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massarray® epitypertm  (Sequenom)

 
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    Sequenom massarray® epitypertm
    Massarray® Epitypertm, supplied by Sequenom, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/massarray%C2%AE+epitypertm/epitypertm/pm29948221-74-13-16
    Average 90 stars, based on 1 article reviews
    massarray® epitypertm - by Bioz Stars, 2026-10
    90/100 stars

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    Related Articles

    DNA Methylation Assay:

    Article Title: DNA methylation of miRNA coding sequences putatively associated with childhood obesity.
    Article Snippet: Material andMethods: DNA isolated fromwhite blood cells of 24 children (identification sample: 12 obese and 12 non-obese) from the Grupo Navarro de Obesidad Infantil study was hybridized in a 450K methylation microarray.. Several CpGs whose DNA methylation levels were statistically different between obese and non-obese were validated by MassArray® in 95 children (validation sample) from the same study.

    Article Title: XIX Reunión Nacional de la Asociación Española de Gastroenterología
    Article Snippet: Introducción: La información al paciente es un derecho que éste tiene, y una obligación ética y legal.. En los procedimientos diagnósticos y terapéuticos invasivos, el consentimiento debe obtenerse después de que el paciente reciba una información adecuada verbal y por escrito del mismo, sus beneficios, complicaciones y alternativas.. Esta información debe proporcionarse de forma oportuna antes del procedimiento.

    Article Title: PTPRS and PER3 methylation levels are associated with childhood obesity: results from a genome-wide methylation analysis.
    Article Snippet: Results: Genome-wide analysis identified 734 CpGs (783 genes) differentially methylated between cases (n = 12) and controls (n = 12).. Ingenuity Pathway Analysis showed that these genes were involved in oxidative stress and circadian rhythm signalling pathways.. Moreover, the DNA methylation levels of VIPR2, GRIN2D, ADCYAP1R1, PER3 and PTPRS regions correlated with the obesity trait.

    Article Title: 10th Congress of the International Society of Nutrigenetics/Nutrigenomics (ISNN). May 22-26, 2016, Tel Aviv, Israel: Abstracts.
    Article Snippet: Several CpGs whose DNA methylation levels were statistically different between obese and non-obese were further validated by Sequenom MassArray® EpiTyperTM in 95 children from the same study.

    Article Title: An integrated transcriptomic and epigenomic analysis identifies CD44 gene as a potential biomarker for weight loss within an energy-restricted program.
    Article Snippet: Purpose The interindividual variable response to weight-loss treatments requires the search for new predictive biomarkers for improving the success of weight-loss programs.. The aim of this study is to identify novel genes that distinguish individual responses to a weight-loss dietary treatment by using the integrative analysis of mRNA expression and DNA methylation arrays.. Methods Subjects from Metabolic Syndrome Reduction in Navarra (RESMENA) project were classified as low (LR) or high (HR) responders depending on their weight loss.

    Article Title: 12th European Nutrition Conference (FENS), Berlin, Germany, October 20-23, 2015: Abstracts.
    Article Snippet: DNA methylation levels of the selected CpG-SNPs were quantified by Sequenom MassArray® EpiTyperTM and MS-HRM approaches Results: Seven of these CpG-SNPs, located in the candidate genes UCP1, POMC, BDNF, SH2B1, FTO, IL6R and CRP, were associated with differential DNA methylation of the CpG-SNPs or surrounding CpG sites.

    Mass Spectrometry:

    Article Title: DNA methylation of miRNA coding sequences putatively associated with childhood obesity.
    Article Snippet: Material andMethods: DNA isolated fromwhite blood cells of 24 children (identification sample: 12 obese and 12 non-obese) from the Grupo Navarro de Obesidad Infantil study was hybridized in a 450K methylation microarray.. Several CpGs whose DNA methylation levels were statistically different between obese and non-obese were validated by MassArray® in 95 children (validation sample) from the same study.

    Article Title: XIX Reunión Nacional de la Asociación Española de Gastroenterología
    Article Snippet: Introducción: La información al paciente es un derecho que éste tiene, y una obligación ética y legal.. En los procedimientos diagnósticos y terapéuticos invasivos, el consentimiento debe obtenerse después de que el paciente reciba una información adecuada verbal y por escrito del mismo, sus beneficios, complicaciones y alternativas.. Esta información debe proporcionarse de forma oportuna antes del procedimiento.

