Datasheet

Biological Description

Specificity	C5b-9 + C5b-8 Antibody [P24G22] detects endogenous levels of total C5b-9 and C5b-8 protein.
Background	C5b-8 and C5b-9 are critical intermediates and the terminal effector of the complement terminal pathway, assembling sequentially on target membranes to form the membrane attack complex (MAC) responsible for innate immune lysis. C5b-8 consists of C5b bound to C6, C7, and heterotrimeric C8 (with α, β, and γ subunits containing MACPF/perforin, thrombospondin type-1, EGF-like, and LDL receptor domains), where the amphiphilic α-to-β hairpin transition in C8α/β enables membrane insertion and catalyzes C9 recruitment and polymerization into a toroidal pore of 16–18 monomers (approximately 100–200 Å in diameter) with a hydrophilic inner channel, β-sheet stem, and outer β-hairpin wall. C5b-8 binds the globular form of C9, inducing allosteric arcuate elongation and rapid oligomerization via lateral contacts that breach the phospholipid bilayer, resulting in uncontrolled Ca²⁺/Na⁺ influx, colloid osmotic swelling, and cell lysis vital for pathogen clearance. Sublytic MAC pores can activate survival pathways (such as Bad phosphorylation and ERK/NF-κB signaling), promoting inflammation, leukocyte recruitment, and prothrombotic effects. Host cells are protected by CD59, which binds C8α’s β-hairpin, forming steric β-sheets that deflect C9 trajectories and halt MAC assembly. Dysregulation of C5b-9 contributes to diseases such as paroxysmal nocturnal hemoglobinuria (PNH), resulting from CD55/CD59 loss and erythrocyte lysis, atypical hemolytic uremic syndrome (aHUS) due to complement regulator deficiencies, and plays a role in transplant rejection and ischemia-reperfusion injury through bystander endothelial damage.

Specificity

C5b-9 + C5b-8 Antibody [P24G22] detects endogenous levels of total C5b-9 and C5b-8 protein.

Background

C5b-8 and C5b-9 are critical intermediates and the terminal effector of the complement terminal pathway, assembling sequentially on target membranes to form the membrane attack complex (MAC) responsible for innate immune lysis. C5b-8 consists of C5b bound to C6, C7, and heterotrimeric C8 (with α, β, and γ subunits containing MACPF/perforin, thrombospondin type-1, EGF-like, and LDL receptor domains), where the amphiphilic α-to-β hairpin transition in C8α/β enables membrane insertion and catalyzes C9 recruitment and polymerization into a toroidal pore of 16–18 monomers (approximately 100–200 Å in diameter) with a hydrophilic inner channel, β-sheet stem, and outer β-hairpin wall. C5b-8 binds the globular form of C9, inducing allosteric arcuate elongation and rapid oligomerization via lateral contacts that breach the phospholipid bilayer, resulting in uncontrolled Ca²⁺/Na⁺ influx, colloid osmotic swelling, and cell lysis vital for pathogen clearance. Sublytic MAC pores can activate survival pathways (such as Bad phosphorylation and ERK/NF-κB signaling), promoting inflammation, leukocyte recruitment, and prothrombotic effects. Host cells are protected by CD59, which binds C8α’s β-hairpin, forming steric β-sheets that deflect C9 trajectories and halt MAC assembly. Dysregulation of C5b-9 contributes to diseases such as paroxysmal nocturnal hemoglobinuria (PNH), resulting from CD55/CD59 loss and erythrocyte lysis, atypical hemolytic uremic syndrome (aHUS) due to complement regulator deficiencies, and plays a role in transplant rejection and ischemia-reperfusion injury through bystander endothelial damage.

Usage Information

Application

IHC, IF, FCM, ELISA

Dilution

IHC

1:10 - 1:500

Reactivity

Human, Baboon, Monkey, Pig, Horse

Source

Mouse Monoclonal Antibody

MW

Storage Buffer

PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage
(from the date of receipt)

-20°C (avoid freeze-thaw cycles), 2 years

References

https://pubmed.ncbi.nlm.nih.gov/28630159/
https://pubmed.ncbi.nlm.nih.gov/28647534/

C5b-9 + C5b-8 Antibody [P24G22]

Biological Description

Usage Information

References

Application Data