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massarray epityper analysis (agena bioscience)

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agena bioscience massarray epityper analysis
Massarray Epityper Analysis, supplied by agena bioscience, 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+epityper+analysis/massarray+epityper/pm38062913-56-31-42
Average 90 stars, based on 1 article reviews

massarray epityper analysis - by Bioz Stars, 2026-11

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Methylation:

Article Title: Association of PPARGC1A gene polymorphism and mtDNA methylation with coal-burning fluorosis: a case–control study
Article Snippet: .. Therefore, we designed this present study using a case-control study approach to examine 16 SNPs within the PPARGC1A gene genotyping and mitochondrial D-ring methylation levels, utilizing MassARRAY SNP and MassARRAY EpiTYPER (Agena Bioscience, Inc.). ..

Article Title: E3 ubiquitin ligase casitas B-lineage lymphoma-b modulates T-cell anergic resistance via phosphoinositide 3-kinase signaling in patients with immune thrombocytopenia.
Article Snippet: Department of Hematology, Qilu Hospital of Shandong University, Jinan, Shandong, China Department of Hematology, Qilu Hospital (Qingdao) of Shandong University, Qingdao, Shandong, China Experimental Asthma and Allergy Research Unit, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden Department of Hand and Foot Surgery, Qilu Hospital (Qingdao) of Shandong University, Qingdao, Shandong, China Jinan Vocational College of Nursing, Jinan, Shandong, China Department of Hematology, Taian Central Hospital, Taian, Shandong, China Shandong Provincial Key Laboratory of Immunohematology, Qilu Hospital of Shandong University, Jinan, Shandong, China Shandong Provincial Clinical Research Center in Hematological Diseases, Jinan, Shandong, China Leading Research Group of Scientific Innovation, Department of Science and Technology of Shandong Province, Qilu Hospital of Shandong University, Jinan, Shandong, China

Article Title: Maternal high-fat diet orchestrates offspring hepatic cholesterol metabolism via MEF2A hypermethylation-mediated CYP7A1 suppression.
Article Snippet: DNA kit (Omega Bio-tek, Inc., Norcross, GA). .. Promoter methylation of the target gene was detected using the MassARRAY EpiTYPER platform (Agena Bioscience, San Diego, CA, USA). ..

Article Title: Intercontinental insights into autism spectrum disorder: a synthesis of environmental influences and DNA methylation
Article Snippet: Lintas et al . [ ] , United States , N/A , Brain tissue , 6 ASD 6 TD , 21± 2.9 years , N/A , Bisulfite treatment, PCR (real time), in silico analysis , Candidate gene( RELN ) , ASD patients have higher methylated CpG islands and heavier methylation in the 5′ region of the RELN gene promoter, compared to controls. Three distinct methylation patterns are discernible, each correlated with different reductions in reelin gene expression in ASD individuals compared to controls. .. Andari et al . [ ] , United States , N/A , Saliva , 35 ASD 64 TD , 27.02 ± 5.34 years , DSM-V| ADOS| ADI-R| SRS , EpiTYPER on the MassARRAY system by Agena Bioscience , Candidate gene( OXTR) , Adults with ASD have higher OXTR methylation in intron 1, linked to clinical symptoms and cortico-cortical hypoconnectivity. Exon 1 CpG site methylation correlates with social deficits and striatal-cortical hyperconnectivity. .. Feinberg et al . [ ] , United States , N/A , Semen , 44 Fathers of ASD , N/A , N/A , Illumina Infinium, HumanMethylation450K BeadChip (Illumina, San Diego, CA) , Genome-wide RR , Identified 193 sperm DMRs linked to offspring AOSI scores, clustering near developmental genes and the SNORD family within the Prader-Willi syndrome gene cluster, indicating hereditary ASD risk factors.

other:

Article Title: Use of Multiple Machine Learning Approaches for Selecting Urothelial Cancer-Specific DNA Methylation Biomarkers in Urine
Article Snippet: Ten amplicons that were shown to be hypermethylated in UCa cases and whose genomic coordinates and primer sequences have been described previously [ ] were analyzed by matrix-assisted laser desorption/ionization–time-of-flight (MALDI-TOF) mass spectrometry (MassARRAY EpiTYPER system, Agena Bioscience GmbH, Hamburg, Germany), enabling the quantitative measurement of CpG methylation at single dinucleotide resolution [ , ].