    Article Title: PTPRS and PER3 methylation levels are associated with childhood obesity: results from a genome-wide methylation analysis.
    Article Snippet: Results: Genome-wide analysis identified 734 CpGs (783 genes) differentially methylated between cases (n = 12) and controls (n = 12).. Ingenuity Pathway Analysis showed that these genes were involved in oxidative stress and circadian rhythm signalling pathways.. Moreover, the DNA methylation levels of VIPR2, GRIN2D, ADCYAP1R1, PER3 and PTPRS regions correlated with the obesity trait.

    Article Title: 10th Congress of the International Society of Nutrigenetics/Nutrigenomics (ISNN). May 22-26, 2016, Tel Aviv, Israel: Abstracts.
    Article Snippet: Several CpGs whose DNA methylation levels were statistically different between obese and non-obese were further validated by Sequenom MassArray® EpiTyperTM in 95 children from the same study.

    Article Title: An integrated transcriptomic and epigenomic analysis identifies CD44 gene as a potential biomarker for weight loss within an energy-restricted program.
    Article Snippet: Purpose The interindividual variable response to weight-loss treatments requires the search for new predictive biomarkers for improving the success of weight-loss programs.. The aim of this study is to identify novel genes that distinguish individual responses to a weight-loss dietary treatment by using the integrative analysis of mRNA expression and DNA methylation arrays.. Methods Subjects from Metabolic Syndrome Reduction in Navarra (RESMENA) project were classified as low (LR) or high (HR) responders depending on their weight loss.

    Article Title: 12th European Nutrition Conference (FENS), Berlin, Germany, October 20-23, 2015: Abstracts.
    Article Snippet: DNA methylation levels of the selected CpG-SNPs were quantified by Sequenom MassArray® EpiTyperTM and MS-HRM approaches Results: Seven of these CpG-SNPs, located in the candidate genes UCP1, POMC, BDNF, SH2B1, FTO, IL6R and CRP, were associated with differential DNA methylation of the CpG-SNPs or surrounding CpG sites.

    Methylation:

    Article Title: DNA methylation of miRNA coding sequences putatively associated with childhood obesity.
    Article Snippet: Material andMethods: DNA isolated fromwhite blood cells of 24 children (identification sample: 12 obese and 12 non-obese) from the Grupo Navarro de Obesidad Infantil study was hybridized in a 450K methylation microarray.. Several CpGs whose DNA methylation levels were statistically different between obese and non-obese were validated by MassArray® in 95 children (validation sample) from the same study.

    Article Title: XIX Reunión Nacional de la Asociación Española de Gastroenterología
    Article Snippet: Introducción: La información al paciente es un derecho que éste tiene, y una obligación ética y legal.. En los procedimientos diagnósticos y terapéuticos invasivos, el consentimiento debe obtenerse después de que el paciente reciba una información adecuada verbal y por escrito del mismo, sus beneficios, complicaciones y alternativas.. Esta información debe proporcionarse de forma oportuna antes del procedimiento.

    Article Title: PTPRS and PER3 methylation levels are associated with childhood obesity: results from a genome-wide methylation analysis.
    Article Snippet: Results: Genome-wide analysis identified 734 CpGs (783 genes) differentially methylated between cases (n = 12) and controls (n = 12).. Ingenuity Pathway Analysis showed that these genes were involved in oxidative stress and circadian rhythm signalling pathways.. Moreover, the DNA methylation levels of VIPR2, GRIN2D, ADCYAP1R1, PER3 and PTPRS regions correlated with the obesity trait.

    Article Title: 10th Congress of the International Society of Nutrigenetics/Nutrigenomics (ISNN). May 22-26, 2016, Tel Aviv, Israel: Abstracts.
    Article Snippet: Several CpGs whose DNA methylation levels were statistically different between obese and non-obese were further validated by Sequenom MassArray® EpiTyperTM in 95 children from the same study.

