miR-155 transgenic mice develop pre-B cell leukemia/lymphoma. Though some targets of miR-155 are known, understanding of the mechanism by which miR-155 overexpression drives malignant transformation is not known. MicroRNAs regulate multiple genes.
miR-155 targets histone deacetylase 4 (HDAC4) and impairs transcriptional activity of B-cell lymphoma 6 (BCL6) in the Eμ-miR-155 transgenic mouse model.
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Prediction of miRNA-mRNA associations in Alzheimer's disease mice using network topology.
Sex, Age, Specimen part
View SamplesWe addressed the integrated analysis of mRNA and miRNA expression levels of Tg6799 AD model mice at 4 month and 8 months of age. Total 8 gene cluster modules for co-expression network were predicted from transcriptome data and 6 modules were show relation with AD or aging. We constructed early stage AD network using data integration between mRNA and miRNA profiles and predicted miRNAs strongly involved in module regulation. We found that ARRDC3 showed AD mutation dependent changes of expression and was related metabolic dysfunction in early stage AD.
Prediction of miRNA-mRNA associations in Alzheimer's disease mice using network topology.
Sex, Age, Specimen part
View SamplesNeutrophils were isolated form peripheral blood of wildtype and Phd3 null mice, cultured for 4 hours in hypoxia (3% O2) and micro array analysis performed
Prolyl hydroxylase 3 (PHD3) is essential for hypoxic regulation of neutrophilic inflammation in humans and mice.
Specimen part, Treatment
View SamplesWe report quantitative transcriptome data in WT and CHD1 mutant. Overall design: RNA-seq in wild-type and CHD1 mutant.
The ATP-dependent chromatin remodeler Chd1 is recruited by transcription elongation factors and maintains H3K4me3/H3K36me3 domains at actively transcribed and spliced genes.
Genetic information, Subject
View SamplesWe report quantitative transcriptome data in WT and CHD1 mutant. Overall design: RNA-seq in wild-type and CHD1 mutant.
The ATP-dependent chromatin remodeler Chd1 is recruited by transcription elongation factors and maintains H3K4me3/H3K36me3 domains at actively transcribed and spliced genes.
Genetic information, Subject
View SamplesWe report quantitative transcriptome data in WT and CHD1 mutant. Overall design: RNA-seq in wild-type and CHD1 mutant.
The ATP-dependent chromatin remodeler Chd1 is recruited by transcription elongation factors and maintains H3K4me3/H3K36me3 domains at actively transcribed and spliced genes.
Genetic information, Subject
View SamplesWe report quantitative transcriptome data in WT and CHD1 mutant. Overall design: RNA-seq in wild-type and CHD1 mutant.
The ATP-dependent chromatin remodeler Chd1 is recruited by transcription elongation factors and maintains H3K4me3/H3K36me3 domains at actively transcribed and spliced genes.
Genetic information, Subject
View SamplesWe report quantitative transcriptome data in WT and CHD1 mutant. Overall design: RNA-seq in wild-type and CHD1 mutant.
The ATP-dependent chromatin remodeler Chd1 is recruited by transcription elongation factors and maintains H3K4me3/H3K36me3 domains at actively transcribed and spliced genes.
Genetic information, Subject
View SamplesWe report quantitative transcriptome data in WT and CHD1 mutant. Overall design: RNA-seq in wild-type and CHD1 mutant.
The ATP-dependent chromatin remodeler Chd1 is recruited by transcription elongation factors and maintains H3K4me3/H3K36me3 domains at actively transcribed and spliced genes.
Genetic information, Subject
View Samples