AGER antibody
- Known as:
- AGER (anti-)
- Catalog number:
- orb10063
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- AGER antibody
Related genes to: AGER antibody
- Gene:
- AGER NIH gene
- Name:
- advanced glycosylation end-product specific receptor
- Previous symbol:
- -
- Synonyms:
- RAGE, SCARJ1
- Chromosome:
- 6p21.32
- Locus Type:
- gene with protein product
- Date approved:
- 1994-10-17
- Date modifiied:
- 2016-10-05
Related products to: AGER antibody
Related articles to: AGER antibody
- Patients with type 2 diabetes mellitus often experience microvascular complications, including diabetic retinopathy, nephropathy, and neuropathy. Despite advances in glucose-lowering treatments, these complications remain a significant clinical and financial burden worldwide. Their pathogenesis is influenced by genetic polymorphism and advanced glycation end products (AGEs). Chronic metabolic stress leads to the formation of AGEs via oxidative and nonenzymatic glycation. AGEs bind to the AGE receptor (RAGE) and actively cause microvascular damage. This occurs through endothelial dysfunction, amplification of oxidative stress, protein cross-linking, and inflammatory activation. Genes controlling AGE production, AGE-RAGE signaling, oxidative stress responses, endothelial nitric oxide bioavailability, and extracellular matrix remodeling affect individual susceptibility to AGE-mediated microvascular damage. Elevated AGE load and genetic polymorphisms influence metabolic memory, microvascular injury, and redox signaling. This review article outlines the molecular mechanisms involving AGEs, genetic polymorphisms, and microvascular complications. Understanding AGE biology and genetic risk analysis could support management of diabetic microvascular complications and foster personalized medicine and preventive approaches beyond traditional glucose-centric frameworks. - Source: PubMed
Publication date: 2026/05/30
Sarangi RajlaxmiSingh SwetaSahoo Jyoti PrakashSatpathy Amrita - Potato ( L.) is an important staple and food security crop to many communities in the world. However, potato production and quality is greatly constrained by bacterial wilt, a disease caused by a soil-borne pathogen, . can be managed through clean seed systems and therefore laboratory testing is a pre-requisite for seed certification to confirm the absence of the pathogen in potato seeds before planting. Molecular diagnostics is the gold standard for detection of in potato seeds. However, the extraction of genomic DNA from for molecular diagnostics is complex, tedious, lengthy and/or costly procedure. A simple, rapid and reliable DNA extraction protocol is required for use in routine molecular diagnosis of , a high-risk quarantine pathogen. In this study, we developed a simple and rapid protocol for extracting genomic DNA from symptomatic and asymptomatic potato tubers infected with and verified its efficiency for the detection and molecular characterization of the pathogen. The protocol was developed from the evaluation of distilled water, Tris-EDTA (TE) and Tris buffer as a base solution for tissue maceration. The DNA quantity and integrity was determined using the NanoDrop 2000C spectrophotometer and agarose gel electrophoresis, respectively. Both hot and cold solutions produced intact high molecular weight genomic DNA of sufficient yield and purity for molecular-based applications. The detection and determination of phylotypes of , based on conventional and multiplex polymerase chain reaction (PCR), amplified the expected 280 and 372 bp amplicons, respectively, confirming that the quantity and quality of the extracted pathogen genomic DNA was sufficient for molecular diagnostic applications. The sequencing of the amplified products of the gene produced good quality sequences, which confirmed the isolates to be members of phylotype II sequevar 1. This protocol is a simple, fast and reliable tool for the extraction of sufficient genomic DNA with high quality, directly from -infected potato tubers for PCR and sequencing applications. Its simplicity and throughput make it valuable for use in routine diagnostics and can be adopted by certification programs to ensure distribution of clean potato seeds to farmers. - Source: PubMed
Publication date: 2026/05/31
Mwangi BrianNjiru Joshua MWandili Sarah AGachoka Kennedy KMburu KennethMuriira GeoffreyRotich HenryAger ElvinceNyaboga Evans N - Chronic hyperglycemia associated with diabetes mellitus (DM) induces systemic metabolic disturbances that progressively promote microvascular and macrovascular complications including the impairment of neuronal integrity and cognitive function. Accumulating evidence has supported that cognitive impairment and Type 2 Diabetes Mellitus (T2DM) share common pathological mechanisms. The current investigation explored potential benefits of alogliptin, a dipeptidyl peptidase IV (DPP-4) inhibitor, on diabetes induced cognitive impairment by revealing its role in attenuating neuroinflammatory pathways. T2DM was induced with a high-fat diet (HFD) for 8 weeks followed by a single low dose of streptozotocin (STZ, 30 mg/kg I.P). Rats of the treatment groups received alogliptin at different doses (20 mg/kg/day or 40 mg/kg/day) for 28 days. Memory function was assessed using the Morris Water Maze (MWM) and Y-maze tests. Blood samples were withdrawn at the end of the experiment, and brain tissue was dissected for biochemical, immunohistochemical, and histopathological examination. Alogliptin reduced diabetes-induced cognitive impairment evident in memory tasks, alleviated histological changes in the brain and attenuated oxidative stress by increasing SOD, CAT and GSH levels while reducing MDA levels. Alogliptin also decreased neuroinflammatory signaling via reducing HMGB1, RAGE, TLR4/ NF-κB which in turn decreased inflammatory cytokines TNF-α and IL-1β. Alogliptin also refined mTOR signaling pathway and improved neuronal health. According to these findings, alogliptin reduces neuroinflammation and alters mTOR action leading to the improvement of neurodegeneration and memory function. - Source: PubMed
Publication date: 2026/06/10
Ata Raneem MEl-Awady El-Sayed EHazem Reem MRadwan Asmaa - D-galactose promotes insulin resistance (IR) and neurodegeneration through hyperglycemia, advanced glycation end products (AGEs), oxidative stress, amyloid-β accumulation, and disruption of the insulin signalling pathway, leading to neuroinflammation and neuroapoptosis. The purpose of this study was to investigate the insulin signalling pathway and efficacy of ZnO nanoparticles (ZnO NPs) in alleviating brain IR and neurodegeneration via regulating IRS/PI3K/AGER/APP signalling. In this study, bioinformatic analysis of hub genes and PIP network revealed the interconnection between PI3K/Akt signalling pathway and neuroinflammation pathway leading to neurodegeneration. Further, analysis on 4-month-old C57BL/6 mice was randomised into control (NC), 50 mg/kg of D-galactose (DC), D-galactose + 450 μg/Kg of ZnO NPs (Z1), D-galactose + 650 μg/Kg of ZnO NPs (Z2), and D-galactose + 20 mg/kg of metformin (MF). Blood glucose, Amadori products, conjugated dienes, amyloid-β deposition, and gene and protein expression of the IRS/PI3K/AGER/APP signalling pathway were analysed. Our findings illustrated that ZnO NPs (Z1) alleviated hyperglycemia, cleared amyloid-β accumulation, maintained neural integrity, lessened fat deposition in the liver, and altered the expression of , , , and genes. Thus, ZnO NPs offer a therapeutic strategy for managing IR and neurodegeneration. - Source: PubMed
Publication date: 2026/05/12
Ramasubbu KanagavalliV Devi Rajeswari - - Source: PubMed
LeSaint Kathy TAger Emily EKaul PranavGeier CurtisSmollin Craig G