|
ORF cDNA clones
|
CRISPR / TALEN
|
Lentivirus
|
AAV
|
TALE-TF
|
ORF knockin clones
|
|
Antibody
|
Proteins
|
miRNA target clones
|
qPCR primers
|
shRNA clones
|
miRNA products
|
Promoter clones
|
Validated All-in-One™ qPCR Primer for AGER(NM_001136.4) Search again
Product ID:
HQP094823
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
RAGE, SCARJ1, sRAGE
Gene Description:
advanced glycosylation end-product specific receptor
Target Gene Accession:
NM_001136.4(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
|
|
| A | B |
|
Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
|
Summary
This gene encodes a member of the immunoglobulin superfamily of cell surface molecules. It is a receptor for various molecules, including the amyloidogenic form of serum amyloid A, amyloid-beta protein, members of the S100/calgranulin superfamily and advanced glycation end products. The gene lies within the major histocompatibility complex (MHC) class III region on chromosome 6.
Gene References into function
- mRNA and protein expression in Caco-2 cells
- this study we have investigated a possible role of RAGE and amphoterin in the retinoic acid-induced differentiation of neuroblastoma cells.
- susceptibility to the development of chronic periodontitis could be influenced by the 1704G/T polymorphism of the RAGE gene, independently of diabetes
- Polymorphisms 1704G/T, 2184A/G, and 2245G/A in the rage gene are not associated with diabetic retinopathy in NIDDM
- allele frequencies and genotype distribution combinations of four polymorphisms in the RAGE gene (6p21.3, G82S, 1704G/T, 2184A/G and 2245A/G) of 272 subjects (130 patients with plaque psoriasis and 142 healthy control).
- increased prevalence of the 82S allele in patients with rheumatoid arthritis compared with control subjects
- There is an association of Gly82Ser polymorphism in this gene with diabetic retinopathy in type II diabetic Asian Indian patients.
- Data show that vascular endothelial cells and pericytes express three novel splice variants of receptor for advanced glycation end-products (RAGE) mRNA.
- co-expression of RAGE and amphoterin is closely associated with invasion and metastasis of colorectal cancer
- These data reinforce the importance of receptor for advanced glycation end products (RAGE)-ligand interactions in modulating properties of CD4+ T cells that infiltrate the central nervous system
- association between -374 T/A RAGE polymorphism and cardiovascular disease and albumin excretion in type 1 diabetics with poor metabolic control suggests gene-environment interaction in development of diabetic nephropathy and cardiovascular complications
- The RAGE is expressed in dying neurons and suggest that RAGE may have a role in neuronal cell death mediated by ischemic stress.
- Advanced glycation end products and receptor for advanced glycation end products are found in AA amyloidosis.
- AGEs can augment inflammatory responses by up-regulating COX-2 via RAGE and multiple signaling pathways, thereby leading to monocyte activation and vascular cell dysfunction
- Results suggest a possible role of S100 protein- and RAGE-mediated signal transduction in the development of specific cancers.
- In vitro binding studies using a series of C-terminal deletion mutants of human RAGE revealed the importance of the membrane-proximal cytoplasmic region of RAGE for the direct ERK-RAGE interaction.
- No association betwween -429T/C and -37T/A polymorphism in RAGE gene promoter with diabetic retinopathy in NIDDM in Chinese patients
- identified three novel RAGE transcripts all encoding truncated soluble forms of RAGE. The relative expression ratios for the full-length RAGE transcript to the sum of its splice-variants encoding the soluble variants varied strongly among tissues.
- Oleate, not ligands of the receptor for advanced glycation end-products, acts as an enhancer of human smooth muscle cell proliferation.
- Our study failed to demonstrate an association between either - 429 T/C or - 374 T/A gene polymorphism of the RAGE gene and diabetic retinopathy in Caucasians with type 2 diabetes
- RAGE G1704T polymorphisms may be useful in identifying the risk for developing diabetic nephropathy in type 2 diabetic patients.
- AGE might be involved in the growth and invasion of melanoma through interactions with RAGE and represent promising candidates for assessing the future therapeutic potential of this therapy in treating patients with melanoma.
- results suggest that the decrease in monocyte RAGE expression can be at least partly accounted for by the ligand engagement and may be a factor contributing to the development of diabetic vascular complications
- AGER mediates S100A13 protein translocation in response to extracellular S100
- Patients with type 2 diabetes and the 63bp deletion in the promoter of RAGE seem to be protected from diabetic nephropathy.
- Only cells expressing RAGE at the cell surface showed hypersensitivity to Abeta.
