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Integrative Low-input Transcriptomic and Cistromic Analyses Identify CREB Target Genes in Cystic Epithelial Cells

ABSTRACT: Integrative Low-input Transcriptomic and Cistromic Analyses Identify CREB Target Genes in Cystic Epithelial Cells

PROVIDER: PRJNA694564 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13519936_1.fastq.gz	Fastqsanger.gz
	SRR13519936_2.fastq.gz	Fastqsanger.gz
	SRR13519937_1.fastq.gz	Fastqsanger.gz
	SRR13519937_2.fastq.gz	Fastqsanger.gz
	SRR13519938_1.fastq.gz	Fastqsanger.gz

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Integrative Low-input Transcriptomic and Cistromic Analyses Identify CREB Target Genes in Cystic Epithelial Cells [RNA-Seq]

Project description:Integrative Low-input Transcriptomic and Cistromic Analyses Identify CREB Target Genes in Cystic Epithelial Cells [RNA-Seq]

| PRJNA694567 | ENA

Integrative Low-input Transcriptomic and Cistromic Analyses Identify CREB Target Genes in Cystic Epithelial Cells [RNA-Seq]

Project description:Transcription factors (TFs) play crucial roles in kidney development and disease by recognizing specific DNA sequences to control gene expression programs. The kidney’s cellular heterogeneity poses substantial challenges to identifying the genomic binding sites and direct target genes of TFs in vivo. We apply the CUT&RUN (cleavage under targets and release using nuclease) technique, together with transcriptomic analysis, to identify cAMP-response element-binding protein (CREB) target genes in cystic epithelial cells of autosomal dominant polycystic kidney disease (ADPKD). Our results reveal that CREB binds to and activates ribosomal biogenesis genes, and that inhibition of CREB retards cyst growth in ADPKD mouse models. Our findings demonstrate that CUT&RUN is a powerful method for genome-scale profiling and identifying direct targets of TFs from small numbers of specific kidney cells.

2022-01-01 | GSE165417 | GEO

Integrative Low-input Transcriptomic and Cistromic Analyses Identify CREB Target Genes in Cystic Epithelial Cells [CUT&RUN, ChIP-Seq]

2022-01-01 | GSE165416 | GEO

Integrative Low-input Transcriptomic and Cistromic Analyses Identify CREB Target Genes in Cystic Epithelial Cells [CUT&RUN, ChIP-Seq]

Project description:Integrative Low-input Transcriptomic and Cistromic Analyses Identify CREB Target Genes in Cystic Epithelial Cells [CUT&RUN, ChIP-Seq]

| PRJNA694566 | ENA

Integrative Cistromic and Transcriptomic Analyses Identify CREB Target Genes in Cystic Renal Epithelial Cells.

Project description:BackgroundGenome-wide mapping of transcription factor (TF) binding sites is essential to identify a TF's direct target genes in kidney development and diseases. However, due to the cellular complexity of the kidney and limited numbers of a given cell type, it has been challenging to determine the binding sites of a TF in vivo. cAMP response element-binding protein (CREB) is phosphorylated and hyperactive in autosomal dominant polycystic kidney disease (ADPKD). We focus on CREB as an example to profile genomic loci bound by a TF and to identify its target genes using low numbers of specific kidney cells.MethodsCleavage under targets and release using nuclease (CUT&RUN) assays were performed with Dolichos biflorus agglutinin (DBA)-positive tubular epithelial cells from normal and ADPKD mouse kidneys. Pharmacologic inhibition of CREB with 666-15 and genetic inhibition with A-CREB were undertaken using ADPKD mouse models.ResultsCUT&RUN to profile genome-wide distribution of phosphorylated CREB (p-CREB) indicated correlation of p-CREB binding with active histone modifications (H3K4me3 and H3K27ac) in cystic epithelial cells. Integrative analysis with CUT&RUN and RNA-sequencing revealed CREB direct targets, including genes involved in ribosome biogenesis and protein synthesis. Pharmacologic and genetic inhibition of CREB suppressed cyst growth in ADPKD mouse models.ConclusionsCREB promotes cystogenesis by activating ribosome biogenesis genes. CUT&RUN, coupled with transcriptomic analysis, enables interrogation of TF binding and identification of direct TF targets from a low number of specific kidney cells.

