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MRNA sequencing analysis of transcripts from hippocampus of Wt1∆ mice

ABSTRACT: mRNA sequencing analysis of transcripts from hippocampus of Wt1∆ mice

PROVIDER: PRJNA494225 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7947410.fastq.gz	Fastqsanger.gz
	SRR7947411.fastq.gz	Fastqsanger.gz
	SRR7947412.fastq.gz	Fastqsanger.gz
	SRR7947409.fastq.gz	Fastqsanger.gz

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mRNA sequencing analysis of transcripts from hippocampus of Wt1∆ mice

Project description:Purpose: Study the differentially expressed genes in the hippocampus of mice, comparing Wt1∆ mice with their control wild type littermates in basal conditions (naïve untrained animals). Methods: Forebrain-specific deletion of Wt1 was achieved by crossing animals homozygous for the conditional Wt1 knockout allele (Wt1fl/fl) with a transgenic line, Camk2a-Cre, (B6.Cg-Tg(Camk2a-cre)T29-1Stl/J; Jackson Lab: http://jaxmice.jax.org/strain/005359.html). Expression of Cre recombinase resulted in the in-frame deletion of exons 8 and 9 and generated a truncated allele encoding a shortened non functional WT1 protein lacking zinc fingers 2 and 3 in their forebrain (starting at P21). Brains of Wt1∆ mice (n=2) and their control littermates (wild type; n=2) were removed, dorsal hippocampi were dissected and used for library preparation. The seq library was prepared using TruSeq RNA Sample Prep Kit v2 protocol (Illumina, CA, USA). For the RNA-Seq data analysis Tophat 2.0.13, bowtie 2.1.0 , samtool 0.1.7 and cufflinks 1.3.0 were used. The rn5-bowtie2 index was generated with the command 'bowtie2-build rn5.fa rn5'. The 'rn5.fa'-file was downloaded from the UCSC genome browser. The mm10-bowtie2 index was downloaded from http://bowtie-bio.sourceforge.net/bowtie2/manual.shtml. RefSeq geneTracks and GTF-files for the rn5 and mm10 genome assembly were downloaded from UCSC genome browser. Common gene ids in the GTF-files were matched to individual transcript_ids using the corresponding official symbols obtained from the geneTracks files. Conclusions: Our study illustrates the nature of the different transcripts in Wt1∆ mice compared to their control wild type littermates at basal state (untrained). This experiment allowed us to identify wich genes are modulated in the hippocampus by the transcription fator WT1.

2018-10-02 | GSE120708 | GEO

Hippocampus of SAMR1 and SAMP8 mice [mRNA]

Project description:Hippocampus of SAMR1 and SAMP8 mice [mRNA]

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N-degradomic analysis of proteolytic processing in WT1 heterozygous mice

Project description:N-degradomic analysis of proteolytic processing in WT1 heterozygous mice, suffering from genetically induced chronic kidney injury, compared to wild type

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Differential mRNA Expression in the hippocampus of arsenic-exposed offspring mice

Project description:Determining the mRNA expression profiles in the hippocampus of developmental arsenic-exposed offspring mice by RNA-seq.

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Wilms' tumor 1 WT1(-KTS) isoform time course induction in U2OS cells

Project description:The Wilms' tumor suppressor gene (WT1) encodes a zinc finger transcription factor that plays important roles during development of several organs including metanephric kidneys. A number of WT1 target genes have been identified, but the detailed mechanisms by which WT1 orchestrates renal development remain elusive. To identify WT1 target genes relevant to development, genome-wide expression profiling was performed using oligonucleotide microarrays representing 39,000 human transcripts Keywords: Wilms' tumor 1 (WT1) gene, -KTS isoform; time course

2007-06-21 | GSE5117 | GEO

Gene expression analysis in the hippocampus of SUMO1 and SUMO2 transgenic mice

Project description:Transgenic mouse lines that express His6-SUMO1 and His6-SUMO2 under the control of the neuron specific Thy1.2 promoter were generated and characterized. The effect of increased levels of SUMO1 and -2 at the level of gene expression in the hippocampus was studied. Pooled (left and right) hippocampi were dissected from adult littermate wild-type control (WT1) and SUMO1 and WT2 and SUMO2 transgenic animals (n=3) and subjected to RNA expression analysis.

2013-12-31 | E-GEOD-47951 | biostudies-arrayexpress

Whole-genome sequencing of chromatin in Hacat cells overexpressing WT1

Project description:We report the application of chip sequencing in the search for target genes of transcription factor .Chip-seq efficiently detect genome-wide segments of DNA interacting with transcription factors.We overexpressed the transcription factor WT1 in hacat cells, and then performed chip experiments to collect the DNA fragments bound to WT1, which were then sequenced.Finally, we proved that interleukinin is the target gene of WT1, providing a new target for clinical research and treatment of skin diseases.

2023-01-03 | GSE142992 | GEO

The differentially long noncoding RNAs and mRNA in the hippocampus of Nrf2-knockout mice

Project description:Non-coding long noncoding RNAs (lncRNAs) and mRNA have displayed dysregulated expression in the hippocampus of Nrf2-knockout mice.

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Project description:Interventions: A patient is vaccinated with Montanide ISA51-adjuvanted WT1 Trio cancer vaccine consisting of two WT1 CTL peptides (WT1-126 and WT1-235) and one WT1 HTL peptide (WT1-332) (2mg each) seven times at the interval of two weeks. Primary outcome(s): Induction of WT1-specific immune responses assessed by WT1-related tests such as WT1-DTH skin reaction and serum levels of WT1 peptide IgG autoantibody at 1M, 2M, and 3M of WT1 Trio vaccine. Study Design: Single arm Non-randomized

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MEF-mKras-WT1

Project description:K-ras is one of the most frequently mutated human oncogenes. Activation of K-ras can lead to either senescence or proliferation in primary cells. The precise mechanism governing these distinct outcomes remains unclear. Here we utilized a loss-of-function screen to assess the role of specific genes identified as potential key regulators of K-ras driven oncogenesis. Using this approach, we identify the transcription factor Wt1 as an inhibitor of senescence in primary cells expressing oncogenic K-ras. Deletion or suppression of Wt1 expression leads to senescence of primary cells expressing oncogenic K-ras under the control of the native promotor at physiological levels, but has no effect on cells expressing wild-type K-ras. Wt1 contributes to K-ras driven lung tumorigenesis in vivo and loss of Wt1 is specifically deleterious to human lung cancer cell lines that are dependent on oncogenic K-ras. Taken together, these observations reveal a novel role for Wt1 as a key regulator of the complex genetic network required for the oncogenic effect of the small GTPase K-ras. We compare the expression profiles of Wild type, K-ras mutant, Wt1-null, and double K-ras mutant/Wt1-null mouse embryonic fibroblasts (MEFs). The study provides insights into the transcriptional role of Wt1 in the context of oncogenic K-ras.

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