- Findings using advanced glycosylation end products (AGEs) with strong RAGE-binding properties indicate that AGEs may not uniformly play a role in cellular activation.
- Review. RAGE is an amplification step in vascular inflammation and acceleration of atherosclerosis.
- the RAGE pathway plays a critical proinflammatory role in vasculitic neuropathy.
- Advanced glycation end products (AGE) by binding to AGE receptor (RAGE) per se could control mesangial cell growth.
- Corellation of expression of tissue factor (TF) and the receptor for advanced glycation end products (RAGEs) and vascular complications in diabetic patients
- RAGE expression is upregulated on monocytes from patients with chronic kidney disease
- RAGE and MMP-9 are expressed concordant with the metastatic ability of the human pancreatic cancer cells. Could be key to regulating metastatic ability of pancreatic cancer.
- AGER has a role as a pleiotropic antagonistic gene (review)
- AGER1 suppressed AGE mediated NF-kappaB and MAPK/p44/p42 activities and suppressed AGE-mediated mesangial cell inflammatory injury through negative regulation of RAGE
- Thiazolidinedione antidiabetics modulate vascular endothelial RAGE expression.
- Down-regulation of RAGE may be considered as a critical step in tissue reorganization and the formation of lung tumours.
- 374T/A polymorphism of the RAGE gene may reduce susceptibility to coronary artery disease
- RAGE may have multiple functions in the human brain, mediated by the individual or coordinated efforts of the different RAGE isoforms
- data demonstrate that the RAGE-NF-kappaB axis operates in diabetic neuropathy, by mediating functional sensory deficits, and that its inhibition may provide new therapeutic approaches
- RAGE, via its interaction with ligands, serves as a cofactor exacerbating diabetic vascular disease. (review)
- DU145 cells, a hormone-independent prostate cancer cell line, showed the highest RAGE mRNA expression
- The RAGE2 haplotype is associated with diabetic nephropathy (DN) in type 2 diabetics and with earlier DN onset and can be regarded as a marker for DN.
- data suggest that G1704T and G82S polymorphisms of the advanced glycation end product receptor (RAGE) gene are not related to microalbuminuria in Japanese type 2 diabetic patients
- 82 Serine allele of the RAGE gene is a risk allele for developing advanced nephropathy in diabettes mellitus.
- Reactive oxygen species generated by the TNF-alpha-stimulated umbilical vein endothelial cells induce RAGE expression.
- results show that the -374A allele (-374T>A polymorphism) in the RAGE gene is related to the susceptibility of developing ischemic heart disease in African-Brazilians with type 2 diabetes
- Antibodies against RAGE receptor blocked Abeta-induced activation of the p38, JNK pathways, and NF-kappaB in CTL cybrids and offered protection against the neurotoxic effects of Abeta.
- results reveal HMGB1 and RAGE as the first known autocrine loop modulating the maturation of plasmacytoid dendritic cells
- data suggest that activation of the receptor for advanced glycation end products (RAGE) pathway may be one of the first steps in the pathogenesis of diabetic polyneuropathies
- ACE inhibition reduces the accumulation of AGE in diabetes partly by increasing the production and secretion of sRAGE into plasma
- polymorphisms G1704T and G82S of the RAGE gene are not related to DR in Japanese type 2 diabetic patients.
- polymorphisms G1704T and G82S of the RAGE gene are not related to DR in Japanese type 2 diabetic patients.
- Advanced glycosylation end-product receptor (RAGE) is required for the effect of high mobility group box 1 (HMGB1) on dendritic cells; HMGB1/RAGE interaction results in downstream activation of MAP kinases and NF-kappa B.
- data suggests that the CML-RAGE-NF-kappaB pathway is an evident proinflammatory pathomechanism in mononuclear effector cells in polymyositis and dermatomyositis
- RAGE, an endogenous decoy receptor, may be related to individual variations in resistance to the development of diabetic vascular complications, observed in transgenic mice.
- The increase in RAGE noted in osteoarthritis(OA) cartilage and the ability of RAGE ligands to stimulate chondrocyte MAP kinase and NF-kappaB activity and to stimulate MMP-13 production suggests that chondrocyte RAGE signaling could play a role in OA.
- S100P plays a major role in the aggressiveness of pancreatic cancer that is likely mediated by its ability to activate RAGE
- These results suggest that RAGE expression appears to be closely associated with the invasiveness of oral squamous cell carcinoma and represents a promising candidate for assessing the future therapeutic potential in treating patients with oral carcinoma
- Analysis of specific manifestations of cardiovascular disease, including coronary heart disease (CHD), cardiovascular disease (CVD), myocardial infarction (MI) and ischemic disease (ISD) revealed no association with RAGE genotype.