    Article Title: An integrated transcriptomic and epigenomic analysis identifies CD44 gene as a potential biomarker for weight loss within an energy-restricted program.
    Article Snippet: Purpose The interindividual variable response to weight-loss treatments requires the search for new predictive biomarkers for improving the success of weight-loss programs.. The aim of this study is to identify novel genes that distinguish individual responses to a weight-loss dietary treatment by using the integrative analysis of mRNA expression and DNA methylation arrays.. Methods Subjects from Metabolic Syndrome Reduction in Navarra (RESMENA) project were classified as low (LR) or high (HR) responders depending on their weight loss.

    Article Title: 12th European Nutrition Conference (FENS), Berlin, Germany, October 20-23, 2015: Abstracts.
    Article Snippet: DNA methylation levels of the selected CpG-SNPs were quantified by Sequenom MassArray® EpiTyperTM and MS-HRM approaches Results: Seven of these CpG-SNPs, located in the candidate genes UCP1, POMC, BDNF, SH2B1, FTO, IL6R and CRP, were associated with differential DNA methylation of the CpG-SNPs or surrounding CpG sites.

    Biomarker Discovery:

    Article Title: DNA methylation of miRNA coding sequences putatively associated with childhood obesity.
    Article Snippet: Material andMethods: DNA isolated fromwhite blood cells of 24 children (identification sample: 12 obese and 12 non-obese) from the Grupo Navarro de Obesidad Infantil study was hybridized in a 450K methylation microarray.. Several CpGs whose DNA methylation levels were statistically different between obese and non-obese were validated by MassArray® in 95 children (validation sample) from the same study.

    Article Title: XIX Reunión Nacional de la Asociación Española de Gastroenterología
    Article Snippet: Introducción: La información al paciente es un derecho que éste tiene, y una obligación ética y legal.. En los procedimientos diagnósticos y terapéuticos invasivos, el consentimiento debe obtenerse después de que el paciente reciba una información adecuada verbal y por escrito del mismo, sus beneficios, complicaciones y alternativas.. Esta información debe proporcionarse de forma oportuna antes del procedimiento.

    Article Title: PTPRS and PER3 methylation levels are associated with childhood obesity: results from a genome-wide methylation analysis.
    Article Snippet: Results: Genome-wide analysis identified 734 CpGs (783 genes) differentially methylated between cases (n = 12) and controls (n = 12).. Ingenuity Pathway Analysis showed that these genes were involved in oxidative stress and circadian rhythm signalling pathways.. Moreover, the DNA methylation levels of VIPR2, GRIN2D, ADCYAP1R1, PER3 and PTPRS regions correlated with the obesity trait.

    Article Title: 10th Congress of the International Society of Nutrigenetics/Nutrigenomics (ISNN). May 22-26, 2016, Tel Aviv, Israel: Abstracts.
    Article Snippet: Several CpGs whose DNA methylation levels were statistically different between obese and non-obese were further validated by Sequenom MassArray® EpiTyperTM in 95 children from the same study.

    Article Title: An integrated transcriptomic and epigenomic analysis identifies CD44 gene as a potential biomarker for weight loss within an energy-restricted program.
    Article Snippet: Purpose The interindividual variable response to weight-loss treatments requires the search for new predictive biomarkers for improving the success of weight-loss programs.. The aim of this study is to identify novel genes that distinguish individual responses to a weight-loss dietary treatment by using the integrative analysis of mRNA expression and DNA methylation arrays.. Methods Subjects from Metabolic Syndrome Reduction in Navarra (RESMENA) project were classified as low (LR) or high (HR) responders depending on their weight loss.

    Article Title: 12th European Nutrition Conference (FENS), Berlin, Germany, October 20-23, 2015: Abstracts.
    Article Snippet: DNA methylation levels of the selected CpG-SNPs were quantified by Sequenom MassArray® EpiTyperTM and MS-HRM approaches Results: Seven of these CpG-SNPs, located in the candidate genes UCP1, POMC, BDNF, SH2B1, FTO, IL6R and CRP, were associated with differential DNA methylation of the CpG-SNPs or surrounding CpG sites.



