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PROVIDER: PRJNA523710 | ENA |
REPOSITORIES: ENA
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Project description:Purpose: The goal of this study is to compare the gene expression profiles of H460, H460-ERT2-RUNX3-WT and H460-ERT2-RUNX3-MT(K94/171R) cells. Methods: H460, H460-ERT2-RUNX3 WT, and H460-ERT2-RUNX3-MT(K94/171R) cells were serum-starved for 24 hr, and then stimulated with 10% serum or 10% serum + 1 uM 4-OHT for 0, 8, or 16 hr. RNA was extracted from the cells. Isolated total RNA was processed for preparation of an RNA-seq library using the Illumina TruSeq Stranded mRNA Sample Preparation kit (Illumina, San Diego, CA, USA). Quality and size of libraries were assessed using the Agilent 2100 Bioanalyzer DNA kit (Agilent, Santa Clara, CA, USA). All libraries were quantified by qPCR using a CFX96 Real Time System (Bio-Rad, Hercules, CA, USA) and sequenced on NextSeq500 sequencers (Illumina). Sequencing adapters and low-quality bases in the raw reads were trimmed using the Cutadapt software. The cleaned high-quality reads were mapped to the human reference genome hg19 (https://genome.ucsc.edu) using STAR software. Genes differentially expressed between two selected biological conditions were identified by Cuffdiff in the Cufflinks package (http://cole-trapnell-lab.github.io/cufflinks/papers/). Results: RNA-Sequencing Data suggest that the R-point defends against oncogenic K-RAS–induced tumorigenesis not only by regulating intracellular programs (cell cycle, apoptosis, and metabolic pathways), but also by regulating extracellular programs (inflammatory response and immune response).
2019-03-13 | GSE128174 | GEO
Project description:Next Generation Sequencing (RNA-Sequencing) for the analysis of RUNX3 targets in H460, H460-ERT2-RUNX3 WT and H460-ERT2-RUNX3 MT(K94/171R mutation)
| PRJNA526672 | ENA
Project description:ChIP-seq was conducted using FACS-isolated CD11chiMHCII+CD4+ splenic WT DC and anti-Runx3 antibodies (Ab). Two biological Runx3 IP repeats and two input controls from sorted CD4 DC
2014-06-22 | E-GEOD-48588 | biostudies-arrayexpress
Project description:ChIP-seq was conducted using freshly isolated (resting) splenic WT CD8+ T cells with anti-Runx3 antibody (Ab), anti-H3K4me1 Ab and non-immune serum (NIS) as control. Two biological Runx3 and two NIS IP repeats from splenic CD8+ T cells isolated by positive selection on anti-CD8 magnetic beads, collected from 18 WT mice.
2013-11-18 | E-GEOD-50130 | biostudies-arrayexpress
Project description:ChIP-seq was conducted using freshly isolated splenic WT NK cells from IL-15/Ra treated mice with anti-Runx3 antibody (Ab) and non-immune serum (NIS) as control. Runx3 and NIS IP from splenic NK cells of IL-15/Ra treated WT mice, isolated by negative selection using NK cell isolation kit (R&D) followed by sorting of NKp46+ cells.
2014-01-22 | E-GEOD-50126 | biostudies-arrayexpress
Project description:ChIP-seq was conducted using freshly isolated (resting) splenic WT NK cells with anti-Runx3 antibody (Ab), anti-H3K4me1 Ab and non-immune serum (NIS) as control. Runx3 and H3K4me1 IP from splenic NK cells isolated by negative selection using NK cell isolation kit (R&D) followed by sorting of NKp46+ cells.
2013-11-18 | E-GEOD-50127 | biostudies-arrayexpress
Project description:ChIP-seq was conducted on isolated splenic WT CD8+ T cells, TCR-activated and cultured with IL-2 using anti-Runx3 antibodies (Ab), anti-H3K4me1 Ab and non-immune serum (NIS) as control. Two biological Runx3 and two NIS IP repeats from TCR-activated and IL-2 cultured splenic CD8+ T cells isolated by positive selection on anti-CD8 magnetic beads.
2013-11-18 | E-GEOD-50128 | biostudies-arrayexpress
Project description:ChIP-seq was conducted using splenic WT NK cells cultured for 7 days with IL-2 using anti-Runx3 antibodies (Ab), anti-H3K4me1 Ab and non-immune serum (NIS) as control. Two biological Runx3, one H3K4me1 and two NIS IP repeats from splenic NK cells isolated from individual mice by negative selection using NK cell isolation kit (R&D) cultured with IL-2.
2013-11-18 | E-GEOD-50129 | biostudies-arrayexpress
Project 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 CBFM-NM-2, 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. 6 mice were analyzed in this study. 3 Runx1;Runx3 double knockout cKit+Sca1+Lin- hematopoietic stem/progenitor cells were compared with their wild type littermate controls. RNA was isolated from 3 independent Runx1;Runx3 WT KSL samples, each pooled from 3 Runx1;Runx3 WT mice, and 3 independent Runx1;Runx3 DKO KSL samples, using the RNeasy Micro Kit (QIAgen). RNA integrity and quantity was assessed using the Agilent 2000 Bioanalyzer system. 3 M-NM-<g to 5 M-NM-<g RNA was processed using WT-Ovation Pico RNA Amplification System (NuGEN) paired with the WT-Ovation Exon Module and FL-Ovation cDNA Biotin Module (NuGEN). A detailed protocol in the userM-bM-^@M-^Ys guide kit was used without modification. cDNA were prepared for hybridization on GeneChip Mouse Gene 1.0 ST Arrays (Affymetrix) according to the instructions in GeneChip Hybridization Wash and Stain Kit for ST arrays (Affymetrix). Microarray hybridization, scanning and preliminary MAS 5.0 normalizations were completed at the A*STAR Biopolis Shared Facilities (BSF).
2014-08-26 | E-GEOD-51107 | biostudies-arrayexpress
Project description:We examine how SUMO post-translational modification of the yeast transcription factor Sko1 affects its binding site selection and affinity. Chromatin immunoprecipitation followed by next-generation sequencing was performed in strains expressing wild-type Sko1 (Sko1-WT) or Sko1 that harbors an Arg-to-Lys mutation at Lys 567 (Sko1-MT), that impairs its sumoylation. We find that, compared with Sko1-WT, SUMO-deficient Sko1 binds numerous additional sites that are near promoters of non-Sko1 target genes. Furthermore, Sko1-MT shows higher occupancy levels than Sko1-WT on most genes that are occupied by both forms. Osmotic stress causes a general rearrangement of Sko1 positions across the genome, but increased numbers of binding sites and occupancy levels are still observed for Sko1-MT after treatment with NaCl. This study indicates that sumoylation attenuates Sko1 association with chromatin and increases its binding specificity.
2019-02-04 | GSE118655 | GEO