AGER Specific Neutra™ Antibody Products
Product listAGER (Advanced glycation end-product receptor) is a multifaceted receptor that, in addition to AGEs, engages with various molecules involved in the maintenance of equilibrium, embryonic growth, and immune response, as well as specific disorders like Alzheimer's disease. Conditions linked with AGER encompass diabetic angiopathy and diabetic neuropathy. Its associated biological pathways include the MyD88-dependent cascade triggered within endosomes and the BBB (Blood-Brain Barrier).
Its Gene ID: 177, UniProtKB ID: Q15109, and OMIM ID: 600214.
AGER Related Pathway
AGER, alias RAGE, can elicit inflammatory responses upon binding with AGEs, which are glycated and oxidized biomolecules, or damage-associated molecular pattern molecules, released from apoptotic cells. The AGER pathway can be triggered by the interaction of DAMPs such as S100B and HMGB1 from dying cells, or AGEs, derived from oxidized proteins, lipids, and nucleic acids. AGER can activate the MAPK signaling cascade involving proteins like Raf, MEK1, and ERK1/2, resulting in the phosphorylation and translocation of key transcription factors such as Ets1, Jun, and NFAT5.
Fig.1 Activation of ERK1/2 signaling by AGE-AGER interaction.1, 3
Antibodies in AGER-Related Therapeutics
- Anti-AGER Antibody Modulation Function in Diabetic Stroke
AGEs play a pivotal role in the onset and progression of diabetic complications, encompassing cardiovascular ailments, stroke, and other maladies. AGER activation exacerbates neural damage post-cerebral ischemia in transgenic mice targeting AGER, while AGER directly contributes to cerebral ischemia pathology. Pro-inflammatory cytokines like TNF-α and ICAM-1 may exacerbate infarction, brain edema, and neuronal demise. To assess the impact of SLI treatment on stroke in T1DM rats and its regulation of the inflammatory factor AGER, immunofluorescence and western blot analyses are conducted using an anti-AGER antibody. Immunofluorescence results confirm a significant reduction in AGER expression following SLI treatment in T1DM+MCAO rats.
Fig.2 Expression of AGER/RAGE in T1DM+MCAo rats.2, 3
- Inhibition of Inflammatory Responses by Anti-AGER Antibody
Systemic inflammation triggers transient or lasting brain dysfunction by exposing it to soluble inflammatory agents. AGER interacts with specific ligands, facilitating and amplifying inflammatory cascades. Using an LPS-induced systemic inflammation model in rats, the impact of AGER blockade is observed in serum, liver, cerebrospinal fluid (CSF), and various brain regions. The AGER antibody mitigates LPS-induced inflammatory effects in serum and liver, reducing levels of proinflammatory cytokines and attenuating phosphorylation/activation of AGER downstream targets in the liver. AGER antibody also prevents LPS-induced TNF-α and IL-1β effects in CSF. In the striatum, it inhibits IL-1β elevation, along with reductions in Iba-1, GFAP, phospho-ERK1/2, and synaptophysin levels. These effects result from systemic AGER inhibition, as the AGER antibody does not penetrate the blood-brain barrier. In summary, AGER blockade effectively suppresses LPS-induced inflammatory responses in serum, liver, CSF, and the brain.
Creative Biolabs presents a wide array of anti-AGER antibody selections, meticulously engineered via recombinant methodologies. Additionally, personalized customization solutions are available to tailor AGER-targeting neutralizing antibodies to specific requirements.
REFERENCES
- Logan, Samantha M., and Kenneth B. Storey. "Pro-inflammatory AGE-RAGE signaling is activated during arousal from hibernation in ground squirrel adipose." PeerJ 6 (2018): e4911.
- Wang, Fujiang, et al. "Neuroprotective effect of salvianolate lyophilized injection against cerebral ischemia in type 1 diabetic rats." BMC complementary and alternative medicine 17 (2017): 1-12.
- Distributed under Open Access license CC BY 4.0, without modification.
