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Translational Research | Citation
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Translational Research | Citations

Methylation Analysis

The following are examples of peer-reviewed studies in which EpiTaq HS polymerase was used for methylation analysis in biomedical research:

Method Targets Disease/Biological state studied Reference
Bisulfite PCR and pyrosequencing ZNF366 Chronic aggression 1
Bisulfite sequencing Lefty Cancer 2
COBRA MENT Human lymphoma 3
Bisulfite sequencing BCL11B Adult T-cell leukemia/lymphoma 4
Bisulfite sequencing SOCS3 Hepatitis C 5
  1. Guilleman, C., et al. (2014) DNA Methylation Signature of Childhood Chronic Physical Aggression in T Cells of Both Men and Women. PLoS ONE 9(1):e86822.

    Summary: In a previous study, the authors reported differential T cell DNA methylation patterns in male humans with history of chronic aggression trajectory. In this longitudinal study, T cell DNA methylation patterns of females with chronic aggression trajectory were analyzed and compared to the signatures observed in males. Methylated DNA immunoprecipitation (MeDIP) was performed on DNA extracted from T cells followed by microarray analysis. Differentially methylated CpG sites in the promoter region of ZNF366 were validated using EpiTaq HS polymerase to amplify bisulfite-treated DNA, followed by pyrosequencing. The authors report finding signature T cell DNA methylation patterns in women with chronic aggression trajectory, as well as a statistically significant overlap between patterns observed in women and men.

  2. Saito, A., et al. (2013) Suppression of Lefty expression in induced pluripotent cancer cells. FASEB J. 27(6):2165–2174.

    Summary: The tumor suppressor gene Lefty (which encodes a negative regulator of the TGF-beta superfamily cytokine Nodal) is highly expressed in embryonic stem cells but not in somatic cancer cells. In this study, researchers investigated methylation of Lefty B CpG island shores in human pancreatic cancer and human liver cancer cell lines in response to TGF-beta stimulation, as well as in embryonic stem cell and induced pluripotent stem cells. EpiTaq HS polymerase was used for amplification of bisulfite-treated genomic DNA.

  3. Alkebsi, L., et al. (2013) DNMT3B7 expression related to MENT expression and its promoter methylation in human lymphomas. Leukemia Res. 37(12):1662–1667.

    Summary: The human proto-oncogene MENT is regulated by DNA methyltransferase 3B (DNMT3B). The DNMT3B gene has over 16 alternative splice variants, one of which, DNMT3B7, lacks a region encoding the catalytic domain. The authors used Combined Bisulfite Restriction Analysis (COBRA) to analyze MENT promoter methylation in human lymphoma and non-malignant/control samples, correlating methylation patterns with MENT and DNMT3B7 expression levels. Significant elevation of DNMT3B7 and MENT expression and MENT promoter hypomethylation was observed in lymphoma cells. EpiTaq HS polymerase was used for COBRA.

  4. Kurosawa, N., et al. (2013) Reduced level of the BCL11B protein is associated with adult T-cell leukemia/lymphoma. PLoS ONE 8(1):e55147.

    Summary: Adult T-cell leukemia/lymphoma (ATLL), an aggressive malignancy of mature CD4+ regulatory T lymphocytes, is thought to be caused by the HTLV-1 virus in combination with chromosomal abnormalities—although the mechanisms of pathogenesis are unknown. The authors focused on BCL11B, a transcriptional regulator that is located near known chromosomal breakpoints in ATLL patients. EpiTaq HS polymerase was used for bisulfite sequencing to assess BCL11B CpG methylation levels in T lymphocytes from ATLL patients as well as several T cell lines.

  5. Yoshikawa, T., et al. (2012) Silencing of microRNA-122 enhances interferon-alpha signaling in the liver through regulating SOCS3 promoter methylation. Scientific Reports 2:637.

    Summary: Interferon (IFN) alpha is a primary therapeutic agent for eradication of hepatitis C virus (HCV), which affects over 170 million people worldwide and is a major cause of liver disease. IFN-alpha activates the JAK-STAT pathway, eliciting transcription of antiviral proteins encoded by genes bearing IFN-stimulated response elements (ISREs) in their promoters. An HCV core protein suppresses this process by inducing transcription of the ISRE negative regulator SOCS3, leading to IFN resistance. In an effort to find new combination therapy strategies, the researchers identified a microRNA regulator of SOCS3 expression. miR-122 affected the methylation status of the SOCS3 promoter, thereby influencing gene expression. EpiTaq HS polymerase was used for bisulfite sequence analysis.

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