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massarray epityper platform  (Sequenom)

 
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    Sequenom massarray epityper platform
    Massarray Epityper Platform, supplied by Sequenom, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/massarray+methylation+platform/massarray+platform/pm41486283-69-20-23
    Average 86 stars, based on 1 article reviews
    massarray epityper platform - by Bioz Stars, 2026-09
    86/100 stars

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    other:

    Article Title: BR-FDP-SKIN: Brazilian forensic DNA Skin phenotyping based on machine learning models
    Article Snippet: ction NA Phenotyping (FDP) enables the prediction of different Externally Visible Characteristics (EVCs), air, and eye color, directly from genetic material (1).. The inference of these traits using a limited set of tide Polymorphisms (SNPs) is extremely valuable in forensic investigations, aiding in the identification dividuals at crime scenes or among victims of mass disasters (2; 3; 4).. Multiple studies have mapped ted with hair, eye, and skin color (2; 5; 6; 7; 8; 9; 10; 11; 12; 13; 14; 15; 16).

    Article Title: Identification of a Novel Genetic Variant responsible for Familial Atrial Fibrillation.
    Article Snippet: This is a PDF of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability.. This version will undergo additional copyediting, typesetting and review before it is published in its final form.. As such, this version is no longer the Accepted Manuscript, but it is not yet the definitive Version of Record; we are providing this early version to give early visibility of the article.

    Article Title: Analysis of MIR155HG gene polymorphisms and ulcerative colitis susceptibility in the Chinese Han Population
    Article Snippet: Four single nucleotide polymorphisms (SNPs) of MIR155HG (rs1893650, rs2282471, rs2829803, and rs2829806) were genotyped using the Sequenom MassARRAY platform.

    Variant Assay:

    Article Title:
    Article Snippet: .. OHSU: Oregon Health & Science University; MassARRAY: Sequenom MassARRAY iPLEX platform; 1KGP: 1000 Genomes Project. a 22 patient DNA samples; b 40 CCL samples and 22 patient DNA samples; c 40 CCL samples; d 40 CCL samples and 6 patient DNA samples analyzed for a single variant in RYR1 ; e 6 patient DNA samples analyzed for 34 variants in RYR1 . ..

    DNA Purification:

    Article Title: Integrating genetic and lifestyle determinants in a risk prediction model for esophageal squamous cell carcinoma in Taiwan.
    Article Snippet: .. Genomic DNA was extracted from peripheral blood using the Puregene DNA Purification Kit (Gentra Systems, Minneapolis, MN, USA) and the resulting DNA was dispensed into 96-well plates (ABgene Limited, Epsom, UK). and samples Samples with concentrations ≥2.5 ng/μl were genotyped using the Sequenom MassARRAY system (with call rate > 95%). ..

    Next-Generation Sequencing:

    Article Title:
    Article Snippet: .. Accuracy studies were performed by comparing the genotypes of the variants determined by the OA-PGx panel with at least one of 2 reference genotyping methods, next-generation sequencing (NGS), and/or Sequenom MassARRAY iPLEX platform (MassARRAY). ..

    Modification:

    Article Title: Midlife insulin resistance and brain beta-amyloid accumulation as predictors of change in late-life cognitive function - A 20-year follow-up study.
    Article Snippet: .. APOE genotype was defined with the MassARRAY System (Sequenom, San Diego, CA, USA) with a modified protocol (Jänis et al., 2004). ..



