Biosimilar Antibodies
C3/C3b/iC3b (alpha chain), Human, clone 18.1, Hycult Biotech, HM2389
The complement system is a key part of our immune system, helping to fight infections and protect the body. It reacts quickly to germs, even before our main immune response kicks in. This system is made up of many proteins and receptors, such as C3, C3b, and iC3b, which are found in the blood, tissues, and different body fluids. Exploring the Three Pathways of Complement Activation The complement system can be activated in three different ways. First, the classical pathway starts when immune complexes are present. Second, the lectin pathway begins with lectins attached to surfaces. Third, the alternative pathway (AP) is triggered on unprotected surfaces. All these pathways create a special enzyme called C3 convertase. This enzyme is important because it cuts the main protein, C3, into a smaller piece known as C3b. The C3 and C5 convertases are enzymatic complexes that initiate and amplify the activity of the complement pathways, leading to the generation of the cytolytic membrane attack complex (MAC). The synthesis of C3, including its forms C3b and iC3b, is tissue-specific and modulated in response to various stimulatory agents. Upon cleavage by C3 convertase, the anaphylotoxin C3a and the activating fragment C3b are formed. C3b, when bound to the cell surface, initiates the terminal pathway of complement by forming the C5 convertase. Understanding C3, C3b, and iC3b: Crucial Components of Immune Defense C3, with a molecular weight of approximately 185kDa, is the most abundant protein in the complement system, featuring serum protein levels of about 1.3 mg/ml. Primarily produced by the liver, C3, as well as its derivatives C3b and iC3b, are also synthesized in macrophages, neutrophils, endothelial, and epithelial cells. Due to its high levels in circulation and low biological reactivity, C3/C3b/iC3b acts swiftly and potently in response to dangers, such as pathogen encounters. However, defects in C3/C3b/iC3b can be detrimental, leading to recurrent infections or autoimmune diseases. C3 deficiency is uncommon, but it does happen. This deficiency affects how well C3b and iC3b work. It leads to frequent infections and problems with the development of immune cells. Polymorphisms in C3 have been associated with conditions like age-related macular degeneration (AMD) and atypical hemolytic uremic syndrome (aHUS). Beyond pathogen clearance, C3/C3b/iC3b plays a vital role in the removal of circulating immune complexes, aiding the phagocytic capacity of macrophages. Malfunctions in this system can lead to autoimmune diseases and complement deposition in tissues. 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
C3, C3b, iC3b, C3c, Human, clone C3-16.4, Hycult Biotech, HM2401
Understanding the Complement System: Focus on C3, C3b, iC3b, and C3c The complement system is a critical component of both innate and adaptive immune responses. It initiates an inflammatory and protective reaction to pathogens, providing an early line of defense before an adaptive immune response is generated. This system comprises a complex family of proteins and receptors present in circulation, tissues, and various body fluids. Among these, the components C3, C3b, iC3b, and C3c play pivotal roles. Pathways of Complement Activation: The Role of C3 and Its Fragments Activation of the complement system can occur through three pathways: the classical pathway, triggered by immune complexes; the lectin pathway, initiated by surface-bound lectins; and the alternative pathway (AP), activated by surfaces not specifically protected against it. Each pathway leads to the formation of a C3 convertase, a serine protease that cleaves the central complement protein C3. This cleavage generates the major fragment C3b, a key player in the complement cascade. The Dynamics of C3, C3b, iC3b, and C3c in Immune Response The C3 and C5 convertases are enzymatic complexes that drive the activity of complement pathways, culminating in the formation of the cytolytic membrane attack complex (MAC). C3 synthesis is tissue-specific and modulated by various stimuli. Upon cleavage by C3 convertase, C3a and C3b are formed, with C3b capable of undergoing further degradation into iC3b, C3c, C3dg, and C3d in the presence of complement regulatory molecules. C3c: A Stable Biomarker in Complement-Mediated Immunity Unlike other C3 fragments, C3c does not bind to structures like pathogens, cell surfaces, or plasma proteins, making it a stable and reliable complement biomarker. It remains solely in the fluid phase, free from interference by other C3-based products. C3 is mainly produced by the liver, but also by macrophages, neutrophils, endothelial, and epithelial cells. Its high levels in circulation and low biological reactivity enable a rapid and potent response to threats like pathogens. Clinical Implications of C3 and Its Fragments Deficiencies or defects in C3 can lead to recurrent infections or autoimmune diseases. C3 deficiency, though rare, results in recurrent infections and impaired immune cell development. Polymorphisms in C3 are linked to diseases like age-related macular degeneration (AMD) and atypical hemolytic uremic syndrome (aHUS). Beyond pathogen clearance, C3 and its fragments assist in the removal of immune complexes, aiding macrophage phagocytic capacity. Dysfunctions in this system can lead to autoimmune diseases and complement deposition in tissues. 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