| S-EPMC8722786 | biostudies-literature

Integrative Low-input Transcriptomic and Cistromic Analyses Identify CREB Target Genes in Cystic Epithelial Cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-01-01 | GSE165418 | GEO

Analyzing CREB binding motif and sites in the mouse lens epithelial cells alpha-TN4 overexpressing Vector, WT-CREB, S133A-CREB, R314A-CREB and S133A/R314A –CREB.

Project description:Transcription factor CREB regulates lens Epithelial-Mesenchymal Transition（EMT）in both S133 phosphorylation dependent and independent manners. We found that S133A-CREB can activate lens EMT, while R314A-CREB attenuated it. To understand the mechanism by which S133A-CREB and R314A-CREB modulates EMT gene expression. ChIP assay using CREB antibody in the in the mouse lens epithelial cells alpha-TN4 overexpressing Vector, WT-CREB, S133A-CREB, R314A-CREB and S133A/R314A-CREB, and ChIP-seq was conducted on the ChIP DNA. We found that WT-CREB, S133A-CREB as well as R314A-CREB binds to the promoter regions of mesenchymal genes, and S133A-CREB retained canonical CREB binding motif, while R314A-CREB exhibited shifted binding motif preference to ATF1.

2025-02-05 | GSE276462 | GEO

Analyzing CREB binding motif and sites in the mouse lens epithelial cells alpha-TN4 overexpressing Vector, WT-CREB, S133A-CREB, R314A-CREB and S133A/R314A –CREB.

Project description:Analyzing CREB binding motif and sites in the mouse lens epithelial cells alpha-TN4 overexpressing Vector, WT-CREB, S133A-CREB, R314A-CREB and S133A/R314A –CREB.

| PRJNA1157419 | ENA

Chromatin immunoprecipitation of human cell lines to identify cAMP-response element binding protein (CREB) binding sites.

Project description:Hormones and nutrients often induce genetic programs via signaling pathways that interface with gene-specific activators. Activation of the cAMP pathway, for example, stimulates cellular gene expression by means of the PKA-mediated phosphorylation of cAMP-response element binding protein (CREB) at Ser-133. Here, we use genome-wide approaches to characterize target genes that are regulated by CREB in different cellular contexts. CREB was found to occupy approximately 4,000 promoter sites in vivo, depending on the presence and methylation state of consensus cAMP response elements near the promoter. The profiles for CREB occupancy were very similar in different human tissues, and exposure to a cAMP agonist stimulated CREB phosphorylation over a majority of these sites. Only a small proportion of CREB target genes was induced by cAMP in any cell type, however, due in part to the preferential recruitment of the coactivator CREB-binding protein to those promoters. These results indicate that CREB phosphorylation alone is not a reliable predictor of target gene activation and that additional CREB regulatory partners are required for recruitment of the transcriptional apparatus to the promoter.

2006-05-09 | E-WMIT-11 | biostudies-arrayexpress

Using RNA-seq to analyze gene expression in the mouse lens epithelial cells alpha-TN4 overexpressing Vector, WT-CREB, KCREB, R314A-CREB, S133A-CREB, S133A-KCREB and S133A/R314A -CREB before and after TGFβ treatment

Project description:CREB regulates lens EMT in both S133 phosphorylation dependent and independent manners. We found that S133A-CREB activated, while R314A-CREB attenuated lens mesenchymal marker gene Fn1 and Snail2. To better understand the mechanism by which S133A and R314A mutations modulate EMT gene expression. RNA-seq on the alpha-TN4 overexpressing Vector, WT-CREB, KCREB, R314A-CREB, S133A-CREB, S133A-KCREB and S133A/R314A -CREB before and after TGFβ treatment.

2025-02-05 | GSE276922 | GEO

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