Mouse Advanced glycosylation end product-specific receptor(AGER) ELISA kit

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. Interaction with S100B after myocardial infarction may play a role in myocyte apoptosis by activating ERK1/2 and p53/TP53 signaling. Can also bind oligonucleotides. 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. RAGE-dependent signaling in microglia contributes to neuroinflammation, amyloid accumulation, and impaired learning/memory in a mouse model of Alzheimer disease.; Is able to advanced glycosylation end product (AGE)-induce nuclear factor NF-kappa-B activation.; Down-regulates receptor for advanced glycosylation end products (RAGE)-ligand induced signaling through various MAPK pathways including ERK1/2, p38 and SAPK/JNK. Significantly affects tumor cell properties through decreasing cell migration, invasion, adhesion and proliferation, and increasing cellular apoptosis. Exhibits drastic inhibition on tumorigenesis in vitro.

1. data, suggests that the dimeric state of RAGE controls its function and ligand mediated signaling which may play important role in RAGE mediated various diseases. PMID: 30076903
2. These novel findings demonstrate that RAGE deficiency protects against aortic valve calcification in high cholesterol diet-fed ApoE(-/-) mice via inhibition of endoplasmic reticulum stress. PMID: 28024939
3. microglial RAGE activation in presence of amyloid beta-enriched environment contributes to the entorhinal cortex vulnerability. PMID: 28205565
4. Established a murine model of myocardial ischemia-reperfusion injury; investigated and found remote ischemic postconditioning protects against IR injury thru RAGE-HMGB1 Pathway. PMID: 29789792
5. In this study, we found that the wnt co-receptor Lrp6 was a potent positive regulator of beta-catenin signaling in TDI-induced asthma models, both in vivo and in vitro. Additionally, for the first time, we demonstrated that RAGE could mediate phosphorylation of Lrp6, suggesting a functional cross talk between RAGE and the canonical wnt/beta-catenin signaling pathway involved in mediating beta-catenin activation. PMID: 29656209
6. Chronic unpredictable stress (CUS) promotes significant morphological changes and causes robust upregulation of HMGB1 messenger RNA in enriched hippocampal microglia and robust and persistent upregulation of RAGE messenger RNA. CUS increased surface expression of RAGE protein on hippocampal microglia and anhedonic behavior. RAGE knockout mice were resilient to stress-induced anhedonia. PMID: 28882317
7. study found that diabetes predisposes to more severe infections because of additional inflammatory output through dual activation of MyD88 by not only TLR4 but also RAGE PMID: 28830942
8. RAGE controls myocardial dysfunction and oxidative stress in high-fat fed mice by sustaining mitochondrial dynamics and autophagy-lysosome pathway. PMID: 28826719
9. these data provide a previously uncharacterized in vivo mechanism contingent on oligodeoxy-nucleotide -administered dose, where TLR9 governs the primary response and RAGE plays a distinct and cooperative function in providing a pivotal role in balancing the immune response. PMID: 28605247
10. data demonstrate that under the diabetic condition, DRG neurons are directly affected by elevated levels of glucose, independent of vascular or glial signals, and dependent on RAGE expression. PMID: 29474476
11. findings suggest that HMGB1 induces the transcytosis of albumin via RAGE-dependent Src phosphorylation and Cav-1 phosphorylation. These studies revealed a new mechanism of HMGB1-induced endothelial hyperpermeability. PMID: 27572515
12. data suggest that S100A8/A9 acts directly on BV-2 microglial cells via binding to TLR4 and RAGE on the membrane and then stimulates the secretion of proinflammatory cytokines through ERK and JNK-mediated NF-kappaB activity in BV-2 microglial cells. PMID: 28498464
13. Activation of RAGE facilitates the development of hypoxia-induced pulmonary hypertension by increasing ECM deposition in pulmonary arteries. PMID: 28407046
14. knockout of RAGE significantly ameliorates mainstream cigarette smoke-induced airway inflammation in mice PMID: 28704797
15. Here, the s show that RAGE deficiency impairs anti-viral immunity during an early-life infection with pneumonia virus of mice (PVM; a murine analogue of RSV). The elevated viral load was associated with the release of high mobility group box-1 (HMGB1) which triggered airway smooth muscle remodelling in early-life. PMID: 28099113
16. We investigated the role of RAGE in postischaemic leukocyte adhesion after myocardial infarction and its effect on postischaemic myocardial function. RAGE represents an additional pro-inflammatory endothelial mediator of ischaemia-reperfusion injury. PMID: 27412300
17. The results indicate that cells respond to advanced glycation end products by increasing matrix assembly and that RAGE is involved in this response. PMID: 27425255
18. Receptor for AGE expression and reactive oxygen species production were upregulated in db/db mouse livers, together with impaired proteolytic, antioxidant and mitochondrial respiratory activities. In parallel, acute exposure of HepG2 cells to glycated albumin also elicited intracellular free radical formation PMID: 27890722
19. RAGE is phosphorylated by the ATM kinase and is recruited to the site of DNA-double-strand break via an early DNA damage response. PMID: 28977635
20. receptor for advanced glycation end products (RAGE) was required for stabilization of beta-catenin in toluene diisocyanate-induced asthma, identifying protective effects of RAGE blockade in this mouse model PMID: 27332707
21. perturbation of Bone marrow mesenchymal stromal cells in diabetes mellitus could be partially explained by chronic RAGE signaling. PMID: 27539289