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    FAEs inhibit DNA demethylation at the MIR-21 promoter in a specific and dose-dependent manner. Naïve (CD45RO−CCR7+) and memory (CD45RO+) CD4 T cells were isolated from human PBMCs by FACS. The baseline DNA methylation levels of naïve (NaïveBL) and memory CD4 T cells (MemoryBL) at the (A) MIR-21 and (B) TNF promoters were measured ex vivo by EpiTYPER™ <t>MassARRAY®.</t> Naïve and memory CD4 T cells were also cultured with or without MMF at the specified concentration and stimulated with anti-CD3 and anti-CD28 coated beads for 3 days either without polarization or under Th17 polarizing conditions, after which DNA methylation levels at the (A) MIR-21 and (B) TNF promoters were measured by EpiTYPER™ MassARRAY®. (A) MMF was able to inhibit DNA demethylation of the MIR-21 promoter in naïve CD4 T cells, but not in memory CD4 T cells, in a dose dependent manner. (B) DNA methylation at the TNF promoter was not significantly changed by MMF in either naïve or memory CD4 T cells. (C) MMF had an even greater hypermethylating effect on the MIR-21 locus of naïve CD4 T cells that were stimulated under Th17 polarizing conditions. (D) MMF was also able to inhibit the demethylation of the MIR-21 promoter of naïve (CD45RO−CCR7+) CD8 T cells after 3 days of activation with anti-CD3 and anti-CD28 coated beads in vitro under Tc17 polarizing conditions. MMF20 = 20 µM of MMF; MMF50 = 50 µM of MMF; Veh = vehicle.
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    massarray® epitypertm  (Sequenom)
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    FAEs inhibit DNA demethylation at the MIR-21 promoter in a specific and dose-dependent manner. Naïve (CD45RO−CCR7+) and memory (CD45RO+) CD4 T cells were isolated from human PBMCs by FACS. The baseline DNA methylation levels of naïve (NaïveBL) and memory CD4 T cells (MemoryBL) at the (A) MIR-21 and (B) TNF promoters were measured ex vivo by EpiTYPER™ <t>MassARRAY®.</t> Naïve and memory CD4 T cells were also cultured with or without MMF at the specified concentration and stimulated with anti-CD3 and anti-CD28 coated beads for 3 days either without polarization or under Th17 polarizing conditions, after which DNA methylation levels at the (A) MIR-21 and (B) TNF promoters were measured by EpiTYPER™ MassARRAY®. (A) MMF was able to inhibit DNA demethylation of the MIR-21 promoter in naïve CD4 T cells, but not in memory CD4 T cells, in a dose dependent manner. (B) DNA methylation at the TNF promoter was not significantly changed by MMF in either naïve or memory CD4 T cells. (C) MMF had an even greater hypermethylating effect on the MIR-21 locus of naïve CD4 T cells that were stimulated under Th17 polarizing conditions. (D) MMF was also able to inhibit the demethylation of the MIR-21 promoter of naïve (CD45RO−CCR7+) CD8 T cells after 3 days of activation with anti-CD3 and anti-CD28 coated beads in vitro under Tc17 polarizing conditions. MMF20 = 20 µM of MMF; MMF50 = 50 µM of MMF; Veh = vehicle.
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    FAEs inhibit DNA demethylation at the MIR-21 promoter in a specific and dose-dependent manner. Naïve (CD45RO−CCR7+) and memory (CD45RO+) CD4 T cells were isolated from human PBMCs by FACS. The baseline DNA methylation levels of naïve (NaïveBL) and memory CD4 T cells (MemoryBL) at the (A) MIR-21 and (B) TNF promoters were measured ex vivo by EpiTYPER™ <t>MassARRAY®.</t> Naïve and memory CD4 T cells were also cultured with or without MMF at the specified concentration and stimulated with anti-CD3 and anti-CD28 coated beads for 3 days either without polarization or under Th17 polarizing conditions, after which DNA methylation levels at the (A) MIR-21 and (B) TNF promoters were measured by EpiTYPER™ MassARRAY®. (A) MMF was able to inhibit DNA demethylation of the MIR-21 promoter in naïve CD4 T cells, but not in memory CD4 T cells, in a dose dependent manner. (B) DNA methylation at the TNF promoter was not significantly changed by MMF in either naïve or memory CD4 T cells. (C) MMF had an even greater hypermethylating effect on the MIR-21 locus of naïve CD4 T cells that were stimulated under Th17 polarizing conditions. (D) MMF was also able to inhibit the demethylation of the MIR-21 promoter of naïve (CD45RO−CCR7+) CD8 T cells after 3 days of activation with anti-CD3 and anti-CD28 coated beads in vitro under Tc17 polarizing conditions. MMF20 = 20 µM of MMF; MMF50 = 50 µM of MMF; Veh = vehicle.
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    Image Search Results


