR is found on cells of the central nervous system, lungs and kidney. In the course of complement activation C3aR functions as the cell surface receptor for C3a, which is the C-terminal 77 amino acid cleavage product of C3. C3a, possesses both anaphylatoxic and immunoregulatory properties, such as smooth muscle contraction, histamine release from mast cells, and enhanced vascular permeability. In addition, C3a induces respiratory burst in neutrophils and has chemotactic properties for eosinophils and mast cells. Moreover, C3a causes release of key cytokines from multiple cell types, including IL-1β, TNF-α, IL-6 and IL-8. A role for C3aR has been implicated in several murine disease models. It was shown that C3aR inhibition reduces neurodegeneration in experimental lupus, whereas in a murine model of allergic airway disease, deletion of the C3a receptor protects against the changes in lung physiology seen after allergen challenge. Finally, it was shown that deletion of C3aR is protective in myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis.
Host
Mouse
Reactivity
Applications
Conjugation
C3aR, Rat, mAb 74, Hycult Biotech, HM3028
The monoclonal antibody 74 reacts with the rat receptor for C3a. The monoclonal antibody 74 is in the literature also referred to as clone rC3aRZ1. In the course of complement activation the C3a receptor functions as the cell surface receptor for the anaphylatoxin C3a, the C-terminal 77 amino acid cleavage product of the alpha chain of C3, but not for C3a-desArg. All cellular responses to C3a are specifically mediated by interactions with the membrane bound C3a receptor, a seven transmembrane GTP-binding-protein-coupled receptor that belongs to the rhodopsin supergene family. The 54 kDa C3a receptor is widely distributed in myeloid cells, peripheral tissues and the central nervous system. Expression of C3aR has been demonstrated on neutrophils, monocytes, eosinophils, astrocytes, neurons and glial cells and is increased in inflammatory conditions. No C3aR expression was detectable on lymphocytes and on tonsillar B cells even after stimulation.
Host
Rat
Reactivity
Applications
Conjugation
C3b/iC3b/C3c, Mouse, mAb 2/11, Hycult Biotech, HM1065
The monocolonal antibody 2/11 recognizes activated fragments of the mouse complement protein C3. The complement system is an important part of the humoral response in innate immunity, consisting of three different pathways. The third complement component, C3, is central to the classical, alternative and lectin pathways of complement activation. Activation products of the complement cascade contain neo-epitopes that are not present in the individual native components. The synthesis of C3 is tissue-specific and is modulated in response to a variety of stimulatory agents. C3 is the most abundant protein of the complement system with serum protein levels of about 1.3 mg/ml. An inherited deficiency of C3 predisposes the person to frequent assaults of bacterial infections. In ulcerative colitis, and idiopathic chronic inflammatory bowel disease, the deposition of C3 in the diseased mucosa has been reported. Proteolysis by certain enzymes results in the cleavage of C3 into C3a and C3b. C3b becomes attached to immune complexes and is further cleaved into iC3b, C3c, C3dg and C3f. The monoclonal antibody 2/11 is specific for cleaved C3 fragments C3b, iC3b, and C3c, and for activated C3. Therefore, positive reactivity in tissues is associated with activation of he complement cascade and C3 cleavage. In case of an acute inflammatory reaction lots of C3 are processed into the products recognized by 2/11 and is as such useful as marker for inflammatory reaction. In chronic inflammatory conditions minimal reactivity with 2/11 may observed. In such cases primarily the C3dg product resides at the place of inflammation (C3c being cleared) which is not recognized by antibody 2/11. The chronic processing/activation of C3 is taking place at a lower level, which would reduce detection of the C3 fragments C3b, iC3b, and C3c. Next to detection of C3 fragments C3b, iC3b, and C3c, the monoclonal antibody 2/11 inhibits the hemolytic activity of mouse complement in a dose-dependent manner.
Host
Mouse
Reactivity
Applications
Conjugation
C3b/iC3b/C3c, Mouse, mAb 3/26, Hycult Biotech, HM1078
The monoclonal antibody 3/26 recognizes mouse complement protein activated C3 fragments C3b, iC3b, and C3c. The complement system is an important factor in innate immunity. The third complement component, C3, is central to the classical, alternative and lectin pathways of complement activation. C3 is the most abundant protein of the complement system with serum protein levels of about 1.3 mg/ml. Proteolysis by certain enzymes results in the cleavage of C3 into C3a and C3b. C3b becomes attached to immune complexes and is further cleaved into iC3b, C3c, C3dg and C3f. Activation products of the complement cascade contain neo-epitopes that are not present in the individual native components. The synthesis of C3 is tissue-specific and is modulated in response to a variety of stimulatory agents. An inherited deficiency of C3 predisposes the person to frequent assaults of bacterial infections. In ulcerative colitis, and idiopathic chronic inflammatory bowel disease, the deposition of C3 in the diseased mucosa has been reported. The monoclonal antibody 3/26 preferably recognizes cleaved C3 fragments C3b, iC3b, and C3c. In case of an acute inflammatory reaction lots of C3 are processed into the products recognized by 3/26 and is as such useful as marker for inflammatory reaction. In chronic inflammatory conditions minimal reactivity with 3/26 may observed. In such cases primarily the C3dg product resides at the place of inflammation (C3c being cleared) which is not recognized by antibody 3/26. The chronic processing/activation of C3 is taking place at a lower level, which would reduce detection of the C3 fragments C3b, iC3b, and C3c.