22. RAGE mediates inflammation that contributes to lung damage, in cigarette smoke-induced lung pathology. PMID: 28678851
23. Ager deletion enhances ischemic muscle inflammation, angiogenesis, and blood flow recovery in diabetic mice. PMID: 28642238
24. HMGB1 neither exerts influence on cardiac remodeling by binding to RAGE nor induces apoptosis of cardiomyocytes under physiological condition PMID: 27355349
25. Our results indicate that lack of RAGE has no significant impact on septic arthritis. However, RAGE-/- mice had significantly higher BMD compared to WT mice, which coincided with lower IL-17A in RAGE-/- mice. In sepsis, RAGE deficiency impairs bacterial kidney clearance. PMID: 27907047
26. SAA is a potential new uremic toxin involved in uremia-related atherosclerosis through interaction with RAGE. PMID: 26988587
27. that selective RAGE regulation reflects a self-protective mechanism to maintain low levels of RAGE ligands PMID: 27221633
28. Data show that receptor for advanced glycation end products (RAGE) impairs collateral growth in a diabetic setting and also in a non-diabetic setting, indicting the importance of RAGE and alternate RAGE ligands in the setting of collateral vessel growth. PMID: 27869797
29. These findings demonstrate the role for RAGE-dependent IL-10 suppression as a key modulator of mortality from Gram-negative sepsis. PMID: 28052995
30. HMGB1 promotes intraoral palatal wound healing through RAGE-dependent mechanisms. PMID: 27886093
31. These findings suggest that the inhibitory effect of these plant extracts on the activation of AGEs/RAGE/SphK1 signaling pathway in db/db diabetic mice kidney is a novel mechanism by which they exert renoprotective effects in diabetic nephropathy. PMID: 26972502
32. Small Molecule Inhibition of Ligand-Stimulated RAGE-DIAPH1 Signal Transduction. PMID: 26936329
33. Interaction of extracellular S100A4 with RAGE prompts prometastatic activation of melanoma cells. PMID: 26928771
34. Study demonstrated that 1,25(OH)2D3, the active form of vitamin D, plays an important role in increasing Abeta1-40 vectorial transport from the brain to blood and systemic clearance from peripheral circulation through increasing LRP1 levels both in vivo and in vitro, and reducing RAGE level in the blood-brain barrier model in vitro PMID: 26820600
35. This present study confirmed an important role of RAGE in vivo and vitro models of pulmonary fibrosis and suggested the therapeutic possibility for pulmonary fibrosis via RAGE regulation PMID: 26545872
36. beta-Caryophyllene protects against GalN/LPS-induced liver injury through down-regulation of the TLR4 and RAGE signaling. PMID: 26254779
37. AGER and its functions to stimulate O-GlcNAcylation are important during liver tumorigenesis, when high blood glucose levels are inadequately controlled. PMID: 26825459
38. HMGB1 and its main receptor, RAGE, appear to be crucial factors in the pathogenesis of TnI-induced experimental autoimmune myocarditis. PMID: 26715748
39. Only one fragment RAGE (60-76) was shown to have a therapeutic activity improving the memory state of bulbectomized mice and leads to decreasing in the level of brain beta-amyloid. PMID: 27125025
40. These data implicate RAGE as a modulator of both vasoreactivity and of proliferative processes in the response of the pulmonary circulation to chronic-hypoxia. PMID: 24417910
41. activation of the RAGE by advanced glycation end products or other ligands suppresses NIPP1 expression in diabetic nephropathy, contributes to podocyte hypertrophy, and glomerular inflammation PMID: 24476693
42. RAGE-/- mice showed reduced inflammation, lower Th2 cytokine production from mononuclear cells, and lower numbers of group 2 innate lymphoid cells in the lung compared with RAGE+/+ mice. PMID: 26472810
43. Mice expressing RAGE on hematopoietic cells, but not radioresistant structural cells, showed reduced neutrophilia and emphysematous change in the lung. PMID: 25188021
44. RAGE has a role in pathogenesis of emphysema in mice. PMID: 25781626
45. RAGE enhances autophagy and neutrophil extracellular traps in pancreatic cancer. PMID: 25908451
46. A soluble receptor for advanced glycation end-products (sRAGE) protects cardiomyocytes from apoptosis induced by ischemia/ reperfusion in vitro and in vivo by activating the JAK2/STAT3 signaling pathway. PMID: 25894538
47. Pulmonary RAGE promotes asthma pathogenesis through IL-33 and accumulation of group 2 innate lymphoid cells. PMID: 25930197
48. Soluble receptor for advanced glycation end-products (sRAGE) is a marker of alveolar type I cell injury. Read More: http://www.atsjournals.org/doi/full/10.1164/rccm.201501-0020OC#.Vh3kYtKFPyA PMID: 25932660
49. Data define a pivotal role for RAGE in initiating the events associated with exposure of sympathetic neurons to high glucose, and strongly support RAGE signaling as a potential therapeutic target in the autonomic complications associated with diabetes PMID: 25431195
50. Data indicate that chronic hypoxia is associated with downregulation of pulmonary receptor for advanced glycation end products (RAGE) protein levels, but a relative increase in sRAGE. PMID: 25703138

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[Isoform 1]: Membrane; Single-pass type I membrane protein.; [Isoform 2]: Secreted.; [Isoform 10]: Cell membrane; Single-pass membrane protein.

Isoform 1: Expressed at higher levels in the coronary arterioles in type 2 diabetic mice (at protein level). Endothelial cells. Expressed in lung, kidney, brain and heart. Most prevalent isoform with the highest level in heart. Isoform 2: Expressed in bra

KEGG: mmu:11596

STRING: 10090.ENSMUSP00000015596

UniGene: Mm.3383