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GSE28853
Caenorhabditis elegans
12 Downloadable Samples
Affymetrix C. elegans Genome Array (celegans)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Chromosome-biased binding and gene regulation by the Caenorhabditis elegans DRM complex.
Sample Metadata Fields
Specimen part
View Samples- Caenorhabditis elegans
- 12 Downloadable Samples
Affymetrix C. elegans Genome Array (celegans)
Description
DRM is a conserved transcription factor complex that includes E2F/DP and pRB family proteins and plays important roles in development and cancer. Here we perform microarray expression profiling analysis of lin-54, a DNA-binding member of the DRM complex. To identify genes regulated by LIN-54 in soma and germline, we analyzed wild-type and lin-54 mutant C. elegans embryos and isolated germlines. We chose embryos because they consist primarily of somatic cells, at a developmental stage with both active cell divisions and dynamic developmental gene expression programs. Since lin-54 null animals are sterile, embryos were obtained from a strain carrying the partial loss-of-function allele lin-54(n2990). Germlines were dissected from lin-54(n3423) null adults that lack detectable transcript and protein. The results revealed conserved roles for DRM in regulating genes involved in cell division, development, and reproduction. We find LIN-54 promotes expression of reproduction genes in the germline, but prevents ectopic activation of germline-specific genes in embryonic soma. Strikingly, genomics and cytological analyses show that DRM binding, a DRM binding motif, and LIN-54-regulated genes are all autosome-enriched. One paradoxical exception occurs the germline, where DRM binds autosomes but genes down-regulated in DRM mutants are enriched on X chromosomes.
Publication Title
Chromosome-biased binding and gene regulation by the Caenorhabditis elegans DRM complex.
Sample Metadata Fields
Specimen part
View Samples- Danio rerio
- 4 Downloadable Samples
IlluminaHiSeq2000
Description
Purpose: The Ikk2 maternal-zygotic mutants are the only vertebrates animals completely depleted globally of the Ikk2 function which is expected to block an activity of the canonical NFkB signaling pathway. Transcriptome profiling of embryos before the midblastula transition (MBT) and after MBT may provide a clean strategy to identify the NFkB target genes. Methods: Zebrafish lines were maintained under standard laboratory procedures. Results: Using an optimized data analysis workflow, we identified 54,276 transcripts in the embryos at 2 hours postfertilization (hpf) and 4 hpf. RNA-seq data confirmed lack of expression of a number of genes in the mutant both prior to and after the MBT, including genes linked to angiogenesis, skin development, cytokinesis, innate immunity and cytoskeletonT, and 4 of these were validated with qRT–PCR. M. add here if required. Conclusions: Our study represents the first detailed analysis of transcriptomes of vertebrates globally depleted of activity of Ikk2, with two biologic replicates, generated by RNA-seq technology.The data reported here should provide a framework for understanding of maternal and zygotic genes which expression is controlled by Ikk2 activity. Our results expands a list of transcripts which expression may be controlled by the canonical NFkB signaling. We conclude that RNA-seq based transcriptome characterization improves analysis of NFkB regulated genes. Overall design: Zebrafish Ikk2 mutants were obtained using zinc-finger nuclease-mediated mutagenesis. Some of the mutant homozygotic embryos grow into fertile adults able to produce embryos totally deplated of maternal and zygotic Ikk2.
Publication Title
Ikk2 regulates cytokinesis during vertebrate development.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 16 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
We performed microarray gene expression profiling in 16 T-ALL cell lines
Publication Title
Aberrant activation of the GIMAP enhancer by oncogenic transcription factors in T-cell acute lymphoblastic leukemia.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Mus musculus
- 8 Downloadable Samples
- Illumina MouseRef-8 v2.0 expression beadchip
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
MYC regulates the core pre-mRNA splicing machinery as an essential step in lymphomagenesis.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Mus musculus
- 8 Downloadable Samples
- Illumina MouseRef-8 v2.0 expression beadchip
Description
Over-expressed MYC binds to virtually all active promoters within a cell, although with different binding affinities, and modulates gene expression, both positively and negatively. Here, we show that during lymphomagenesis in E-myc transgenic mice, MYC directly up-regulates the transcription of the core snRNP assembly genes, including PRMT5, an arginine methyltransferase, that methylates Sm proteins as an early step in lymphomagenesis. This coordinated regulatory effect is direct and is critical for snRNP biogenesis, the maintenance of effective mRNA splicing and cellular viability in cycling cells, in either fibroblasts or B-cells.