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    MiR‐9‐1 is downregulated by promoter methylation in nasopharyngeal carcinoma (NPC). A, CpG islands in miR‐9‐1. The transcription start site (TSS) is indicated by a curved arrow. The regions analyzed by methylation‐specific PCR (MSP) and <t>MassARRAY</t> are shown. B, Relative miR‐9‐1 expression in normal nasopharyngeal NP69 cells and NPC cell lines. Glyceraldehyde‐3‐phosphate dehydrogenase ( GAPDH ) was used as the endogenous control. C, Relative miR‐9‐1 expression in 11 normal nasopharyngeal tissues (N) and 16 NPC tissues (T). U6 was used as the endogenous control. * P < .05. D, Quantitative MassARRAY methylation analysis of miR‐9‐1 in normal tissues (NT), NPC tissue (P), NP69 cell lines, NPC cell lines. E, F, MSP analysis of miR‐9‐1 promoter methylation in NPC cell lines and tissue specimens. M, methylated; U, unmethylated; L, marker; 1‐14, NPC tissue specimen numbers. G, Demethylation treatment with 5‐Aza‐2’‐deoxycytidine (DAC) restored the expression of miR‐9‐1 in NPC cell lines
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    During transforming growth factor β1 (TGFβ1)-induced epithelial-to-mesenchymal transition (EMT), stomatin was downregulated through <t>methylation-dependent</t> transcription mechanism. (A) Real-time polymerase chain reaction (PCR) was performed to validate the transcriptional change of stomatin identified in the microarray. **, P<0.001; (B) Two CpG islands spanning from −768 to −223 bp and from −143 to +122 bp upstream of STOM gene were identified by EMBOSS cpgplot program (upper). Schematic representation of −768/−223 and −143/+122 (marked with the grey square) CpG islands in the upstream of stomatin gene (lower). Red box marked the exon. The translation start site was position +1; (C) Measuring stomatin promoter methylation levels by Sequenom <t>MassARRAY</t> assay; (D) Sequenom MassARRAY analysis of methylation percentages of CpG sites at the stomatin promoter. The top panel showed the methylation percentages of 30 sites in human bronchial epithelial (HBE) and A549 cells. Dots with different color depths represent different methylation status. Dark dots represent high degrees of methylation. Light dots represent low degrees of methylation. The methylation percentages of 30 CpG sites were compared by two-tailed paired Student’s t test. In line graph, each dot represents an individual CpG dinucleotide. Green dots represent CpG dinucleotides in HBE cells. Red dots represent CpG sites in A549 cells. The corresponding detection sites were connected in a straight line. Real-time PCR was performed to evaluate the expression of stomatin in HBE and A549 cells (P<0.01); (E) The same sequenom MassArray and statistical analyses were also implemented to assess the methylation status of the indicated promoter region of stomatin in A549 and A549-5Aza cells (P<0.01); (F) A549 cells were exposed to TGFβ1 (5 ng/mL) for 2 d or 5 d with or without 5-Aza. Expression of DNMT3A and stomatin was analyzed by western blotting. β-actin was used as a loading control; (G) Sequenom MassArray analysis was implemented to assess the stomatin promoter methylation levels in A549, A549-TGFβ1, and A549-TGFβ1/5-Aza cells (P=0.005, P=0.004, respectively).
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    During transforming growth factor β1 (TGFβ1)-induced epithelial-to-mesenchymal transition (EMT), stomatin was downregulated through <t>methylation-dependent</t> transcription mechanism. (A) Real-time polymerase chain reaction (PCR) was performed to validate the transcriptional change of stomatin identified in the microarray. **, P<0.001; (B) Two CpG islands spanning from −768 to −223 bp and from −143 to +122 bp upstream of STOM gene were identified by EMBOSS cpgplot program (upper). Schematic representation of −768/−223 and −143/+122 (marked with the grey square) CpG islands in the upstream of stomatin gene (lower). Red box marked the exon. The translation start site was position +1; (C) Measuring stomatin promoter methylation levels by Sequenom <t>MassARRAY</t> assay; (D) Sequenom MassARRAY analysis of methylation percentages of CpG sites at the stomatin promoter. The top panel showed the methylation percentages of 30 sites in human bronchial epithelial (HBE) and A549 cells. Dots with different color depths represent different methylation status. Dark dots represent high degrees of methylation. Light dots represent low degrees of methylation. The methylation percentages of 30 CpG sites were compared by two-tailed paired Student’s t test. In line graph, each dot represents an individual CpG dinucleotide. Green dots represent CpG dinucleotides in HBE cells. Red dots represent CpG sites in A549 cells. The corresponding detection sites were connected in a straight line. Real-time PCR was performed to evaluate the expression of stomatin in HBE and A549 cells (P<0.01); (E) The same sequenom MassArray and statistical analyses were also implemented to assess the methylation status of the indicated promoter region of stomatin in A549 and A549-5Aza cells (P<0.01); (F) A549 cells were exposed to TGFβ1 (5 ng/mL) for 2 d or 5 d with or without 5-Aza. Expression of DNMT3A and stomatin was analyzed by western blotting. β-actin was used as a loading control; (G) Sequenom MassArray analysis was implemented to assess the stomatin promoter methylation levels in A549, A549-TGFβ1, and A549-TGFβ1/5-Aza cells (P=0.005, P=0.004, respectively).
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    Image Search Results


