Mus musculus
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-54931
PROVIDER: PRJNA238053 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Comparison of gene expression pattern between Wild-type and Setd2 knockout mESCs [Affymetrix]
2014-10-28 | E-GEOD-54931 | ExpressionAtlas
Project description:SETD2/HYPB has been known as a histone H3K36 specific methyltransferase. However, its roles in physiology such as development and cellular function remain unclear. In this study, using mESCs as cellular model, we show that Setd2 mainly regulates differentiation of murine embryonic stem cells (mESCs) towards primitive endoderm. This study aimed at exploring how did Setd2 regulate primitive endoderm. differentiation. We used microarrays to detail the global programme of gene expression controled by setd2, which is required for endoderm differentiation. Wild type and Setd2 knockout mESCs were selected for RNA extraction and hybridization on Affymetrix GeneChip® mouse genome 430 2.0 arrays. We sought to obtain some deregulated genes, which were required for primitive endoderm differentiation. For comparison, three biological repeats of each were performed.
2014-10-14 | E-GEOD-54931 | biostudies-arrayexpress
Project description:Comparison of gene expression pattern between Wild-type and Hypb knockout embryo yolk sacs
| PRJNA108263 | ENA
Project description:Quantitative Analysis of Wild Type(wt) and Setd2 knockout(ko) mESCs Transcriptomes [RNA-Seq]
| PRJNA238051 | ENA
Project description:Comparison of gene expression pattern between wild-type and RhoE knockout embryo hearts
| PRJNA479470 | ENA
Project description:Purpose: This study aimed at exploring the deregulated genes in setd2 knockout mESCs compared with wt, more particularly to find the mechanism controlled by setd2,which was required for endoderm differentiation. Methods: Setd2 wt and ko mESCs were generated by deep sequencing, using Illumina GAIIx. Using Avadis NGS (version:1.3) software to analyze the sequence reads that passed quality filter to acquire the expression level of all genes. qRT–PCR validation was performed usingSYBR Green assays. Results: Using an optimized data analysis workflow, we mapped about 80 million sequence reads per sample to the mouse genome (build mm9) and identified 17,827 transcripts in the sted2 wt and ko mESCs. About 2,516 genes were deregulated in setd2 ko mESCs, more than 10 genes were validated using qRT-PCR. Conclusions: Through RNA-seq,we noticed that a subset of genes that related to MAPK signaling pathways were down-regulated in ko mESCs. This provided a bridge to connect setd2 and mESCs endoderm differentiation. One wt and one ko mESCs were generated by deep sequencing, using Illumina GAIIx.
2014-10-14 | E-GEOD-54932 | biostudies-arrayexpress
Project description:Comparison of gene expression between wild-type and SERT knockout ileal mucosa
| PRJNA371612 | ENA
Project description:Purpose: This study aimed at exploring the deregulated genes in setd2 knockout mESCs compared with wt, more particularly to find the mechanism controlled by setd2,which was required for endoderm differentiation. Methods: Setd2 wt and ko mESCs were generated by deep sequencing, using Illumina GAIIx. Using Avadis NGS (version:1.3) software to analyze the sequence reads that passed quality filter to acquire the expression level of all genes. qRT–PCR validation was performed usingSYBR Green assays. Results: Using an optimized data analysis workflow, we mapped about 80 million sequence reads per sample to the mouse genome (build mm9) and identified 17,827 transcripts in the sted2 wt and ko mESCs. About 2,516 genes were deregulated in setd2 ko mESCs, more than 10 genes were validated using qRT-PCR. Conclusions: Through RNA-seq,we noticed that a subset of genes that related to MAPK signaling pathways were down-regulated in ko mESCs. This provided a bridge to connect setd2 and mESCs endoderm differentiation.
2014-10-14 | GSE54932 | GEO
Project description:Differential expression between Sh2b3 knockout and wild type mice
| PRJNA273746 | ENA