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R&D Systems monoclonal anti rage antibody
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R&D Systems esrage variants
Comparison of AGEs, <t> sRAGE </t> isoforms, and their ratios between healthy controls (CTR) and patients with type 2 diabetes
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Comparison of AGEs, <t> sRAGE </t> isoforms, and their ratios between healthy controls (CTR) and patients with type 2 diabetes
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R&D Systems human s100a12 en rage duoset elisa
Comparison of AGEs, <t> sRAGE </t> isoforms, and their ratios between healthy controls (CTR) and patients with type 2 diabetes
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Cell Signaling Technology Inc rage
In A, chondrocytes were pretreated with <t>anti-RAGE</t> (5 μg/ml) for 12 hours before AGEs (100 μg/ml) stimulation. In B, chondrocytes were pretreated with SB203580, SP600125, PD98059 (10 μM) for 30 minutes prior to AGEs (100 μg/ml) stimulation. The expression of PPARγ was quantified by real-time PCR and western blotting using β-actin as an internal control. In A, densitometric analysis for PPARγ levels corrected to β-actin is shown. All data are expressed as means ± SD and are representative of three independent experiments. *: p< 0 . 05 versus control, #: p< 0 . 05 versus AGEs treatment, &: p> 0 . 05 versus AGEs treatment.
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R&D Systems rat anti rage
In A, chondrocytes were pretreated with <t>anti-RAGE</t> (5 μg/ml) for 12 hours before AGEs (100 μg/ml) stimulation. In B, chondrocytes were pretreated with SB203580, SP600125, PD98059 (10 μM) for 30 minutes prior to AGEs (100 μg/ml) stimulation. The expression of PPARγ was quantified by real-time PCR and western blotting using β-actin as an internal control. In A, densitometric analysis for PPARγ levels corrected to β-actin is shown. All data are expressed as means ± SD and are representative of three independent experiments. *: p< 0 . 05 versus control, #: p< 0 . 05 versus AGEs treatment, &: p> 0 . 05 versus AGEs treatment.
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R&D Systems mab11795 synaptophysin presynaptic vesicles mouse
List of antibodies used in this study
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Boster Bio rage
EGCG inhibits balloon <t>injury-induced</t> <t>HMGB1</t> and <t>RAGE</t> expression levels. mRNA expression levels of (A) HMGB1 and (B) RAGE in artery tissues were determined by reverse transcription-quantitative polymerase chain reaction. Protein expression levels of (C) HMGB1 and (D) RAGE in artery tissues were detected by western blotting. β-actin was used as a loading control. The protein bands were quantified by gray scanning. Data are presented as the mean + standard deviation (n=6). *P<0.05, **P<0.01 and ***P<0.001 vs. the sham group; # P<0.05, ## P<0.01 and ### P<0.001 vs. the injury group. EGCG, epigallocatechin-3-gallate; HMGB1, high mobility group box 1; RAGE, receptor of advanced glycation end products.
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Image Search Results


Comparison of AGEs,  sRAGE  isoforms, and their ratios between healthy controls (CTR) and patients with type 2 diabetes

Journal: Cardiovascular Diabetology

Article Title: Circulating levels of AGEs and soluble RAGE isoforms are associated with all-cause mortality and development of cardiovascular complications in type 2 diabetes: a retrospective cohort study

doi: 10.1186/s12933-022-01535-3

Figure Lengend Snippet: Comparison of AGEs, sRAGE isoforms, and their ratios between healthy controls (CTR) and patients with type 2 diabetes

Article Snippet: Specifically, total human sRAGE included the detection of both cRAGE and esRAGE variants (DY1145, Human RAGE DuoSet ELISA, R&D Systems Inc., MN, USA) and esRAGE concentration was evaluated by an ELISA assay with an antibody raised against the exclusive C-terminal amino acids (332–347) sequence (K1009-1, B-bridge International, CA, USA). cRAGE was determined by subtracting esRAGE from sRAGE as already described [ , , ].