    MiR‐9‐1 is downregulated by promoter methylation in nasopharyngeal carcinoma (NPC). A, CpG islands in miR‐9‐1. The transcription start site (TSS) is indicated by a curved arrow. The regions analyzed by methylation‐specific PCR (MSP) and MassARRAY are shown. B, Relative miR‐9‐1 expression in normal nasopharyngeal NP69 cells and NPC cell lines. Glyceraldehyde‐3‐phosphate dehydrogenase ( GAPDH ) was used as the endogenous control. C, Relative miR‐9‐1 expression in 11 normal nasopharyngeal tissues (N) and 16 NPC tissues (T). U6 was used as the endogenous control. * P < .05. D, Quantitative MassARRAY methylation analysis of miR‐9‐1 in normal tissues (NT), NPC tissue (P), NP69 cell lines, NPC cell lines. E, F, MSP analysis of miR‐9‐1 promoter methylation in NPC cell lines and tissue specimens. M, methylated; U, unmethylated; L, marker; 1‐14, NPC tissue specimen numbers. G, Demethylation treatment with 5‐Aza‐2’‐deoxycytidine (DAC) restored the expression of miR‐9‐1 in NPC cell lines

    Journal: Cancer Science

    Article Title: Methylation‐associated silencing of miR‐9‐1 promotes nasopharyngeal carcinoma progression and glycolysis via HK2

    doi: 10.1111/cas.15103

    Figure Lengend Snippet: MiR‐9‐1 is downregulated by promoter methylation in nasopharyngeal carcinoma (NPC). A, CpG islands in miR‐9‐1. The transcription start site (TSS) is indicated by a curved arrow. The regions analyzed by methylation‐specific PCR (MSP) and MassARRAY are shown. B, Relative miR‐9‐1 expression in normal nasopharyngeal NP69 cells and NPC cell lines. Glyceraldehyde‐3‐phosphate dehydrogenase ( GAPDH ) was used as the endogenous control. C, Relative miR‐9‐1 expression in 11 normal nasopharyngeal tissues (N) and 16 NPC tissues (T). U6 was used as the endogenous control. * P < .05. D, Quantitative MassARRAY methylation analysis of miR‐9‐1 in normal tissues (NT), NPC tissue (P), NP69 cell lines, NPC cell lines. E, F, MSP analysis of miR‐9‐1 promoter methylation in NPC cell lines and tissue specimens. M, methylated; U, unmethylated; L, marker; 1‐14, NPC tissue specimen numbers. G, Demethylation treatment with 5‐Aza‐2’‐deoxycytidine (DAC) restored the expression of miR‐9‐1 in NPC cell lines

    Article Snippet: The Sequenom MassARRAY platform (Agena Bioscience) was applied to examine the promoter methylation level of miR‐9‐1 quantitatively.