- Data suggest that re-expression of the receptor for advanced glycation end-products in lung cancer cells impairs the proliferative stimulus mediated by fibroblasts.
- a cross-talk exists between the AGE-RAGE system and the angiotensin II receptor (renin-angiotensin system), and serum levels of sRAGE may reflect endothelial RAGE expression
- Patients with Alzheimer disease have reduced levels of sRAGE in plasma compared with patients with vascular dementia and controls.
- RAGE is mainly expressed in fibroblasts, dendrocytes, and keratinocytes and to a minor extent in endothelial and mononuclear cells.
- study found a modest association with the -RAGE 374T/A polymorphism in the nonproliferative diabetic retinopathy subgroup
- The existence of splice variants of RAGE in endothelial cells might explain the lack of interaction of extracellular AGEs with endothelial cells.
- Association of level in serum with albuminuria may be a marker of microvascular damage in type 2 diabetes.
- 3 AGER genetic variants: -429T>C, -374T>A, and Gly82Ser were determined in cerebral ischemia and stroke patients. Specific haplotypes were associated with reduced risk of incident myocardial infarction & ischemic stroke, independent of diabetes status.
- CRP at concentrations known to predict future vascular events upregulates RAGE expression in human endothelial cells at both the protein and mRNA level. Silencing of the RAGE gene prevents CRP-induced macrophage chemoattractant protein 1 activation.
- adhesion of red blood cells from type 2 diabetes patients was mediated by RAGE
- AGER1 negatively regulates AGE-mediated oxidant stress-dependent signaling via the EGFR and Shc/Grb2/Ras pathway.
- observation suggests that the RAGE gene polymorphism is not associated with in-stent restenosis after coronary artery stenting in non-diabetic patients in the Korean population
- results show an association between the AGER -374 T/A polymorphism & type 1 diabetes; the polymorphism was associated with diabetic nephropathy in both type 1 & type 2 diabetes & with sight-threatening retinopathy in type 1 diabetic patients
- Serum levels are associated with the severity of nephropathy in type 2 diabetic patients.
- Telmisartan: it may work as an anti-inflammatory agent against AGE by suppressing RAGE expression via PPAR-gamma activation in the liver.
- Serum levels are significantly higher in type 2 diabetic patients than in non-diabetics and are positively associated with the presence of coronary artery disease.
- data suggest that the autocrine/paracrine release of HMGB1 and the integrity of the HMGB1/RAGE pathway are required for the migratory function of dendritic cells
- Soluble RAGE forms tetramers that bind to hexamers of Ca2+-calgranulin C, creating a large platform for effectively transmitting RAGE-dependent signals from extracellular S100 proteins to the cytoplasmic signaling complexes.
- association of RAGE and its ligands with sarcoidosis and suggest that an intrinsic genetic factor could be in part involved in its expression. In Italian patients, the -374 T/A polymorphism seems to be significantly associated with this disease.
- The results of this large population study demonstrate that the AA/GA genotypes of the RAGE +557G>A polymorphism are associated with a significantly decreased risk of significant coronary artery disease.
- study demonstrates that HOCl-modified albumin acts as a ligand for RAGE and promotes RAGE-mediated inflammatory complications
- subjects with homozygosity for the minor S allele of the G82S polymorphism of RAGE had higher risk factors for cardiovascular disease
- We demonstrated that after successful TX, PAPP-A and sRAGE decrease and early chronic vascular changes in the kidney TX are associated with elevation of their serum levels.
- Soluble but not sescretory protein is associated with albuminuria in type 2 diabetic paaatients, whil neither is associated with markers of glucose control or macrovascular disease.
- evidence provided for activation of the NF-kappaB system in intervertebral discs in vivo which correlates with accumulated oxidative stress & increases in age & disc degeneration; oxidative stress may lead to RAGE activation & NF-kappaB translocation
- the RAGE Ser82 allele does not predispose to cardiovascular events in rheumatoid arthritis.
- Accumulation of AGE may have a role in the development of osteoarthritis.
- Expression of Endogenous secretory receptor for advanced glycation endproducts was significantly higher in chondrosarcomas
- High level bacterial expression systems and purification protocols were generated for the extracellular region of RAGE (sRAGE) and the five permutations of single and tandem domain constructs.