DNA Methylation Assay:

Article Title: Association of methylation risk score with incident type 2 diabetes mellitus: A nested case-control study.
Article Snippet: We used MALDI-TOF mass spectrometry based on the MassARRAY System (Bio Miao Biological Technology, Beijing) to analyze the mass spectra of products, and nloaded from https://onlinelibrary.w iley.com /doi/10.1111/1753-0407.13512 by G itam U niversity, W iley O nline L ibrary on [22/12/2023]. .. See the T erm s and C onditions (https://onlinelibrary.w iley.com /term s-and-conditions) on W iley O nline L ibrary for rules of use; O A articles are governed by the applicable C reative C om m ons L icense MassARRAY EpiTYPER analysis (Agena Bioscience, San Diego, CA) to measure the DNA methylation levels. ..

Article Title: Visit to visit transition in TXNIP gene methylation and the risk of type 2 diabetes mellitus: a nested case-control study.
Article Snippet: Our study aimed to investigate the association between the transition of the TXNIP gene methylation level and the risk of incident type 2 diabetes mellitus (T2DM).. This study included 263 incident cases of T2DM and 263 matched non-T2DM participants.. According to the methylation levels of five loci (CpG1–5; chr1:145441102-145442001) on the TXNIP gene, the participants were classified into four transition groups: maintained low, low to high, high to low, and maintained high methylation levels.

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Epigenome-wide DNA methylation analysis reveals MIR-21 as the top hypermethylated region in CD4 T cells from FAE-treated patients. CD4 T cell DNA from 47 treatment-naïve, 35 FAE-treated and 16 GA-treated multiple sclerosis patients was analysed by using the Infinium MethylationEPIC BeadChip array. To identify differentially methylated regions between treated and untreated patients, we utilized a linear regression model at each individual CpG site to identify the contribution of treatment status in DNA methylation changes after controlling for age, gender, race, disease duration, the total CD4 T cell percentage as well as the percentage of CCR6−CCR4+, CCR6+CCR4+ and CCR6+CCR4− CD4 T cells in each sample. We then used a 1-kb sliding window to define genomic regions with closely located CpG sites, and then combined each CpG specific P-value from our previous linear regression model within a single region with the Stouffer’s method. This was followed by the Bonferroni correction for multiple hypothesis testing. DMRs were defined as regions with more than four CpG sites that have an absolute median β-value change > 0.02 and an adjusted combined P-value of < 0.01. Based on this analysis we uncovered 202 hypermethylated DMRs (containing 1545 CpGs) and only 13 hypomethylated DMRs (containing 158 CpGs) in FAE-treated patients compared to controls. (A and B) The CpGs distribution of these hypermethylated (hyperCpGs) and hypomethylated (hypoCpGs) DMRs was compared to that of the CpG distribution in the Illumina Infinium MethylationEPIC BeadChip (allCpGs). (C) Circos plot showing (from inside out); innermost first circle: chromosomal colors, numbers and size; second circle: a scatter plot with each point representing the genomic location and mean change in β-value of hypomethylated (in blue) and hypermethylated (in red) CpG sites; third circle: dark red perpendicular lines represent the genomic location of significantly hypermethylated DMRs; fourth circle: dark red scatter plot with each point representing the genomic location and mean beta change of significantly hypermethylated DMRs spanning more than 10 CpGs; outermost fifth circle: contains the names of genes whose promoters are located in these large DMRs (MIR-21 is shown in red). (D) Manhattan plot of the discovery cohort analysis showing mean beta change of significantly hypermethylated DMRs spanning more than 10 CpGs, where MIR-21 was the top differentially methylated locus. (E) Manhattan plot from the pair-wise longitudinal analysis showing that MIR-21 was the hypermethylated DMR with the most consistent and greatest methylation change in the validation cohort.

Journal: Brain

Article Title: Fumarates target the metabolic-epigenetic interplay of brain-homing T cells in multiple sclerosis