    Techniques: Methylation, Expressing, Marker

    During transforming growth factor β1 (TGFβ1)-induced epithelial-to-mesenchymal transition (EMT), stomatin was downregulated through methylation-dependent transcription mechanism. (A) Real-time polymerase chain reaction (PCR) was performed to validate the transcriptional change of stomatin identified in the microarray. **, P<0.001; (B) Two CpG islands spanning from −768 to −223 bp and from −143 to +122 bp upstream of STOM gene were identified by EMBOSS cpgplot program (upper). Schematic representation of −768/−223 and −143/+122 (marked with the grey square) CpG islands in the upstream of stomatin gene (lower). Red box marked the exon. The translation start site was position +1; (C) Measuring stomatin promoter methylation levels by Sequenom MassARRAY assay; (D) Sequenom MassARRAY analysis of methylation percentages of CpG sites at the stomatin promoter. The top panel showed the methylation percentages of 30 sites in human bronchial epithelial (HBE) and A549 cells. Dots with different color depths represent different methylation status. Dark dots represent high degrees of methylation. Light dots represent low degrees of methylation. The methylation percentages of 30 CpG sites were compared by two-tailed paired Student’s t test. In line graph, each dot represents an individual CpG dinucleotide. Green dots represent CpG dinucleotides in HBE cells. Red dots represent CpG sites in A549 cells. The corresponding detection sites were connected in a straight line. Real-time PCR was performed to evaluate the expression of stomatin in HBE and A549 cells (P<0.01); (E) The same sequenom MassArray and statistical analyses were also implemented to assess the methylation status of the indicated promoter region of stomatin in A549 and A549-5Aza cells (P<0.01); (F) A549 cells were exposed to TGFβ1 (5 ng/mL) for 2 d or 5 d with or without 5-Aza. Expression of DNMT3A and stomatin was analyzed by western blotting. β-actin was used as a loading control; (G) Sequenom MassArray analysis was implemented to assess the stomatin promoter methylation levels in A549, A549-TGFβ1, and A549-TGFβ1/5-Aza cells (P=0.005, P=0.004, respectively).

    Journal: Chinese Journal of Cancer Research

    Article Title: Stomatin plays a suppressor role in non-small cell lung cancer metastasis

    doi: 10.21147/j.issn.1000-9604.2019.06.09

    Figure Lengend Snippet: During transforming growth factor β1 (TGFβ1)-induced epithelial-to-mesenchymal transition (EMT), stomatin was downregulated through methylation-dependent transcription mechanism. (A) Real-time polymerase chain reaction (PCR) was performed to validate the transcriptional change of stomatin identified in the microarray. **, P<0.001; (B) Two CpG islands spanning from −768 to −223 bp and from −143 to +122 bp upstream of STOM gene were identified by EMBOSS cpgplot program (upper). Schematic representation of −768/−223 and −143/+122 (marked with the grey square) CpG islands in the upstream of stomatin gene (lower). Red box marked the exon. The translation start site was position +1; (C) Measuring stomatin promoter methylation levels by Sequenom MassARRAY assay; (D) Sequenom MassARRAY analysis of methylation percentages of CpG sites at the stomatin promoter. The top panel showed the methylation percentages of 30 sites in human bronchial epithelial (HBE) and A549 cells. Dots with different color depths represent different methylation status. Dark dots represent high degrees of methylation. Light dots represent low degrees of methylation. The methylation percentages of 30 CpG sites were compared by two-tailed paired Student’s t test. In line graph, each dot represents an individual CpG dinucleotide. Green dots represent CpG dinucleotides in HBE cells. Red dots represent CpG sites in A549 cells. The corresponding detection sites were connected in a straight line. Real-time PCR was performed to evaluate the expression of stomatin in HBE and A549 cells (P<0.01); (E) The same sequenom MassArray and statistical analyses were also implemented to assess the methylation status of the indicated promoter region of stomatin in A549 and A549-5Aza cells (P<0.01); (F) A549 cells were exposed to TGFβ1 (5 ng/mL) for 2 d or 5 d with or without 5-Aza. Expression of DNMT3A and stomatin was analyzed by western blotting. β-actin was used as a loading control; (G) Sequenom MassArray analysis was implemented to assess the stomatin promoter methylation levels in A549, A549-TGFβ1, and A549-TGFβ1/5-Aza cells (P=0.005, P=0.004, respectively).

    Article Snippet: The methylation status of Stomatin promoter was detected using Sequenom MassARRAY quantitative methylation analysis platform (BGI tech, Shenzhen, China).

    Techniques: Methylation, Real-time Polymerase Chain Reaction, Microarray, Sequenom Massarray Assay, Two Tailed Test, Expressing, Western Blot, Control