Techniques: Comparison

Boxplots for the comparison of A total sRAGE, esRAGE, and cRAGE isoforms and ) AGEs/sRAGE, AGEs/esRAGE, AGEs/cRAGE, cRAGE/esRAGE ratio among healthy control subjects (CTR) and type 2 diabetes patients without (T2DM-NC) or with (T2DM-C) complications. **p < 0.01; ***p < 0.001; ****p < 0.0001 for Dunn’s post-hoc tests following Kruskal-Wallis H test

Journal: Cardiovascular Diabetology

Article Title: Circulating levels of AGEs and soluble RAGE isoforms are associated with all-cause mortality and development of cardiovascular complications in type 2 diabetes: a retrospective cohort study

doi: 10.1186/s12933-022-01535-3

Figure Lengend Snippet: Boxplots for the comparison of A total sRAGE, esRAGE, and cRAGE isoforms and ) AGEs/sRAGE, AGEs/esRAGE, AGEs/cRAGE, cRAGE/esRAGE ratio among healthy control subjects (CTR) and type 2 diabetes patients without (T2DM-NC) or with (T2DM-C) complications. **p < 0.01; ***p < 0.001; ****p < 0.0001 for Dunn’s post-hoc tests following Kruskal-Wallis H test

Article Snippet: Specifically, total human sRAGE included the detection of both cRAGE and esRAGE variants (DY1145, Human RAGE DuoSet ELISA, R&D Systems Inc., MN, USA) and esRAGE concentration was evaluated by an ELISA assay with an antibody raised against the exclusive C-terminal amino acids (332–347) sequence (K1009-1, B-bridge International, CA, USA). cRAGE was determined by subtracting esRAGE from sRAGE as already described [ , , ].

Techniques: Comparison, Control

Spearman correlations of AGEs and the different isoforms of  sRAGE  isoforms with age in healthy controls (CTR) and patients with type 2 diabetes

Journal: Cardiovascular Diabetology

Article Title: Circulating levels of AGEs and soluble RAGE isoforms are associated with all-cause mortality and development of cardiovascular complications in type 2 diabetes: a retrospective cohort study

doi: 10.1186/s12933-022-01535-3

Figure Lengend Snippet: Spearman correlations of AGEs and the different isoforms of sRAGE isoforms with age in healthy controls (CTR) and patients with type 2 diabetes

Article Snippet: Specifically, total human sRAGE included the detection of both cRAGE and esRAGE variants (DY1145, Human RAGE DuoSet ELISA, R&D Systems Inc., MN, USA) and esRAGE concentration was evaluated by an ELISA assay with an antibody raised against the exclusive C-terminal amino acids (332–347) sequence (K1009-1, B-bridge International, CA, USA). cRAGE was determined by subtracting esRAGE from sRAGE as already described [ , , ].

Techniques:

Age- and HbA1c-adjusted multiple quantile regression model for the evaluation of AGEs and  sRAGE  isoforms in type 2 diabetes complications

Journal: Cardiovascular Diabetology

Article Title: Circulating levels of AGEs and soluble RAGE isoforms are associated with all-cause mortality and development of cardiovascular complications in type 2 diabetes: a retrospective cohort study

doi: 10.1186/s12933-022-01535-3

Figure Lengend Snippet: Age- and HbA1c-adjusted multiple quantile regression model for the evaluation of AGEs and sRAGE isoforms in type 2 diabetes complications

Article Snippet: Specifically, total human sRAGE included the detection of both cRAGE and esRAGE variants (DY1145, Human RAGE DuoSet ELISA, R&D Systems Inc., MN, USA) and esRAGE concentration was evaluated by an ELISA assay with an antibody raised against the exclusive C-terminal amino acids (332–347) sequence (K1009-1, B-bridge International, CA, USA). cRAGE was determined by subtracting esRAGE from sRAGE as already described [ , , ].