- The -429 T>C polymorphism in the RAGE promoter is associated with type 1 diabetes in a Brazilian population, with a 2-fold increase of C-allele frequency compared to non-diabetic subjects
- Data show that soluble RAGE blocks scavenger receptor CD36-mediated uptake of hypochlorite-modified low-density lipoprotein.
- it is concluded that CDK5RAP3, CCNB2, and RAGE genes may be used as a very reliable biomarkers of lung adenocarcinoma
- Olmesartan may play a protective role against proliferative diabetic retinopathy by attenuating the deleterious effects of AGEs via down-regulation of RAGE.
- RAGE was found throughout the testis, caput epididymis, particularly the principle cells apical region, and on sperm acrosomes in men with diabetes mellitus.
- Serum levels of sRAGE are associated with inflammatory markers in patients with type 2 diabetes.
- Multivariate analysis showed high-grade expression of RAGE to be an independent prognostic factor for disease-free survival in oral squamous cell carcinoma.
- Higher levels of plasma RAGE measured shortly after reperfusion predicted poor short-term outcomes from lung transplantation. Elevated plasma RAGE levels may have both pathogenetic and prognostic value in patients after lung transplantation.
- Treating type 2 diabetic patients with thiazolidinedione can increase circulating levels of RAGE.
- Data suggest that deregulation of RAGE expression in myoblasts might concur in rhabdomyosarcomagenesis and that increasing RAGE expression in rhabdomyosarcoma cells might reduce their tumor potential.
- Structural and the binding data suggest that tetrameric S100B triggers RAGE activation by receptor dimerisation.
- The receptor of advanced glycation end product (RAGE) -374 T/A single nucleotide polymorphism affected the dialysate-to-plasma ratio of creatinine at baseline, suggesting that the RAGE polymorphism may effect the basal peritoneal solute transport rate.
- De-N-glycosylation or G82S mutation of RAGE increases affinity for AGE ligands, and may sensitize cells or conditions with it to AGE.
- result confirms that the -374AA genotype of the RAGE gene promoter is a protective factor against the severity of coronary artery disease lesions in type 2 diabetic patients
- Suggest key mechanisma by which AGER1 maintains cellular resistance against AGE-induced oxidative stress.
- Plasma soluble RAGE and endogenous secretory RAGE are not associated with measures of diabetic neuropathy in type 2 diabetes patients.
- Calculating the S100A12:sRAGE ratio might help to detect patients with KD who are at risk of being unresponsive to IVIG therapy.
- serum sRAGE levels were influenced by genetic polymorphisms (-429 T/C, Gly82Ser and 2184 A/G) of the RAGE gene in breast cancer.
- HMGB-1 and BSA-AGE stimulated the invasiveness of fibroblast-like synoviocytes in rheumatoid arthritis by activation of RAGE.
- Single nucleotide polymorphisms may contribute to development of glucose intolerance and type 2 diabetes.
- endothelial RAGE and its ligands mediate vascular and inflammatory stresses that culminate in atherosclerosis in the vulnerable vessel wall
- HCC during the early stage of tumorigenesis with less blood supply may acquire resistance to stringent hypoxic milieu by hypoxia-induced RAGE expression.
- RAGE_v1 variant is the primary secreted soluble isoform of RAGE. identification of functional splice variants of RAGE underscores biological diversity of the RAGE gene & will aid in understanding of the gene in the normal & pathological state.
- the -374AA genotype of the RAGE gene promoter could be associated with a reduced risk of in-stent restenosis after coronary stent implantation
- This preliminary study supports the hypothesis that the RAGE system might participate in the disease pathway of primary Sjogren's syndrome (SS), and that sRAGE may be a potential biomarker to aid in the diagnosis of primary SS.
- Loss of RAGE contributes to idiopathic pulmonary fibrosis pathogenesis.
- Endothelial dysfunction in chronic kidney disease may be partly mediated by advanced glycation end product-induced inhibition of endothelial nitric oxide synthase through RAGE activation.
- RAGE could also behave as a receptor for Mycobacterium tuberculosis
- -374T/A RAGE polymorphism is an independent protective factor for cardiac events in nondiabetic patients with coronary artery disease
- study identified advanced glycation end products as the ligand for RAGE on both invasive and non-invasive prostate cancer cells
- The SAA-RAGE-stimulated NF-kappaB signaling pathway has an important role in the pathogenesis of rheumatoid arthritis.
- S100A8/A9-promoted cell growth occurs through RAGE signaling and activation of NF-kappaB.
- These findings reveal new aspects of RAGE regulation and signaling and also provide a new interaction between RAGE and human pathologies.