    FAEs inhibit DNA demethylation at the MIR-21 promoter in a specific and dose-dependent manner. Naïve (CD45RO−CCR7+) and memory (CD45RO+) CD4 T cells were isolated from human PBMCs by FACS. The baseline DNA methylation levels of naïve (NaïveBL) and memory CD4 T cells (MemoryBL) at the (A) MIR-21 and (B) TNF promoters were measured ex vivo by EpiTYPER™ MassARRAY®. Naïve and memory CD4 T cells were also cultured with or without MMF at the specified concentration and stimulated with anti-CD3 and anti-CD28 coated beads for 3 days either without polarization or under Th17 polarizing conditions, after which DNA methylation levels at the (A) MIR-21 and (B) TNF promoters were measured by EpiTYPER™ MassARRAY®. (A) MMF was able to inhibit DNA demethylation of the MIR-21 promoter in naïve CD4 T cells, but not in memory CD4 T cells, in a dose dependent manner. (B) DNA methylation at the TNF promoter was not significantly changed by MMF in either naïve or memory CD4 T cells. (C) MMF had an even greater hypermethylating effect on the MIR-21 locus of naïve CD4 T cells that were stimulated under Th17 polarizing conditions. (D) MMF was also able to inhibit the demethylation of the MIR-21 promoter of naïve (CD45RO−CCR7+) CD8 T cells after 3 days of activation with anti-CD3 and anti-CD28 coated beads in vitro under Tc17 polarizing conditions. MMF20 = 20 µM of MMF; MMF50 = 50 µM of MMF; Veh = vehicle.

    Journal: Brain

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    doi: 10.1093/brain/awy344

    Figure Lengend Snippet: FAEs inhibit DNA demethylation at the MIR-21 promoter in a specific and dose-dependent manner. Naïve (CD45RO−CCR7+) and memory (CD45RO+) CD4 T cells were isolated from human PBMCs by FACS. The baseline DNA methylation levels of naïve (NaïveBL) and memory CD4 T cells (MemoryBL) at the (A) MIR-21 and (B) TNF promoters were measured ex vivo by EpiTYPER™ MassARRAY®. Naïve and memory CD4 T cells were also cultured with or without MMF at the specified concentration and stimulated with anti-CD3 and anti-CD28 coated beads for 3 days either without polarization or under Th17 polarizing conditions, after which DNA methylation levels at the (A) MIR-21 and (B) TNF promoters were measured by EpiTYPER™ MassARRAY®. (A) MMF was able to inhibit DNA demethylation of the MIR-21 promoter in naïve CD4 T cells, but not in memory CD4 T cells, in a dose dependent manner. (B) DNA methylation at the TNF promoter was not significantly changed by MMF in either naïve or memory CD4 T cells. (C) MMF had an even greater hypermethylating effect on the MIR-21 locus of naïve CD4 T cells that were stimulated under Th17 polarizing conditions. (D) MMF was also able to inhibit the demethylation of the MIR-21 promoter of naïve (CD45RO−CCR7+) CD8 T cells after 3 days of activation with anti-CD3 and anti-CD28 coated beads in vitro under Tc17 polarizing conditions. MMF20 = 20 µM of MMF; MMF50 = 50 µM of MMF; Veh = vehicle.

    Article Snippet: DNA methylation analysis of ex vivo and in vitro stimulated cells was performed with EpiTYPERTM MassARRAY® system (Agena Bioscience) as previously described ( Moyon et al. , 2016 ) at the Epigenetics Core facility at the CUNY Advanced Science Research Center (ASRC).

    Techniques: Isolation, DNA Methylation Assay, Ex Vivo, Cell Culture, Concentration Assay, Activation Assay, In Vitro