doi: 10.1093/brain/awy344

Figure Lengend Snippet: Epigenome-wide DNA methylation analysis reveals MIR-21 as the top hypermethylated region in CD4 T cells from FAE-treated patients. CD4 T cell DNA from 47 treatment-naïve, 35 FAE-treated and 16 GA-treated multiple sclerosis patients was analysed by using the Infinium MethylationEPIC BeadChip array. To identify differentially methylated regions between treated and untreated patients, we utilized a linear regression model at each individual CpG site to identify the contribution of treatment status in DNA methylation changes after controlling for age, gender, race, disease duration, the total CD4 T cell percentage as well as the percentage of CCR6−CCR4+, CCR6+CCR4+ and CCR6+CCR4− CD4 T cells in each sample. We then used a 1-kb sliding window to define genomic regions with closely located CpG sites, and then combined each CpG specific P-value from our previous linear regression model within a single region with the Stouffer’s method. This was followed by the Bonferroni correction for multiple hypothesis testing. DMRs were defined as regions with more than four CpG sites that have an absolute median β-value change > 0.02 and an adjusted combined P-value of < 0.01. Based on this analysis we uncovered 202 hypermethylated DMRs (containing 1545 CpGs) and only 13 hypomethylated DMRs (containing 158 CpGs) in FAE-treated patients compared to controls. (A and B) The CpGs distribution of these hypermethylated (hyperCpGs) and hypomethylated (hypoCpGs) DMRs was compared to that of the CpG distribution in the Illumina Infinium MethylationEPIC BeadChip (allCpGs). (C) Circos plot showing (from inside out); innermost first circle: chromosomal colors, numbers and size; second circle: a scatter plot with each point representing the genomic location and mean change in β-value of hypomethylated (in blue) and hypermethylated (in red) CpG sites; third circle: dark red perpendicular lines represent the genomic location of significantly hypermethylated DMRs; fourth circle: dark red scatter plot with each point representing the genomic location and mean beta change of significantly hypermethylated DMRs spanning more than 10 CpGs; outermost fifth circle: contains the names of genes whose promoters are located in these large DMRs (MIR-21 is shown in red). (D) Manhattan plot of the discovery cohort analysis showing mean beta change of significantly hypermethylated DMRs spanning more than 10 CpGs, where MIR-21 was the top differentially methylated locus. (E) Manhattan plot from the pair-wise longitudinal analysis showing that MIR-21 was the hypermethylated DMR with the most consistent and greatest methylation change in the validation cohort.

Article Snippet: EpiTYPER MassArray® analysis 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: DNA Methylation Assay, Methylation, Biomarker Discovery

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

Article Title: Fumarates target the metabolic-epigenetic interplay of brain-homing T cells in multiple sclerosis

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.

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

FAE therapy modifies the metabolic-epigenetic interplay in multiple sclerosis to reduce pathogenic CCR6+ CD4 and CD8 T cells. (A) CD4 T cells from treatment naïve patients with multiple sclerosis exhibit low DNA methylation levels at the MIR-21 locus and high expression of CCR6. CD8 T cells from treatment naïve multiple sclerosis patients also exhibit high levels of CCR6. (B) FAE therapy epigenetically modulates the MIR-21 locus in CD4 and CD8 T cells, which results in hypermethylation and downregulation of miR-21 expression in FAE-treated Th17 and Tc17 cells. This in turn allows for the upregulation of SMAD7 in both CD4 and CD8 T cells, a miR-21-5p and miR-21-3p target with inhibitory feedback on the TGF-b signalling pathway. Finally, FAEs reduce CCR6 expression and lower this potentially pathogenic brain-homing CCR6+ CD4 and CD8 T cell population in FAE-treated multiple sclerosis patients.

Journal: Brain

Article Title: Fumarates target the metabolic-epigenetic interplay of brain-homing T cells in multiple sclerosis

doi: 10.1093/brain/awy344

Figure Lengend Snippet: FAE therapy modifies the metabolic-epigenetic interplay in multiple sclerosis to reduce pathogenic CCR6+ CD4 and CD8 T cells. (A) CD4 T cells from treatment naïve patients with multiple sclerosis exhibit low DNA methylation levels at the MIR-21 locus and high expression of CCR6. CD8 T cells from treatment naïve multiple sclerosis patients also exhibit high levels of CCR6. (B) FAE therapy epigenetically modulates the MIR-21 locus in CD4 and CD8 T cells, which results in hypermethylation and downregulation of miR-21 expression in FAE-treated Th17 and Tc17 cells. This in turn allows for the upregulation of SMAD7 in both CD4 and CD8 T cells, a miR-21-5p and miR-21-3p target with inhibitory feedback on the TGF-b signalling pathway. Finally, FAEs reduce CCR6 expression and lower this potentially pathogenic brain-homing CCR6+ CD4 and CD8 T cell population in FAE-treated multiple sclerosis patients.

Techniques: DNA Methylation Assay, Expressing

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massarray epityper analysis (agena bioscience)

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