Publication Title
MYC regulates the core pre-mRNA splicing machinery as an essential step in lymphomagenesis.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 6 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
In order to investigate the role of PRL-3 in the leukemogenesis, we transfected a control vector (pEGFP) and (human) PRL-3 gene into an acute myeloid leukemia (AML) cell line TF-1, respectively. After drug selection and FACS sorting, we established TF1-pEGFP and TF1-hPRL-3 isogenic cell lines. In vitro and in vivo experiments were conducted to characterized this pair of isogenic cell lines. Results provided insight into the molecular basis of PRL-3 in contributing the development of AML.
Publication Title
LIN28B Activation by PRL-3 Promotes Leukemogenesis and a Stem Cell-like Transcriptional Program in AML.
Sample Metadata Fields
Cell line
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
The RUNX genes encode for transcription factors involved in development and human disease. RUNX1 and RUNX3 are frequently associated with leukemias, yet the basis for their involvement in leukemogenesis is not fully understood. Here we show that Runx1;Runx3 double knockout (DKO) mice exhibited lethal phenotypes due to bone marrow failure and myeloproliferative disorder. These contradictory clinical manifestations are reminiscent of human inherited bone marrow failure syndromes like Fanconi anemia (FA), caused by defective DNA repair. Indeed, Runx1;Runx3 DKO cells showed mitomycin C hypersensitivity, due to impairment of monoubiquitinated-FANCD2 recruitment to DNA damage foci, although FANCD2 monoubiquitination in the FA pathway was unaffected. RUNX1 and RUNX3 interact with FANCD2 independent of CBF, suggesting non-transcriptional role for RUNX in DNA repair. These findings suggest that RUNX dysfunction causes DNA repair defect, besides transcriptional misregulation, and promotes development of leukemias and other cancers.
Publication Title
Disruption of Runx1 and Runx3 leads to bone marrow failure and leukemia predisposition due to transcriptional and DNA repair defects.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 36 Downloadable Samples
- NextSeq 500
Description
The present study aimed to determine mRNA expression profilling of indirect immobilized Jagged1 treated human dental pulp cells. Human dental pulp cells were seeded on indirect immobilized Jagged1 surface for 24 h. Cells on hFc immobilized surface was employed as the control. RNA sequencing was performed using NextSeq500, Illumina. Data were processed on FastQC and FastQ Toolkit and subsequently mapped with Homo sapiens hg38 using TopHat2. Mapped data were processed through Cufflink2 and Cuffdiff2. Results demonstrated 1,465 differentially expressed genes in Jagged1 treated cells compared with the control. Enriched pathway analysis revealed that Jagged1 treated cells upregulated genes mainly involved in extracellular matrix organization, disease, and signal transduction categories. However, genes related to cell cycle, DNA replication and DNA repair categories were downregulated. In conclusion, Jagged1 activates Notch signaling and regulates cell cycle pathway in hDPs. Overall design: The mRNA profiles of human dental pulp cells treated with indirect immobilized Jagged1 (10nM) for 24 h was evaluated by next genereation RNA sequencing (NextSeq 500, Illumina) in triplicates. Cells on hFc immobilized surface was used as the control. In some condition, cells were pretreated with a gamma secretase inhibitor (DAPT; 20 uM) for 30 mins prior to Jagged1 exposure.
Publication Title
RNA sequencing data of Notch ligand treated human dental pulp cells.
Sample Metadata Fields
Specimen part, Treatment, Subject
View Samples- Mus musculus
- 2 Downloadable Samples
- Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)
Description
The change in gene expression on the 8th day of gestation was investigated using DNA microarrays.
Publication Title
Cystathionine β-synthase deficiency causes infertility by impairing decidualization and gene expression networks in uterus implantation sites.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples