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Polyclonal Antibody Classical Pathway

Also showing Polyclonal Antibody Western Blotting Classical Pathway

$260
100 µl
APPLICATIONS
REACTIVITY
Human, Monkey, Mouse, Rat

Application Methods: Western Blotting

Background: C1QBP, also referred to as p32, p33, gC1q receptor (gC1qR), and hyaluronic acid binding protein 1 (HABP1), was originally identified via its binding interactions with Splicing Factor (SF-2) (1). Multiple, diverse binding partners of C1QBP were subsequently identified, including the globular heads of complement component C1q, hyaluronic acid, selected protein kinases (2), the tumor suppressor ARF (3-5), and multiple antigens of bacterial and viral origin (6). Research studies have shown that C1QBP is overexpressed in a number of cancer cell types (7), and has been implicated in the Warburg effect, whereby cancer cells shift their metabolism from oxidative phosphorylation to glycolysis (7). C1QBP has also been shown to inhibit the Mitochondrial Permeability Transition (MPT) pore, possibly serving a protective function against damage from oxidative stress (8).

$260
100 µl
APPLICATIONS
REACTIVITY
Human

Application Methods: Western Blotting

Background: Decay-accelerating factor (DAF/CD55) is a GPI-linked plasma membrane glycoprotein normally expressed on the surface of vascular endothelial and hematopoietic cells, which are continuously exposed to autologous complement components. In conjunction with other membrane complement regulatory proteins (CD35, CD46, and CD59), DAF/CD55 protects healthy cells from inappropriate complement-mediated lysis (1). DAF/CD55 inhibits activation of the complement cascade by promoting membrane dissociation and inactivation of C3 convertase, which inhibits amplification of the classical and alternative complement cascades (2). Research studies have demonstrated that DAF/CD55 is overexpressed in a variety of solid and liquid tumors, which functions to protect tumor cells from complement-mediated attack (3,4). Given its ability to disable the complement cascade and facilitate immune evasion by tumor cells, DAF/CD55 has received attention as a potential therapeutic target for the treatment of human malignancies. CD55 deficiency is also linked to human disease. The inability to express CD55 on the surface of erythrocytes renders them highly susceptible to complement-mediated lysis, which contributes to the development of paroxymal noctural hemoglobinuria (PNH). PNH is characterized by hemolytic anaemia, pancytopenia, and venous thrombosis (5).

$260
100 µl
APPLICATIONS
REACTIVITY
Human

Application Methods: Western Blotting

Background: Complement receptor type 2 (CR2/CD21) is a type 1 transmembrane glycoprotein whose expression is largely restricted to B lymphocytes and follicular dendritic cells (1,2). Research studies have shown that CR2/CD21 functions to bind the complement fragments iC3b, C3dg, and C3d, which function to activate the alternative complement pathway and MAC formation (3,4). In addition to its function as a complement receptor, CR2/CD21 also functions as the B-lymphocyte receptor for Epstein-Barr virus (5) and interferon alpha (6). Research studies have also shown that CR2/CD21 participates in B-cell activation, proliferation, and protection from apoptosis through its association with components of the B-cell coreceptor signaling complex such as CD19 and CD21 (7-9).