C3c

GWB-D0DE6C

718

10-02A

This product recognises 135kDa complement component 3c (C3c) present in blood serum. C3c is generated over the course of complement activation where convertase C4b2a (classical pathway) and convertase C3bBb (alternative pathway) cleave C3 to C3b and C3a. C3b is further degraded into iC3b and C3dg/C3d. iC3b is then slowly cleaved (possibly by factor I) to form C3c (beta chain + alpha\' chain fragment 1 + alpha\' chain fragment 2) C3dg and C3f. C3 is crucial in the induction of tolerance generated when an antigen is introduced into immunoprivileged sites and this is exploited by pathogens and cancer cells to evade the immune system by inhibiting complement activation. Histology: Kidney from post streptococal glomerulonephritis patients.

Borate buffered saline pH8. 4

Western Blot: This product binds both C3c and C3 and so is not suitable for all ELISA applications.

Derived from proteolytic degradation of complement C3 C3a anaphylatoxin is a mediator of local inflammatory process. It induces the contraction of smooth muscle increases vascular permeability and causes histamine release from mast cells and basophilic leukocytes.

Secreted.

There are two alleles: C3S (C3 slow) the most common allele in all races and C3F (C3 fast) relatively frequent in Caucasoids less common in Black Americans extremely rare in Orientals.

Genetic variation in C3 is associated with susceptibility to age-related macular degeneration type 9 (ARMD9) [MIM:611378]. ARMD is a multifactorial eye disease and the most common cause of irreversible vision loss in the developed world. In most patients the disease is manifest as ophthalmoscopically visible yellowish accumulations of protein and lipid that lie beneath the retinal pigment epithelium and within an elastin-containing structure known as Bruch membrane.

Contains 1 NTR domain. 1. Janssen. B. J. et al. (2005) Structures of complement component C3 provide insights into the function and evolution of immunity.