Techniques:

Univariate and multivariate Cox regression analysis for the prediction of 15-year all-cause mortality in patients with type 2 diabetes

Journal: Cardiovascular Diabetology

Article Title: Circulating levels of AGEs and soluble RAGE isoforms are associated with all-cause mortality and development of cardiovascular complications in type 2 diabetes: a retrospective cohort study

doi: 10.1186/s12933-022-01535-3

Figure Lengend Snippet: Univariate and multivariate Cox regression analysis for the prediction of 15-year all-cause mortality in patients with type 2 diabetes

Article Snippet: Specifically, total human sRAGE included the detection of both cRAGE and esRAGE variants (DY1145, Human RAGE DuoSet ELISA, R&D Systems Inc., MN, USA) and esRAGE concentration was evaluated by an ELISA assay with an antibody raised against the exclusive C-terminal amino acids (332–347) sequence (K1009-1, B-bridge International, CA, USA). cRAGE was determined by subtracting esRAGE from sRAGE as already described [ , , ].

Techniques:

In A, chondrocytes were pretreated with anti-RAGE (5 μg/ml) for 12 hours before AGEs (100 μg/ml) stimulation. In B, chondrocytes were pretreated with SB203580, SP600125, PD98059 (10 μM) for 30 minutes prior to AGEs (100 μg/ml) stimulation. The expression of PPARγ was quantified by real-time PCR and western blotting using β-actin as an internal control. In A, densitometric analysis for PPARγ levels corrected to β-actin is shown. All data are expressed as means ± SD and are representative of three independent experiments. *: p< 0 . 05 versus control, #: p< 0 . 05 versus AGEs treatment, &: p> 0 . 05 versus AGEs treatment.

Journal: PLoS ONE

Article Title: The Role of PPARγ in Advanced Glycation End Products-Induced Inflammatory Response in Human Chondrocytes

doi: 10.1371/journal.pone.0125776

Figure Lengend Snippet: In A, chondrocytes were pretreated with anti-RAGE (5 μg/ml) for 12 hours before AGEs (100 μg/ml) stimulation. In B, chondrocytes were pretreated with SB203580, SP600125, PD98059 (10 μM) for 30 minutes prior to AGEs (100 μg/ml) stimulation. The expression of PPARγ was quantified by real-time PCR and western blotting using β-actin as an internal control. In A, densitometric analysis for PPARγ levels corrected to β-actin is shown. All data are expressed as means ± SD and are representative of three independent experiments. *: p< 0 . 05 versus control, #: p< 0 . 05 versus AGEs treatment, &: p> 0 . 05 versus AGEs treatment.

Article Snippet: Rabbit monoclonal antibodies specific for IL-1β, NF-κB p65, PPARγ, TNF-α, IκBα, β-actin and RAGE were purchased from Cell signaling Technology (Danvers, MA, USA).

Techniques: Expressing, Real-time Polymerase Chain Reaction, Western Blot, Control

List of antibodies used in this study

Journal: Acta neuropathologica

Article Title: Beta-Amyloid pathology in human brain microvessel extracts from the parietal cortex: Relation with cerebral amyloid angiopathy and Alzheimer’s Disease

