Anti-C4D Polyclonal Antibody, FITC

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12-5001
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Product Name Anti-C4D Polyclonal Antibody, FITC
Description This gene encodes the acidic form of complement factor 4, part of the classical activation pathway. The protein is expressed as a single chain precursor which is proteolytically cleaved into a trimer of alpha, beta, and gamma chains prior to secretion. The trimer provides a surface for interaction between the antigen-antibody complex and other complement components. The alpha chain may be cleaved to release C4 anaphylatoxin, a mediator of local inflammation. Deficiency of this protein is associated with systemic lupus erythematosus and type I diabetes mellitus. This gene localizes to the major histocompatibility complex (MHC) class III region on chromosome 6. Varying haplotypes of this gene cluste exist, such that individuals may have 1, 2, or 3 copies of this gene. Two transcript variants encoding different isoforms have been found for this gene. Rabbit polyclonal Antibody to human C4d FITC conjugate
Host Rabbit
Clonality Polyclonal
Immunogen Synthetic peptide specific for human C4d conjugated to KLH (keyhole limpet hemocyanin)
Specificity Human C4d
Reactivity Human
Applications IHC, IHC-P
Form FITC, affinity purified, in PBS, containing Stabilizer and 0.1% sodium azide
Storage 2-8C
References 1. Akalin, E., Dinavahi, R., Friedlander, R., Ames, S., de Boccardo, G., Sehgal, V., Schröppel, B., Bhaskaran, M., Lerner, S., Fotino, M., Murphy, B., Bromberg, J.S. Addition of Plasmapheresis Decreases the Incidence of Acute Antibody-Mediated Rejection in Sensitized Patients with Strong Donor-Specific Antibodies. (2008), Clinical Journal of the American Society of Nephrology, 3: 1160-1167. Astor, T. L., Galantowicz, M., Phillips, A., Palafox, J. and Baker, P. (2009), Pulmonary Capillaritis as a Manifestation of Acute Humoral Allograft Rejection Following Infant Lung Transplantation. American Journal of Transplantation, 9: 409–412. Crystal P. Jenkins, Diana M. Cardona, Jennifer N. Bowers, Bahram R. Oliai, Robert W. Allan, and Sigurd J. Normann (2010) The Utility of C4d, C9, and Troponin T Immunohistochemistry in Acute Myocardial Infarction. Archives of Pathology & Laboratory Medicine: February 2010, Vol. 134, No. 2, pp. 256-263. Csaba Galambos, Brian Feingold, and Steven A. Webber (2008) Characterization of C4d Immunostaining Utilizing Paraffin-Embedded Tissue of Nonpresensitized Pediatric Heart Transplant Patients. Pediatric and Developmental Pathology: May 2008, Vol. 11, No. 3, pp. 181-184. De Kort, H., Munivenkatappa, R. B., Berger, S. P., Eikmans, M., Van Der Wal, A., De Koning, E. J., Van Kooten, C., De Heer, E., Barth, R. N., Bruijn, J. A., Philosophe, B., Drachenberg, C. B. and Bajema, I. M. (2010), Pancreas Allograft Biopsies with Positive C4d Staining and Anti-Donor Antibodies Related to Worse Outcome for Patients. American Journal of Transplantation, 10: 1660–1667. Fedson, S.E., Daniel, S.S., Husain, A.N. (2008), Immunohistochemistry Staining of C4d to Diagnose Antibody-mediated Rejection in Cardiac Transplantation. The Journal of Heart and Lung Transplantation, 27: 372-379. Hisashi, Y., Yamada, K., Kuwaki, K., Tseng, Y.-L., Dor, F. J. M. F., Houser, S. L., Robson, S. C., Schuurman, H.-J., Cooper, D. K. C., Sachs, D. H., Colvin, R. B. and Shimizu, A. (2008), Rejection of Cardiac Xenografts Transplanted from α1,3-Galactosyltransferase Gene-Knockout (GalT-KO) Pigs to Baboons. American Journal of Transplantation, 8: 2516–2526. Rafiq, M. A., De Boccardo, G., Schröppel, B., Bromberg, J. S., Sehgal, V., Dinavahi, R., Murphy, B. and Akalin, E. (2009), Differential outcomes in 3 types of acute antibody-mediated rejection. Clinical Transplantation, 23: 951–957. Shimizu, A., Hisashi, Y., Kuwaki, K., Tseng, YL., Dor, F.J.M.F., Houser, S.L., Robson, S.C., Schuurman, HJ., Cooper, D.K.C., Sachs, D.H., Yamada, K., Colvin, R.B. Thrombotic Microangiopathy Associated with Humoral Rejection of Cardiac Xenografts from α1, 3-Galactosyltransferase Gene-Knockout Pigs in Baboons. (2008), American Journal of Pathology, 172(6): 1471–1481. Shimizu, A., Yamada, K., Yamamoto, S., Lavelle, J.M., Barth, R.N., Robson, S.C., Sachs, D.H., Colvin, R.B. (2005), Thrombotic Microangiopathic Glomerulopathy in Human Decay Accelerating Factor–Transgenic Swine-to-Baboon Kidney Xenografts. J Am Soc Nephrol, 16: 2732-2745. Torrealba, J. R., Samaniego, M., Pascual, J., Becker, Y., Pirsch, J., Sollinger, Hans., Odorico, J. (2008), C4d-Positive Interacinar Capillaries Correlates With Donor-Specific Antibody-Mediated Rejection in Pancreas Allografts. Transplantation, 86: 1849-1856. Taner, T., Gandhi, M. J., Sanderson, S. O., Poterucha, C. R., De Goey, S. R., Stegall, M. D. and Heimbach, J. K. (2012), Prevalence, Course and Impact of HLA Donor-Specific Antibodies in Liver Transplantation in the First Year. American Journal of Transplantation, 12: 1504–1510.
Background This gene encodes the acidic form of complement factor 4, part of the classical activation pathway. The protein is expressed as a single chain precursor which is proteolytically cleaved into a trimer of alpha, beta, and gamma chains prior to secretion. The trimer provides a surface for interaction between the antigen-antibody complex and other complement components. The alpha chain may be cleaved to release C4 anaphylatoxin, a mediator of local inflammation. Deficiency of this protein is associated with systemic lupus erythematosus and type I diabetes mellitus. This gene localizes to the major histocompatibility complex (MHC) class III region on chromosome 6. Varying haplotypes of this gene cluste exist, such that individuals may have 1, 2, or 3 copies of this gene. Two transcript variants encoding different isoforms have been found for this gene.
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