Key features and details
- Produced recombinantly (animal-free) for high batch-to-batch consistency and long term security of supply
- Rabbit monoclonal [EPR16849-75] to RAGE - Low endotoxin, Azide free
- Suitable for: IP, WB
- Reacts with: Mouse, Rat
Product nameAnti-RAGE antibody [EPR16849-75] - Low endotoxin, Azide free
See all RAGE primary antibodies
DescriptionRabbit monoclonal [EPR16849-75] to RAGE - Low endotoxin, Azide free
Tested applicationsSuitable for: IP, WBmore details
Species reactivityReacts with: Mouse, Rat
Recombinant fragment. within Mouse RAGE aa 100-350. The exact sequence is proprietary.
Database link: Q62151
- WB: Mouse and rat lung lysates. IP: Mouse lung whole cell lysate.
ab225533 is a carrier-free antibody designed for use in antibody labeling, including fluorochromes, metal isotopes, oligonucleotides, enzymes.
Our Low endotoxin, azide-free formats have low endotoxin level (≤ 1 EU/ml, determined by the LAL assay) and are free from azide, to achieve consistent experimental results in functional assays.
Our RabMAb® technology is a patented hybridoma-based technology for making rabbit monoclonal antibodies. For details on our patents, please refer to RabMab® patents.
Storage instructionsShipped at 4°C. Store at +4°C. Do Not Freeze.
Storage bufferConstituent: PBS
Concentration information loading...
PurityProtein A purified
Our Abpromise guarantee covers the use of ab225533 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|IP||Use at an assay dependent concentration.|
|WB||Use at an assay dependent concentration.|
FunctionMediates 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. Interaction with S100B after myocardial infarction may play a role in myocyte apoptosis by activating ERK1/2 and p53/TP53 signaling (By similarity). 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.
Tissue specificityEndothelial cells.
Sequence similaritiesContains 2 Ig-like C2-type (immunoglobulin-like) domains.
Contains 1 Ig-like V-type (immunoglobulin-like) domain.
Cellular localizationSecreted and Cell membrane.
- Information by UniProt
- Advanced glycosylation end product-specific receptor antibody
- Ager antibody
- DAMA 358M23.4 antibody
This IP data was generated using the same anti-RAGE antibody clone [EPR16849-75] in a different buffer formulation (cat# ab181293).
RAGE was immunoprecipitated from 1 mg of mouse lung whole cell lysate with ab181293 at 1/50 dilution.
Western blot was performed from the immunoprecipitate using ab181293 at 1/1000 dilution.
VeriBlot for IP Detection Reagent (HRP) (ab131366), was used for detection at 1/10000 dilution.
Lane 1: Mouse lung whole cell lysate 10µg (Input).
Lane 2: ab181293 IP in mouse lung whole cell lysate.
Blocking and dilution buffer and concentration: 5% NFDM/TBST.
Exposure time: 1 second.
To our knowledge, customised protocols are not required for this product. Please try the standard protocols listed below and let us know how you get on.
ab225533 has not yet been referenced specifically in any publications.