C3, Mouse, mAb 11H9 – 100 µg - HM1045-100UG
Quantity
100 µg
Catalog #
HM1045-100UG
510,00 €
Verwandte Produkte
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.
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.
| Datasheet URL | https://www.hycultbiotech.com/wp-content/uploads/2022/06/coa-tds_hm1045-100ug.pdf |
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| Quantity | 100ug |
| Quantity | 100 µg |
| Species | MOUSE |
| Alias | omplement component C3, HSE-MSF Gene name: C3 |
| Application | Flow cytometry, Frozen sections, Immuno assays, Immuno fluorescence, Western blot |
| Precautions | For research use only. Not for use in or on humans or animals or for diagnostics. It is the responsibility of the user to comply with all local/state and Federal rules in the use of this product. Hycult Biotech is not responsible for any patent infringements that might result with the use of or derivation of this product. |
| References | 1. Kremmer, E et al; Monoclonal antibodies to complement components without the need of their prior purification. II. Antibodies to mouse C3 and C4. Hybridoma 1990, 9: 309 2. Pan, W et al; CR3 (CD11b/CD18) is the major macrophage receptor for IgM antibodymediated phagocytosis of African trypanosomes: Diverse effect on subsequent synthesis of tumor necrosis factor a and nitric oxide. Microb Infect 2006, 8: 1209 3. Zhou, J et al; Complement C3 and C4 expression in C1q sufficient and deficient mouse models of Alzheimer's disease. J Neurochem 2008, 106: 2080 4. Heurich, B et al; Complement upregulation and activation on motor neurons and neuromuscular junction in the SOD1 G93A mouse model of familial amyotrophic lateral sclerosis. Journal of Neuroimmunology 2011, 235: 104 5. Lewis, R et al; CD55 Deficiency Protects against Atherosclerosis in ApoE-Deficient Mice via C3a Modulation of Lipid Metabolism. Am J Path 2011, 179: 1601 6. Lesher, A et al; Combination of Factor H Mutation and Properdin Deficiency Causes Severe C3 Glomerulonephritis. Am Soc Nephrol 2013, 24: 53 7. Antunes, A et al; The Phosphocarrier Protein HPr Contributes to Meningococcal Survival during Infection. PLos One 2015, 11: e0162434 8. Ramaglia, V et al; Complement activation and expression during chronic relapsing. Clin Exp Immunol 2015, 180:432 |
| Disease | Infectious diseases, Nephrology |
| Application: | Flow cytometry Frozen sections Immuno assays Immuno fluorescence Western blot |
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