doi: 10.1007/s00401-019-01967-4

Figure Lengend Snippet: List of antibodies used in this study

Article Snippet: Protein Role/localization Host Dilution Company Catalog number WB IF α-SMA Smooth muscle cell Rabbit 1:1000 1:100 Abcam ab5694 Aβ40 Aβ peptide Mouse ---------- 1:100 BioLegend 805401 Aβ42 Aβ peptide Mouse ---------- 1:100 BioLegend 805501 ABCB1 BBB transporter Rabbit 1:2000 1:100 Abcam ab170904 APP Aβ precursor Mouse 1:500 ---------- BioLegend 803003 BACE1 Aβ production Rabbit 1:500 ---------- Abcam ab108394 CD31 EC intercellular junctions Rabbit 1:1000 ---------- Abcam ab28364 Claudin-5 EC intercellular junctions Rabbit 1:2000 1:100 Santa Cruz Biotechnology sc-28670; discontinued Cyclophilin B Loading control Rabbit 1:1000 ---------- Abcam ab16045 LRP1 BBB receptor Rabbit 1:20000 ---------- Abcam ab92544 Neprilysin Aβ-degrading enzyme Rabbit 1:2000 ---------- Abcam ab79423 NeuN Neuronal nuclei Rabbit 1:1000 1:1000 Abcam ab177487 Occludin EC intercellular junctions Rabbit 1:1000 ---------- Invitrogen 71-1500 PDGFRβ Pericyte receptor Rabbit 1:2000 1:100 Abcam ab32570 RAGE BBB receptor Rat 1:2000 ---------- R&D Systems MAB11795 Synaptophysin Presynaptic vesicles Mouse 1:20000 ---------- Millipore MAB368; discontinued Type IV collagen Basal membrane Goat ---------- 1:500 Millipore AB769 Open in a separate window Abbreviations: Aβ, beta amyloid peptides; ABCB1, P-glycoprotein; APP, amyloid protein precursor; BACE1, β-secretase; BBB, blood-brain barrier; CD31, platelet endothelial cell adhesion molecule; EC, endothelial cell; IF, immunofluorescence; LRP1, low density lipoprotein receptor-related protein 1; NeuN, neuronal nuclei; RAGE, receptor for advanced glycation end-products; WB, Western blot.

Techniques: Control, Membrane

EGCG inhibits balloon injury-induced HMGB1 and RAGE expression levels. mRNA expression levels of (A) HMGB1 and (B) RAGE in artery tissues were determined by reverse transcription-quantitative polymerase chain reaction. Protein expression levels of (C) HMGB1 and (D) RAGE in artery tissues were detected by western blotting. β-actin was used as a loading control. The protein bands were quantified by gray scanning. Data are presented as the mean + standard deviation (n=6). *P<0.05, **P<0.01 and ***P<0.001 vs. the sham group; # P<0.05, ## P<0.01 and ### P<0.001 vs. the injury group. EGCG, epigallocatechin-3-gallate; HMGB1, high mobility group box 1; RAGE, receptor of advanced glycation end products.

Journal: Experimental and Therapeutic Medicine

Article Title: Epigallocatechin-3-gallate attenuates neointimal hyperplasia in a rat model of carotid artery injury by inhibition of high mobility group box 1 expression

doi: 10.3892/etm.2017.4774

Figure Lengend Snippet: EGCG inhibits balloon injury-induced HMGB1 and RAGE expression levels. mRNA expression levels of (A) HMGB1 and (B) RAGE in artery tissues were determined by reverse transcription-quantitative polymerase chain reaction. Protein expression levels of (C) HMGB1 and (D) RAGE in artery tissues were detected by western blotting. β-actin was used as a loading control. The protein bands were quantified by gray scanning. Data are presented as the mean + standard deviation (n=6). *P<0.05, **P<0.01 and ***P<0.001 vs. the sham group; # P<0.05, ## P<0.01 and ### P<0.001 vs. the injury group. EGCG, epigallocatechin-3-gallate; HMGB1, high mobility group box 1; RAGE, receptor of advanced glycation end products.

Article Snippet: Subsequent to blocking with 5% skimmed milk for 1 h at room temperature, the membranes were incubated with primary antibodies against HMGB1 (Boster Biological Technology, Ltd., Wuhan, China; catalogue no. BA4277; 1:400), RAGE (Boster Biological Technology, Ltd.; catalogue no. PB0530; 1:400), nuclear factor (NF)-κB (Boster Biological Technology, Ltd.; catalogue no. BA0610; 1:400) and β-actin (Santa Cruz Biotechnology, Dallas, USA; catalogue no. sc-47778; 1:400), respectively at 4°C overnight.

Techniques: Expressing, Reverse Transcription, Real-time Polymerase Chain Reaction, Western Blot, Control, Standard Deviation