C3, Human, ELISA kit, Hycult Biotech, HK366
C3, a central component in the complement system, plays a crucial role in both innate and adaptive immune responses. It acts as a frontline defense against pathogens, triggering inflammatory and protective reactions. Found in circulation, tissues, and body fluids, C3 is part of a complex protein and receptor family. Activation occurs via three pathways: the classical pathway, triggered by immune complexes; the lectin pathway, initiated by surface-bound lectins; and the alternative pathway (AP), activated by unprotected surfaces. These pathways converge to produce C3 convertase, which cleaves C3 into C3b, a major fragment. This process escalates into the formation of the membrane attack complex (MAC). C3 synthesis varies across tissues, responding to diverse stimuli. Its cleavage results in anaphylotoxin C3a and C3b, the latter kickstarting the terminal complement pathway. Weighing around 185kDa, C3 stands as the most abundant complement protein, primarily produced by the liver and also by macrophages, neutrophils, and endothelial and epithelial cells. C3’s high concentration and swift response to threats like pathogens make it a potent immune component. Deficiencies in C3 can lead to recurrent infections and autoimmune diseases. Although rare, C3 deficiency cases involve recurrent infections and impaired immune cell development. C3 polymorphism is linked to age-related macular degeneration (AMD) and atypical hemolytic uremic syndrome (aHUS). Furthermore, C3 assists in removing immune complexes, enhancing macrophage phagocytic capabilities. Dysfunctions in this system can lead to autoimmune diseases and tissue complement deposition, underscoring C3’s pivotal role in immune regulation.
Host
Human
Reactivity
Applications
Conjugation
C3, Mouse, ELISA, Hycult Biotech, HK2002
The C3 and C5 convertases are enzymatic complexes that initiate and amplify the activity of the complement pathways and ultimately generate the cytolytic MAC. The synthesis of C3 is tissue-specific and is modulated in response to a variety of stimulatory agents. After cleavage by C3 convertase the anaphylotoxin C3a and activating C3b are formed. When bound to the cell surface C3b forms the start of the terminal pathway of complement by initiating the formation of the C5 convertase. C3 has a molecular weight of app. 185kDa and is the most abundant protein of the complement system with serum protein levels of about 1.3 mg/ml. C3 is primarily produced by the liver but is also generated in macrophages, neutrophils, endothelial end epithelial cells. Due to the high levels in circulation with low biological reactivity, C3 is able to act in a fast and potent way when danger by eg pathogens is encountered . Defects in C3 can be unfavorable to the host leading to recurrent infections or auto-immune diseases. Although rare, C3 deficiency has been reported. These patients suffer from recurrent infections of e.g. S. pneumoniae or N. meningitidis due to lack of opsonization, but also impaired DC and Treg development. Polymorphism of C3 has been associated with AMD and aHUS. Besides clearance of pathogens, C3 is also important in removal of circulating immune-complexes by assisting the phagocytic capacity of macrophages. Malfunction of this system can lead to development of auto-immune disease and complement deposition in tissues. The complement system plays important roles in both innate and adaptive immune response and can produce an inflammatory and protective reaction to challenges from pathogens before an adaptive response can occur. The complement system consist of a complex family of proteins and receptors which are found in the circulation, in tissues and other body-fluids. There are three pathways of complement activation. The classical pathway is initiated by Immune complexes; the lectin pathway by surface bound lectins; and the AP by all the surfaces that are not specifically protected against it. Each generates a C3 convertase, a serine protease that cleaves the central complement protein C3, and generates the major cleavage fragment C3b.
