MeDIP-chip combines methylated DNA immunoprecipitation (MeDIP) with microarray technology to give a detailed profile of genome-wide methylation, and provides insight into the mechanisms of DNA methylation. We provide services for methylation arrays designed by Arraystar.
Arraystar Epigenetic Arrays
|Arraystar Human RefSeq Promoter Array
||23,148 RefSeq promoters (-1,300 bp ~ 500 bp of TSS) |
|Arraystar Mouse RefSeq Promoter Array
||22,327 RefSeq promoters (-1,300 bp ~ 500 bp of TSS) |
|Arraystar Rat RefSeq Promoter Array
||15,987RefSeq promoters (-1,300 bp ~ 500 bp of TSS) |
|Arraystar Human ncRNA Promoter Array
||27,248 lncRNA promoters (-1,300 bp ~ 500 bp of TSS) 622 miRNA promoter (-50 kb~ 50 kb) |
|Arraystar Mouse ncRNA Promoter Array
||18,552 lncRNA promoters (-1,300 bp ~ 500 bp of TSS) 346 miRNA promoter (-50 kb~ 50 kb) |
|Arraystar Human Cancer DMR Array
||12,113 DMRs and nearby 11,380 CpG islands and shores |
|Arraystar Human Cancer Block Array
||7,088 blocks containing 2,554 mRNA, 8,481 lncRNA and 463 miRNA genes |
Arraystar has vast experience performing MeDIP-chip on many sample types, such as FFPE (Formalin-Fixed, Pariffin-Embeded), serum, and plasma. Just send us your samples, and we'll do the rest! (Please refer to the Sample Submission Guidelines to help you start your project).
* For quotations and inquiries, please specify the type of service that you need: Option A, Option B or Option C.
Arraystar's bioinformatics team has extensive experience in analyzing MeDIP-chip data. We provide our customers with thorough, comprehensive data analysis.
• Raw data files derived from the NimbleScan software or Agilent GeneSpring software
• Defferentially Enriched Peak (DEP) analysis
• Summary Report
• Analysis Report Files in GFF format (Genome annotation file, Scaled Log2-ratio Data, P-value Data, Peaks Data, Multi-sample comparison)
The overall promoter CpG content is an excellent predictor of transcriptional repression. Arraystar's bioinformatics team is expert at analyzing MeDIP-chip data. Our unique MeDIP-chip analysis determines the CpG methylation state of mammalian gene promoters (Table 1). The degree of CpG methylation at promoters falls into three classes: High-CpG density promoters (HCP), low-CpG density promoters (LCP) and intermediate-CpG-density promoters (ICP), based on the CpG ratio, GC content and the length of the CpG-rich region.
Table 1. Results of a MeDIP-chip experiment that uncovered genes whose promoters contain methylated CpG islands. . Each gene is listed in the column on the left. The promoter type (LCP, ICP, or HCP) is indicated in the column highlighted by the blue box.
• Identification of Differentially Methylated Regions (DMRs)
DMRs represent regions of the genome that display significant differences in DNA methylation levels among various cell and tissue types, disease states such as cancers, therapeutic treatments, etc. DMRs are associated with diverse regulatory roles and can serve as epigenetic biomarkers for diagnosis, prognosis and treatment options in clinical settings, as well as for drug design. Arraystar's Advanced Data Analysis uses the most sophisticated analytical methods available for using MeDIP data to identify DMRs.Some examples of DMR results from MeDIP are given in Tables 2 and 3.
1) DMRs in Promoter Region
Table 2. Differentially Methylated Regions in Promoters. The columns in the "dmr_attribution" section (red rectangle) display the differences in methylation status at a given locus between 2 different experimental conditions (represented by "Group A" and "Group B". You can find detailed information of the DMRs in this table, including coordinates, length, methylation status and annotations of the related genes.
2) DMRs in CpG Island region
Table 3. Differentially Methylated Regions in CpG islands. The columns in the "dmr_attribution" section (red rectangle) display the differences in methylation status at a given locus between 2 different experimental conditions (represented by "Group A" and "Group B". You can find detailed information of the DMRs in this table, including coordinates, length, methylation status and annotations of the CpG islands.
MSC Transplantation Improves Osteopenia via Epigenetic Regulation of Notch Signaling in Lupus. Shiyu Liu, et al. Cell Metabolism, 2016
TET3 Mediates Alterations in the Epigenetic Marker 5hmC and Akt Pathway in Steroid-Associated Osteonecrosis. Zhao J, et al. Journal of Bone and Mineral Research, 2016
TFIIS. h, a new target of p53, regulates transcription efficiency of pro-apoptotic bax gene. JM Liao, et al. Scientific Reports, 2016
Epigenetic inactivation of the CpG demethylase TET1 as a DNA methylation feedback loop in human cancers. Li L, et al. Scientific reports?, 2016
Genome-Wide DNA Methylation in Mixed Ancestry Individuals with Diabetes and Prediabetes from South Africa. Matsha T E, et al. International Journal of Endocrinology?, 2016
DNA methylation differences in monozygotic twin pairs discordant for schizophrenia identifies psychosis related genes and networks. Castellani CA, et al. BMC Med Genomics, 2015
Long-term parental methamphetamine exposure of mice influences behavior and hippocampal DNA methylation of the offspring. Y Itzhak, et al. Molecular Psychiatry, 2014
Characterization of the nasopharyngeal carcinoma methylome identifies aberrant disruption of key signaling pathways and methylated tumor suppressor genes. Li L, et al.Epigenomics, 2014
Olanzapine-induced methylation alters cadherin gene families and associated pathways implicated in psychosis. MG Melka, et al. BMC Neuroscience, 2014.
Olanzapine-induced DNA methylation in the hippocampus and cerebellum in genes mapped to human 22q11 and implicated in schizophrenia. MG Melka, et al.Psychiatric genetis, 2014.
Long lasting alterations to DNA methylation and ncRNAs may underlie the effects of fetal alcohol exposure. Benjamin I. Laufer, et al. Disease Models & Mechanisms, 2013.
Olanzapine induced DNA methylation changes support the dopamine hypothesis of psyhosis. Melkaye G Melka, et al. Journal of Molecular Psychiatry, 2013.
P10-017 Volatile biomarkers of cisplatin-induced toxicity in vitro. R. Fijten, et al. Abstracts / Toxicology Letters, 2015
A Long-Term Neuroepigenomic Profile of Prenatal Alcohol Exposure. Benjamin I. Laufer. Electronic Thesis and Dissertation Repository.Paper 3913, 2016