C5b-9 + C5b-8 Antibody [P24G22] | Primary Antibodies

Application: Reactivity: Human, Baboon, Monkey, Pig, Horse

Usage Information

Dilution
IHC1:10 - 1:500

Application
IHC, IF, FCM, ELISA

Reactivity
Human, Baboon, Monkey, Pig, Horse

Source
Mouse Monoclonal Antibody

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

Datasheet & SDS

Biological Description

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

Clone
P24G22

Synonym(s)
CPAMD4; C5; Complement C5; C3 and PZP-like alpha-2-macroglobulin domain-containing protein 4

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.

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.

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

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%