Host
Mouse
Reactivity
Applications
Conjugation
C3, Mouse, mAb 11H9, Hycult Biotech, HM1045
The monoclonal antibody 11H9 recognizes mouse complement component C3 and its activation products, C3b, iC3b, C3d and C3dg. 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 complement factor C3 consists of an alpha- and a beta-chain. 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 11H9 recognizes both intact C3 and its cleaved products C3b, iC3b, C3d and C3dg. These activation products are present in acute as well as chronic inflammatory conditions. In chronic inflammatory condition, primarily the C3dg product resides at the place of inflammation (C3c being cleared) which is recognized by antibody 11H9. 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
C3, Mouse, pAb, Hycult Biotech, HP8012
The complement factor C3 consists of an alpha- and a beta-chain. C3 is a central factor in the complement cascade. It is central to the alternative pathway that leads to the C3 convertase C3bBb. The classical and mannose binding lectin activation pathways lead to the C3 convertase C4b2a. These convertases cleave C3 resulting in C3a and C3b. Further degradation leads to formation of the alpha-chain products C3d, C3g and C3c. C3 is an acute phase protein that is produced by a wide range of tissues including renal epithelial cells and hepatocytes.
Host
Mouse
Reactivity
Applications
Conjugation
C3, Pig, pAb, Hycult Biotech, HP7003
The polyclonal antibody recognizes pig complement component 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 complement factor C3 consists of an alpha- and a beta-chain. 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.
Host
Reactivity
Applications
Conjugation
C3, Rat, pAb, Hycult Biotech, HP8022
The polyclonal antibody reacts with Rat C3. The complement factor C3 consists of an alpha- and a beta-chain. C3 is a central factor in the complement cascade. It is central to the alternative pathway that leads to the C3 convertase C3bBb. The classical and mannose binding lectin activation pathways lead to the C3 convertase C4b2a. These convertases cleave C3 resulting in C3a and C3b. Further degradation leads to formation of the alpha-chain products C3d, C3g and C3c. C3 is an acute phase protein that is produced by a wide range of tissues including renal epithelial cells and hepatocytes.
Host
Rat
Reactivity
Applications
Conjugation
C3a/C3a des Arg, Human, mAb 2991, Hycult Biotech, HM2074
Exploring the Role of C3a/C3a des Arg in Innate Immunity The complement system is a crucial component of the humoral response in innate immunity, and it operates through three distinct pathways. At the heart of these pathways is the third complement component, C3, which is integral to the classical, alternative, and lectin pathways of complement activation. The activation products of the complement cascade, including C3a and C3a des Arg, are key to understanding this system’s function. C3a/C3a des Arg: Understanding Its Significance Activation products like C3a and C3a des Arg contain unique neo-epitopes, which are absent in their native forms. These epitopes are essential for direct quantification of activation at various stages in the complement cascade, often detected through monoclonal antibodies. C3, the most abundant protein in the complement system, has serum levels of about 1.3 mg/ml. Its synthesis is tissue-specific, influenced by various stimulatory agents. The Clinical Importance of C3a and C3a des Arg Inherited C3 deficiency can lead to frequent bacterial infections. In conditions like ulcerative colitis, C3 deposition in diseased mucosa has been observed. The cleavage of C3 by specific enzymes releases C3a anaphylatoxin and C3b. C3a, a short-lived protein of 74 amino acids, quickly transforms in the serum into the more stable form, C3a des Arg, also known as acylation stimulating protein (ASP). Measuring C3a des Arg provides reliable insights into complement activation levels in test samples. C3a and C3a des Arg in Inflammatory Responses C3a is a potent mediator in local inflammatory processes. It can induce smooth muscle contraction, increase vascular permeability, and trigger histamine release from mast cells and basophilic leukocytes. Its involvement is significant in conditions like gram-negative bacterial sepsis, trauma, ischemic heart disease, post-dialysis syndrome, and various autoimmune diseases. Normal plasma values of C3a/C3a des Arg in control individuals typically range between 48-150 ng/ml. 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
C3a, Human, ELISA kit, Hycult Biotech, HK354
C3a, a vital component in innate immunity, central to complement activation, rapidly converts in serum to its stable form, C3a-desArg, offering a reliable measure of immune response. This transformation is key for researchers tracking inflammation and immune reactions in conditions like sepsis, heart disease, and autoimmune disorders. Our precision-focused human C3a ELISA kit, targeting a unique neo-epitope on C3a-desArg, guarantees accurate results without interference from C3. This makes C3a an indispensable biomarker for groundbreaking immunological research.
Host
Human
Reactivity
Applications
Conjugation
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