Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA167279 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:De novo methylation of CpG islands is seen in many tumors, but the general rules governing this process are not known. By analyzing DNA from tumors, as well as normal tissues, and by utilizing a wide range of published data, we have been able to identify a well-defined set of tumor targets, each of which has its own M-bM-^@M-^\coefficientM-bM-^@M-^] of methylation that is largely determined by its inherent relative ability to recruit the polycomb complex. This pattern is initially formed by a slow process of de novo methylation that occurs during aging and then undergoes expansion early in tumorigenesis, where it may play a role as an inhibitor of development-associated gene activation. We also demonstrate that DNA methylation patterns can be used to diagnose the primary tissue source of tumor metastases. CpG-methylated genomic DNA was enriched using a methyl-DNA immunoprecipitation (mDIP) assay. DNA from the input and bound (enriched) DNA for each sample were labeled and hybridized on the array to define the methylation state of each region.
2014-03-26 | E-GEOD-38142 | biostudies-arrayexpress
Project description:De novo methylation of CpG islands is seen in many tumors, but the general rules governing this process are not known. By analyzing DNA from tumors, as well as normal tissues, and by utilizing a wide range of published data, we have been able to identify a well-defined set of tumor targets, each of which has its own “coefficient” of methylation that is largely determined by its inherent relative ability to recruit the polycomb complex. This pattern is initially formed by a slow process of de novo methylation that occurs during aging and then undergoes expansion early in tumorigenesis, where it may play a role as an inhibitor of development-associated gene activation. We also demonstrate that DNA methylation patterns can be used to diagnose the primary tissue source of tumor metastases.
2014-03-26 | GSE38142 | GEO
Project description:Gene methylation profiling of immortalized human mesenchymal stem cells comparing HPV E6/E7-transfected MSCs cells with human telomerase reverse transcriptase (hTERT)- and HPV E6/E7-transfected MSCs. hTERT may increase gene methylation in MSCs. Goal was to determine the effects of different transfected genes on global gene methylation in MSCs.
2011-08-25 | GSE23936 | GEO
Project description:Gene methylation profiling of immortalized human mesenchymal stem cells comparing HPV E6/E7-transfected MSCs cells with human telomerase reverse transcriptase (hTERT)- and HPV E6/E7-transfected MSCs. hTERT may increase gene methylation in MSCs. Goal was to determine the effects of different transfected genes on global gene methylation in MSCs. Two-condition experiment, KP MSCs vs. 3A6 MSCs.
2011-08-24 | E-GEOD-23936 | biostudies-arrayexpress
Project description:To understand what dictates the emerging patterns of de novo DNA methylation, we mapped DNA methylation, chromatin, and transcription changes in purified fetal mouse germ cells using MIRA-chip, ChIP-chip, and strand-specific RNA-seq, respectively. De novo methylation occurred without any apparent trigger from preexisting repressing chromatin marks but was preceded by broad, low-level transcription along the entire genome in prospermatogonia. Only distinct short sequences remained unmethylated, precisely aligned with constitutive or emerging peaks of H3K4me2. Establishment of methylation at differentially methylated regions (DMRs) of imprinted genes, CpG islands, and IAPs followed these same default rules. Transcription run-through occurred at paternal DMRs with no- or diminishing H3K4me2 peaks. Maternal DMRs remained unmethylated among highly methylated DNA at precisely aligned H3K4me2 peaks with transcription initiating at least in one strand. Our results suggest that the pattern of de novo DNA methylation in prospermatogonia is dictated by opposing actions of broad, low-level transcription and dynamic patterns of active chromatin.
2013-07-31 | GSE45836 | GEO
Project description:Epigenetic regulation plays an important role in cellular development and differentiation. A detailed map of the DNA methylation dynamics that occur during cell differentiation would contribute to decipher the molecular networks governing cell fate commitment. We used the most recent Illumina MethylationEPIC Beadchip platform to describe the genome-wide DNA methylation changes observed throughout hematopoietic maturation by analyzing multiple hematopoietic cell types at different developmental stages. We identified a plethora of DNA methylation changes that occur during human hematopoietic differentiation. Interestingly, we observed that T lymphocytes display a substantial enhancement of de novo CpG hypermethylation as compared to other hematopoietic cell populations.
2018-06-08 | E-MTAB-6315 | biostudies-arrayexpress
Project description:To understand what dictates the emerging patterns of de novo DNA methylation, we mapped DNA methylation, chromatin, and transcription changes in purified fetal mouse germ cells using MIRA-chip, ChIP-chip, and strand-specific RNA-seq, respectively. De novo methylation occurred without any apparent trigger from preexisting repressing chromatin marks but was preceded by broad, low-level transcription along the entire genome in prospermatogonia. Only distinct short sequences remained unmethylated, precisely aligned with constitutive or emerging peaks of H3K4me2. Establishment of methylation at differentially methylated regions (DMRs) of imprinted genes, CpG islands, and IAPs followed these same default rules. Transcription run-through occurred at paternal DMRs with no- or diminishing H3K4me2 peaks. Maternal DMRs remained unmethylated among highly methylated DNA at precisely aligned H3K4me2 peaks with transcription initiating at least in one strand. Our results suggest that the pattern of de novo DNA methylation in prospermatogonia is dictated by opposing actions of broad, low-level transcription and dynamic patterns of active chromatin. ChIP-chip and MIRA-chip were performed to map histone modifications and DNA methylation at different devlopmental time points in germ cells and somatic cells along known imprinted domains and control regions, using custom NimbleGen tiling arrays.
2013-07-31 | E-GEOD-45836 | biostudies-arrayexpress
Project description:To understand what dictates the emerging patterns of de novo DNA methylation, we mapped DNA methylation, chromatin, and transcription changes in purified fetal mouse germ cells using MIRA-chip, ChIP-chip, and strand-specific RNA-seq, respectively. De novo methylation occurred without any apparent trigger from preexisting repressing chromatin marks but was preceded by broad, low-level transcription along the entire genome in prospermatogonia. Only distinct short sequences remained unmethylated, precisely aligned with constitutive or emerging peaks of H3K4me2. Establishment of methylation at differentially methylated regions (DMRs) of imprinted genes, CpG islands, and IAPs followed these same default rules. Transcription run-through occurred at paternal DMRs with no- or diminishing H3K4me2 peaks. Maternal DMRs remained unmethylated among highly methylated DNA at precisely aligned H3K4me2 peaks with transcription initiating at least in one strand. Our results suggest that the pattern of de novo DNA methylation in prospermatogonia is dictated by opposing actions of broad, low-level transcription and dynamic patterns of active chromatin. Strand-specific RNA-seq was done in male and female fetal germ cells and somatic gonadal cells at 15.5 dpc to map transcription.
2013-07-31 | E-GEOD-46953 | biostudies-arrayexpress
Project description: Not available
| S-EPMC2531291 | biostudies-literature
Project description:RNA extracted at 240min. Samples are rRNA depleted. Expression measurement of Homo sapiens genes.
2019-07-31 | GSE114179 | GEO