Host
Mouse
Reactivity
Applications
Conjugation
C3b/iC3b/C3d, Human, mAb 1H8, Hycult Biotech, HM2287
The Critical Role of C3b/iC3b/C3d in the Complement System Activation C3 plays a crucial role in our immune system, ensuring it functions correctly through two main pathways: the classical and the alternative pathway. People with insufficient C3 have a higher risk of contracting bacterial infections. This fact underscores the importance of C3 components, namely C3b, iC3b, and C3d, in defending our bodies against infections. C3-convertase and Its Impact on C3b/iC3b/C3d Formation A heterodimer of activated C4 and C2 forms one form of C3-convertase, known as C4b2a. This enzyme plays a crucial role in actively cleaving C3 into C3a and C3b during activation in both the classical and lectin pathways. C3a acts as an anaphylotoxin and a precursor to cytokines like ASP, while C3b functions as an opsonizing agent. Factor I actively cleaves C3b into C3c and C3d, a process that significantly enhances B cell responses. This underscores the essential roles of C3b, iC3b, and C3d in the immune system. Alternative Pathway and the Dynamics of C3b/iC3b/C3d In the alternative complement pathway, C3 is cleaved by C3bBb, another form of C3-convertase, consisting of activated C3 (C3b) and factor B (Bb). The activation of C3 to C3b reveals a reactive thioester, crucial for its binding to various surfaces. The complex C3bBb, known as the alternative pathway C3 convertase, plays a significant role in this process. Regulation and Clinical Implications of C3b/iC3b/C3d The process to turn off C3bBb, a part of our immune system, involves a few steps. First, a part of it called Bb is removed by something called decay-accelerating factor (DAF). Then, C3b, which is a piece of C3bBb, gets broken down into smaller pieces. It first turns into iC3b, then into C3c and C3dg, and finally into C3d. This breaking down is helped by Factor I and CR1. This whole process of breaking down C3b into smaller parts is really important for controlling how active our immune system is. Checking the levels of C3 in the blood, including its parts like C3b, iC3b, and C3d, is really helpful for doctors. It can give them clues about certain health problems. For example, if someone has low levels of C3, it might mean they have a specific type of kidney disease such as post-infectious glomerulonephritis or shunt nephritis. So, these parts of C3 are really important for figuring out certain medical conditions. Not sure which C3 antibody to use? With numerous options available, it is essential to select the right C3 antibody to ensure the success of your research. We designed a guide to assist you in making an informed decision: Go to our C3 researcher’s guide and choose the right antibody
Host
Human
Reactivity
Applications
Conjugation
C3b/iC3b, Human, mAb 3E7, Hycult Biotech, HM2286
Understanding the Complement System: The Role of C3b/iC3b in Immune Response The complement system is integral to both innate and adaptive immune responses, capable of producing an inflammatory and protective reaction against pathogens. This system operates via three pathways of complement activation: the classical pathway, initiated by immune complexes; the lectin pathway, triggered by surface-bound mannan-binding lectin; and the alternative pathway (AP), which activates on unprotected surfaces. Each of these pathways generates a C3 convertase, a serine protease that cleaves C3, resulting in the formation of the crucial fragment C3b, a component central to understanding the C3b/iC3b dynamic. The Dynamics of C3b and iC3b in Complement Activation Upon activation, C3 splits into two fragments: the smaller anaphylatoxin C3a and the larger, short-lived C3b. C3b is highly reactive, binding to complement-activating particles or immune complexes. In contrast to the classical pathway, the AP is continuously active, playing a significant role in tissue damage and inflammation in autoimmune diseases and ischemia-reperfusion injury. Recent evidence suggests that inhibiting AP activation could reduce certain disease pathologies while maintaining the host defense mechanisms provided by the classical and lectin pathways. The inhibition of the alternative pathway at C3b and iC3b can be measured with the Alternative Pathway Assay ( HK3012 ). The Clinical Implications of C3b and iC3b C3b is a substance that can attach to the surfaces of cells. When this happens, it can mark the cells for destruction – a process known as opsonization. However, once C3b is attached to a cell, it can change into different, inactive forms. The most important of these is iC3b, followed by C3dg. This change from C3b to iC3b is very important because it helps control how active the complement system is. The complement system is a part of our immune system that helps fight diseases. By understanding how C3b changes into iC3b, scientists can find new ways to treat diseases where this part of the immune system is involved. Not sure which C3 antibody to use? With numerous options available, it is essential to select the right C3 antibody to ensure the success of your research. We designed a guide to assist you in making an informed decision: Go to our C3 researcher’s guide and choose the right antibody
