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GSE26020
Homo sapiens
3 Downloadable Samples
Affymetrix Human Gene 1.0 ST Array (hugene10st), Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Relationship between gene body DNA methylation and intragenic H3K9me3 and H3K36me3 chromatin marks.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Homo sapiens
- 3 Downloadable Samples
Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
This is one of expressional parts of the study. These data were correlated to epigenetic marks and CG density of genes in analyzed cells. The whole study has a following summary: To elucidate possible roles of DNA methylation and chromatin marks in transcription, we performed epigenetic profiling of chromosome 19 in human bronchial epithelial cells (HBEC) and in the colorectal cancer cell line HCT116 as well as its counterpart with double knockout of DNMT1 and DNMT3B (HCT116-DKO). We found that H3K9me3 forms intragenic chromatin blocks along genes with low CpG density in the gene body. Analysis of H3K36me3 profiles indicated that this mark associates either with active genes with low CpG density and H3K9me3 in the gene body or with active genes with high CpG density and DNA hypermethylation in the gene body. In HCT116 cells with double knockout of DNMT1 and DNMT3B, transcription of genes with low CpG density in the gene body was highly elevated and associated with promoter DNA demethylation and rearrangement of H3K9me3 and H3K36me3 occupation. Our finding suggests that similar to DNA methylation, H3K9me3 may play a role in intragenic gene regulation. Further, we observed that a combination of low CpG density in gene bodies together with H3K9me3 and H3K36me3 marking is a specific epigenetic feature of zinc finger (ZNF) genes, which comprise 90% of all genes carrying both histone marks on chromosome 19. For high CpG density genes, transcription and H3K36me3 occupancy were not changed in condition of partial or intensive loss of DNA methylation in gene bodies in the HCT116-DKO cell line. siRNA experiments with SETD2 knockdown in both HBEC and HCT116-DKO cell lines failed to reduce DNA methylation in gene bodies under conditions of H3K36me3 depletion. Our study suggests that the H3K36me3 and DNA methylation marks in gene bodies are established independently from each other and points to similar functional roles of intragenic DNA methylation and intragenic H3K9me3 for CpG-rich and CpG-poor genes, respectively.
Publication Title
Relationship between gene body DNA methylation and intragenic H3K9me3 and H3K36me3 chromatin marks.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Homo sapiens
- 44 Downloadable Samples
- Affymetrix HT Human Genome U133A Array (hthgu133a)
Description
Gene expression data from AML cell lines, MOLM-14, U937, THP-1 and HL-60, that were infected with a scrambled control hairpin (shControl), two shRNAs directed against GSK-3B (shGSK3B_1 and shGSK3B_2), or two shRNAs directed against GSK-3A (shGSK3A_5 and shGSK3A_6).
Publication Title
The intersection of genetic and chemical genomic screens identifies GSK-3α as a target in human acute myeloid leukemia.
Sample Metadata Fields
Cell line
View Samples- Homo sapiens
- 4 Downloadable Samples
- (imblegenhumandnamethylation3x720kcpgislandplusrefseqpromoterarray[100718hg18cpgrefseqprommedip), Affymetrix Human Gene 2.0 ST Array (hugene20st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Loss of the polycomb mark from bivalent promoters leads to activation of cancer-promoting genes in colorectal tumors.
Sample Metadata Fields
Specimen part, Disease, Subject
View Samples- Homo sapiens
- 4 Downloadable Samples
- Affymetrix Human Gene 2.0 ST Array (hugene20st)
Description
Analysis of expression changes between colon tumors (Duke's stage II) and matching colon mucosa tissues using Affymetrix GeneChip Human Gene 2.0 ST arrays.
Publication Title
Loss of the polycomb mark from bivalent promoters leads to activation of cancer-promoting genes in colorectal tumors.
Sample Metadata Fields
Specimen part, Disease, Subject
View Samples- Homo sapiens
- 32 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Keloids are scars that extend beyond original wounds and are resistant to treatment. In order to improve understanding of the molecular basis of keloid scarring, we have assessed the genomic profiles of keloid fibroblasts and keratinocytes.
Publication Title
Keloid-derived keratinocytes exhibit an abnormal gene expression profile consistent with a distinct causal role in keloid pathology.
Sample Metadata Fields
Sex, Age, Specimen part, Race
View Samples- Saccharomyces cerevisiae
- 16 Downloadable Samples
- Affymetrix Yeast Genome 2.0 Array (yeast2)
Description
RNA Pol II transcription has been implied to be either regulated by the general transcription factor TFIID or the co-activator SAGA. Also, this dominancy of either SAGA or TFIID might be according to the existance, or not, of a TATA consensus sequence.
