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MRNA profiles of WT and STAT6-/- mice colon tissue

ABSTRACT: mRNA profiles of WT and STAT6-/- mice colon tissue

PROVIDER: PRJNA451477 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7057551.fastq.gz	Fastqsanger.gz
	SRR7057552.fastq.gz	Fastqsanger.gz
	SRR7057553.fastq.gz	Fastqsanger.gz
	SRR7057554.fastq.gz	Fastqsanger.gz
	SRR7057555.fastq.gz	Fastqsanger.gz

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mRNA profiles of WT and STAT6-/- mice colon tissue

Project description:Colon tissues from 6-8 week BALB/c mice and STAT6-/- mice having 3% DSS for 3 days were obtained. Total RNAs were isolated with Trizol (invitrogen) and the RNA-seq library was prepared by the Beijing Genomics Institute. Sequence reads were obtained using BGIseq500 and successfully mapped to mouse genome. Reads counts were normalized based on FPKM, fold changes were calculated for all possible comparisons.

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Gene expression in WT and Stat6 KO intestinal stem cells

Project description:Purpose: To examine the expression profile of WT and Stat6 KO intestinal stem cells. Methods: We isolated Lgr5+ ISCs from the intestine tissue, and generated Stat6 KO ISCs through CRISPR/Cas9 approach. Results: Many genes are changed upon Stat6 KO cells. We pay special attention on Wnt/β-catenin signaling that is the most critical pathway in ISCs, and discovered Stat6 drove the expression of Wnt target genes. Conclusions: Stat6 crosstalks with Wnt signaling to drive ISC self-renewal.

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Transcriptome analysis in the colon of mice with constitutive active STAT6 expression in intestinal epithelial cells

Project description:We investigated which genes in colon tissue are differentially expressed due to constitutive active STAT6 signaling in intestinal epithelial cells (VillinCre_STAT6vt). Therefore, we performed RNA sequencing of colon tissue from naive VillinCre_STAT6vt mice and littermate controls (STAT6vt).

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STAT6 mutations compensate for CREBBP mutations and hyperactivate IL4/STAT6/RRAGD/mTOR signaling in follicular lymphoma

Project description:Activating mutations in STAT6 are common in Follicular Lymphoma (FL) and transformed FL and various other B cell lymphomas. Here, we report RNA-seq based gene expression data on normal human lymph node derived B lymphocytes (NBC; N = 6), and primary human FL WT (N = 11) or mutant (N = 4) for STAT6 before and after ex vivo stimulation with IL4. We found that STAT6 mutants result in broad based augmentation of IL4-induced gene expression. Unexpectedly, in FL with WT STAT6 we measured reduced baseline and IL4-induced gene expression levels when compared with NBC lymphocytes or FL with STAT6 mutations. We tracked the attenuated IL4/JAK/STAT6 response to co-existing CREBBP mutations and experimentally verified that intact CREBBP is required for the induction of many IL4-induced genes. One of the IL4-induced genes here identified is RRAGD, a small G-protein involved in lysosomal mTOR activation. We show that IL4 treatment induced RRAGD expression, that RRAGD is required for mTOR activation in lymphoma cells and that IL4-enhanced BCR signaling induced mTOR activation. The IL4 and BCR-induced mTOR activation was reduced by CREBBP mutants and augmented by mutant STAT6, establishing a link between STAT6 mutations and mTOR regulated pro-growth pathways in lymphoma.

2025-03-10 | GSE261465 | GEO

STAT6 mutations compensate for CREBBP mutations and hyperactivate IL4/STAT6/RRAGD/mTOR signaling in Follicular Lymphoma

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WT distal colon RNA-seq

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RNAseq of WT and Stat6 knockout Tfh21 and Tfh4 cells

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Gene expression in WT and Stat6 KO intestinal stem cells

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Project description:We report that Stat6-driven gene transcription regulates the transition from Tfh21 to Tfh4 cells, suppressing IL-21 production and promoting IL-4 secretion. We identified a cis-enhancer in the second intron of Il21 as a regulator of Tfh cell cytokine transition, via an effect of Stat6 on chromatin accessibility with repression of Il21 transcription. We conclude that Stat6 is necessary for coordinated regulation of IL-21 and IL-4 production by Tfh cells, leading to appropriate maturation of the germinal center B cell response.

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Activation of STAT6 by STING Is Critical for Antiviral Innate Immunity

Project description:Analysis of the transcriptional response of HEK293 or HEK293-STAT6 stable cell lines to poly(I:C) transfection. The hypothesis tested was that poly(I:C) transfection is capable of inducing the expression of STAT6-dependent antiviral genes. mRNA isolated from HEK293 or HEK293-STAT6 stable cell lines with control treatment or poly(I:C) transfection for 16 hours.

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