Host
Human
Reactivity
Applications
Conjugation
C3b/iC3b, Human, mAb 5G9, Hycult Biotech, HM2285
The Vital Role of C3b/iC3b in Complement System Activation C3 plays a pivotal role in activating the complement system, a key component of our immune response. This activation is crucial for both the classical and alternative complement pathways. A deficiency in C3 can increase susceptibility to bacterial infections, underlining the importance of understanding the C3b/iC3b dynamic. C3 Convertases: The Pathway to C3b/iC3b Formation One form of C3 convertase, C4b2a, is vital in the classical and lectin pathways. It catalyzes the cleavage of C3 into C3a and C3b. While C3a functions as an anaphylotoxin and cytokine precursor like ASP, C3b acts as an opsonizing agent. The transformation of C3b into C3c and C3d, facilitated by Factor I, plays a crucial role in enhancing B cell responses. In the alternative pathway, C3b is also generated by C3bBb, another form of C3 convertase, leading to the creation of the C3b/iC3b forms. Mechanics of C3b/iC3b in Immune Regulation Once formed, C3b can bind to surfaces via a reactive thioester, a crucial step in the complement activation process. The alternative pathway’s C3 convertase, C3bBb, undergoes deactivation in several steps. Initially, the Bb component is removed by proteins with decay-accelerating factor activity. Subsequently, C3b is methodically broken down to iC3b, then to C3c and C3dg, and finally to C3d. This process, involving Factor I and CR1 as a cofactor, is pivotal in the regulation of the complement system. The inhibition of the classical complement pathway at C3 and iC3b can be measured with the Classical complement pathway assay ( HK3010 ). Clinical Relevance of C3b/iC3b Levels in Diagnosis Monitoring levels of C3, and by extension C3b/iC3b, in the blood can provide valuable diagnostic insights. For example, low levels of C3 are linked with certain kidney diseases such as post-infectious glomerulonephritis and shunt nephritis. Understanding the behavior and levels of C3b/iC3b is thus critical in both the diagnosis and potential treatment of various medical conditions. Not sure which C3 antibody to use? With numerous options available, it is essential to select the right C3 antibody to ensure the success of your research. We designed a guide to assist you in making an informed decision: Go to our C3 researcher’s guide and choose the right antibody
Host
Human
Reactivity
Applications
Conjugation
C3b, Mouse, ELISA kit, Hycult Biotech, HK216
The mouse C3b ELISA assay is specific for the cleaved C3 fragments C3b, iC3b, and C3c, and for activated C3. The complement system is an important component of innate immunity. Complement-derived products mediate functions contributing to pathogen killing and elimination. However, inappropriate activation of the system contributes to the pathogenesis of immunological and inflammatory diseases. Complement component 3 (C3) occupies a central position because of the manifold biological activities of its activation fragments, including the major fragment, C3b, which anchors the assembly of convertases effecting C3 and C5 activation. C3 is converted to C3b by proteolysis of its anaphylatoxin domain, by either of two C3 convertases. This activates a stable thioester bond, leading to the covalent attachment of C3b to cell-surface or protein-surface hydroxyl groups through transesterification. C3b is further cleaved into iC3b, C3c, C3dg and C3f. C3b and iC3b function as opsonins, they act through different complement receptors, complement receptor 1 (CD35) and complement receptor 3 (CD11b/CD18), respectively. The mouse C3b ELISA assay is specific for the cleaved C3 fragments C3b, iC3b, and C3c, and for activated C3. Therefore, positive reactivity in plasma or serum is associated with activation of the complement cascade and C3 cleavage. In case of an acute inflammatory reaction, lots of C3 are processed into the products recognized by the assay, making this assay a useful tool for measuring the acute inflammatory response. The assay is less useful for assessing chronic inflammatory conditions since minimal reactivity may be observed. In such cases, primarily the C3dg product resides at the place of inflammation (C3c being cleared) which is not recognized by the assay. The chronic processing/activation of C3 is taking place at a lower level, which would reduce detection of the C3 fragments C3b, iC3b, and C3c. Beware that complement activity levels are mouse strain dependent and might be affected by the way the samples are collected and processed. C3 levels can differ between healthy and diseased animals, the optimal dilution can be different between these statuses.
Host
Mouse
Reactivity
Applications
Conjugation
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