- results indicate that RAGE serves a protective role in the lung, and that loss of the receptor is related to functional changes of pulmonary cell types, with the consequences of fibrotic disease
- results show significant downregulation of the total RAGE mRNA transcripts in peripheral blood mononuclear cells of patients with probable Alzheimer disease
- low expression of endogenous secretory RAGE in the hippocampus would be associated with the development of Alzheimer's disease
- shedding of RAGE might occur as reactive oxygen species accumulate in brain cells and be part of the process of neurodegeneration
- AGEs induce ROS generation and intensify the proliferation and activation of HSCs, supporting the possibility that antioxidants may represent a promising treatment for prevention of the development of hepatic fibrosis in NASH.
- the peritoneal membrane of the uraemic patients showed an increased submesothelial thickness and a marked induction of RAGE expression and NFkappaB-binding activity
- Distinct regions of RAGE are involved in Abeta-induced cellular and neuronal toxicity with respect to the Abeta aggregation state, suggesing the blockage of particular sites of the receptor as a therapeutic strategy to attenuate neuronal death.
- RAGE Gly82Ser polymorphism may confer not only an increased risk of gastric cancer but also with invasion of gastric cancer in the Chinese population.
- Serum AGER levels are associated with the severity of renal dysfunction and duration of diabetes in type 2 diabetic patients/
- association between diabetic complications and LTA, TNF and AGER polymorphisms is complex, with partly different alleles conferring susceptibility in type 1 and type 2 diabetic patients
- Advanced oxidation protein products might be new ligands of endothelial RAGE. AOPPs-HSA activates vascular ECs via RAGE-mediated signals.
- The sheddase ADAM10 was identified as a membrane protease responsible for RAGE cleavage.
- study defines RAGE (receptor for advanced glycation end products) as the hS100A7 receptor, whereas hS100A15 functions through a Gi protein-coupled receptor; hS100A7-RAGE binding, signaling, and chemotaxis are zinc-dependent in vitro
- GFR is a principal determinant of sRAGE concentration and gradual sRAGE increase in subjects with advancing impairment of renal function is paralleled by AGE and its receptor
- Mediation of RAGE affects the balance of cellular proliferation and apoptosis
- RAGE levels increase in conjunction with the onset of Alzheimer's disease, and continue to increase linearly as a function of pathologic severity
- Structural basis for pattern recognition by the receptor for advanced glycation end products (RAGE).
- RAGE, carboxylated glycans and S100A8/A9 play essential roles in tumor-stromal interactions, leading to inflammation-associated colon carcinogenesis.
- maternal esRAGE concentrations are significantly increased in patients with preeclampsia during pregnancy
- association of low soluble isoform of RAGE (sRAGE) with high CML-protein levels in diabetic patients who developed severe diabetic complications supports the hypothesis that sRAGE protects vessels AGE-mediated diabetic microvascular damage
- RAGE was markedly and diffusely expressed in blood vessels, neurons, and the choroid plexus in the brains of two patients who died as the result of brain edema that developed during the treatment of severe diabetic ketoacidosis
- likely that circulating soluble RAGE and endogenous secretory RAGE are distinct markers and that circulating esRAGE levels are associated with the status of early-stage atherosclerosis.
- Advanced glycation end products (AGE) and circulating receptor for AGE (RAGE) levels are independently associated with decreased glomerular filtration rate (GFR) and seem to predict decreased GFR.
- We found no consistent association between prevalent type 2 diabetes mellitus and insulin indices and AGER polymorphisms
- HNRNP K and microRNA-16 have roles in cyclooxygenase-2 RNA stability induced by S100b, a ligand of the receptor for advanced glycation end products
- the interaction of the RAGE cytoplasmic domain with Dia-1 is required to transduce extracellular environmental cues evoked by binding of RAGE ligands to their cell surface receptor, resulting in Rac-1 and Cdc42 activation and cellular migration
- RAGE signaling contributes to neuroinflammation in infantile neuronal ceroid lipofuscinosis.
- ADAM10 and MMP9 to be involved in RAGE shedding.
- Thus, HMGB1-RAGE signaling links necrosis with macrophage activation and may provide a target for anti-inflammatory therapy in stroke.
- new insight into AGE-RAGE interaction
- A set of tumours, healthy tissues and various cancer cell lines were screened for RAGE splicing variants and analysed their structure.
- These results indicate that RAGE signaling directly contributes to pathology in cerebral ischemia.
- several differences in the levels of advanced glycation end products, sRAGE, and proinflammatory cytokines between euglycemic and diabetic pregnancies
- No significant correlation between serum levels off RAGE in hypertensive agents.