Anti-RAGE Polyclonal Antibody 2 is a Rabbit antibody targeting RAGE. Anti-RAGE Polyclonal Antibody 2 can be used in IF,IHC-Fr,IHC-P,WB.

IgG

Mouse,Rat (predicted:Human,Dog,Pig,Cow)

1. Tissue/cell: rat skeletal muscle; 4% Paraformaldehyde-fixed and paraffin-embedded;
Antigen retrieval: citrate buffer (0.01M, pH6.0), Boiling bathing for 15 min; Block endogenous peroxidase by 3% Hydrogen peroxide for 30 min; Blocking buffer (normal goat serum) at 37°C for 20 min;
Incubation: Anti-RAGE Polyclonal Antibody, Unconjugated (TMAB-01605) 1:200, overnight at 4°C, followed by conjugation to the secondary antibody and DAb staining.
2. Sample:
Lane 1: Kidney (Mouse) Lysate at 40 μg
Lane 2: Cerebrum (Mouse) Lysate at 40 μg
Lane 3: Cerebrum (Rat) Lysate at 40 μg
Primary: Anti-RAGE (TMAB-01605) at 1/1000 dilution
Secondary: IRDye800CW Goat Anti-Rabbit IgG at 1/20000 dilution
Predicted band size: 50/43/55 kDa
Observed band size: 58/50 kDa

WB: 1:500-2000; IHC-P: 1:100-500; IHC-Fr: 1:100-500; IF: 1:100-500

Polyclonal

KLH conjugated synthetic peptide: human AGER Isoform 1, not for Isoform 2

Human

Ager

Advanced glycosylation end product-specific receptor

Diabetes associated,Inflammatory mediators,Amyloid,Alzheimer's disease,Visual system

Mediates interactions of advanced glycosylation end products (AGE). These are nonenzymatically glycosylated proteins which accumulate in vascular tissue in aging and at an accelerated rate in diabetes. Acts as a mediator of both acute and chronic vascular inflammation in conditions such as atherosclerosis and in particular as a complication of diabetes. AGE/RAGE signaling plays an important role in regulating the production/expression of TNF-alpha, oxidative stress, and endothelial dysfunction in type 2 diabetes. Interaction with S100A12 on endothelium, mononuclear phagocytes, and lymphocytes triggers cellular activation, with generation of key proinflammatory mediators. Receptor for amyloid beta peptide. Contributes to the translocation of amyloid-beta peptide (ABPP) across the cell membrane from the extracellular to the intracellular space in cortical neurons. ABPP-initiated RAGE signaling, especially stimulation of p38 mitogen-activated protein kinase (MAPK), has the capacity to drive a transport system delivering ABPP as a complex with RAGE to the intraneuronal space. Interaction with S100B after myocardial infarction may play a role in myocyte apoptosis by activating ERK1/2 and p53/TP53 signaling.