Publication Title
Transcription of Nearly All Yeast RNA Polymerase II-Transcribed Genes Is Dependent on Transcription Factor TFIID.
Sample Metadata Fields
Treatment
View Samples- Mus musculus
- 12 Downloadable Samples
- Illumina MouseWG-6 v2.0 expression beadchip
Description
The concept of age-dependent host control of cancer development raises the natural question of how these effects manifest across the host tissue/organ types with which a tumor interacts, one important component of which is the aging immune system. To investigate this, changes in the spleen, an immune nexus in the mouse, was examined for its age-dependent interactive influence on the carcinogenesis process. The model is the C57BL/6 male mice (adolescent, young adult, middle-aged, and old or 68, 143, 551 and 736 days old respectively) with and without a syngeneic murine tumor implant. Through global transcriptome analysis, immune-related functions were found to be key regulators in the spleen associated with tumor progression as a function of age with CD2, CD3, CCL19, and CCL5 being the key molecules involved. Surprisingly, other than CCL5, all key factors and immune-related functions were not active in spleens from non-tumor bearing old mice. Our findings of age-dependent tumor-spleen signaling interaction suggest the existence of a global role of the aging host in carcinogenesis. Suggested is a new avenue for therapeutic improvement that capitalizes on the pervasive role of host aging in dictating the course of this disease.
Publication Title
Tumor-host signaling interaction reveals a systemic, age-dependent splenic immune influence on tumor development.
Sample Metadata Fields
Sex, Age, Specimen part, Disease, Disease stage
View Samples- Mus musculus
- 32 Downloadable Samples
- Illumina MouseWG-6 v2.0 expression beadchip
Description
The concept of age-dependent host control of cancer development raises the natural question of how these effects manifest across the host tissue/organ types with which a tumor interacts, one important component of which is the aging immune system. To investigate this, changes in the spleen, an immune nexus in the mouse, was examined for its age-dependent interactive influence on the carcinogenesis process. The model is the C57BL/6 male mice (adolescent, young adult, middle-aged, and old or 68, 143, 551 and 736 days old respectively) with and without a syngeneic murine tumor implant. Through global transcriptome analysis, immune-related functions were found to be key regulators in the spleen associated with tumor progression as a function of age with CD2, CD3, CCL19, and CCL5 being the key molecules involved. Surprisingly, other than CCL5, all key factors and immune-related functions were not active in spleens from non-tumor bearing old mice. Our findings of age-dependent tumor-spleen signaling interaction suggest the existence of a global role of the aging host in carcinogenesis. Suggested is a new avenue for therapeutic improvement that capitalizes on the pervasive role of host aging in dictating the course of this disease.
Publication Title
Tumor-host signaling interaction reveals a systemic, age-dependent splenic immune influence on tumor development.
Sample Metadata Fields
Age, Specimen part, Disease, Disease stage
View Samples- Homo sapiens
- 12 Downloadable Samples
Ion Torrent S5
Description
Although several studies have uncovered abnormal signaling pathways in RASopathy disorders, little is known about the alterations of the cardiac transcriptome induced by Noonan syndrome (NS) mutations. Hence, to gain insights into the transcriptional alterations induced by the NS-associated RAF1S257L/+ mutation in human iPSC-derived cardiomyocytes, we performed quantitative transcriptome profiling by RNA-sequencing. Since we have found that inhibition of ERK5 and MEK1/2 pathways could normalized hypertrophy and myofibrillar disarray in mutant cardiomyocytes, we also aimed at identifying gene transcriptional profiles that were specifically affected by either MEK5-ERK5 or MEK1/2-ERK1/2 activation in RAF1S257L/+ iCMs. Overall design: mRNA profiles of human RAF1 S257L/+ and isogenic corrected iPSC-derived cardiomyocytes were generated by RNA-sequencing, in triplicate, using Ion S5.
Publication Title
Inducible Pluripotent Stem Cell-Derived Cardiomyocytes Reveal Aberrant Extracellular Regulated Kinase 5 and Mitogen-Activated Protein Kinase Kinase 1/2 Signaling Concomitantly Promote Hypertrophic Cardiomyopathy in RAF1-Associated Noonan Syndrome.
Sample Metadata Fields
Specimen part, Subject
View Samples