Global Gene expression changes in cholangiocytes with TGF beta treatment
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA606585 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11080776_1.fastq.gz | Fastqsanger.gz | |||
| SRR11080776_2.fastq.gz | Fastqsanger.gz | |||
| SRR11080777_1.fastq.gz | Fastqsanger.gz | |||
| SRR11080777_2.fastq.gz | Fastqsanger.gz | |||
| SRR11080778_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 12 |
Similar Datasets
Project description:Growth factor, TGF beta can have profound effect on global gene expression changes. Since TGF beta signalling is not well studied in liver epithelia , we decided to do Next gen RNA-seq analysis to look at TGF beta signaling in cholangiocytes
2020-02-20 | GSE145271 | GEO
Project description:The growth factor, TGF-beta can have profound effect on global gene expression changes. Since TGF-beta signaling is not well studied in liver epithelia, RNA-seq analysis was performed to evaluate TGF-beta signaling in cholangiocytes.
2019-01-25 | GSE125577 | GEO
Project description:Global Gene Expression Changes in Cholangiocytes Treated with TGF-beta
| PRJNA516867 | ENA
Project description:TGF beta has profound effects on global gene expression changes. To understand the epigenetic changes associated with TGF beta stimulation, we performed ATAC-seq of cholangiocytes to understand the changes in chromatin accessibility associated with TGF beta. We also wanted to determine if H3K9ac played a role in TGF beta induced changes in chromatin accessibility. Therefore, H3K9ac inhibitor CPTH6 was used to treat cells.
2020-02-20 | GSE145252 | GEO
Project description:TGF beta has profound effects on global gene expression changes. To understand the epigenetic mechanisms associated with TGF beta stimulation, we performed ChIP-seq of cholangiocytes to understand the changes in histone modifications associated with TGF beta. We choose H3K27ac and H3K9ac, histone modification associated with gene expression. These histone modifications were correlated with SMAD3 occupancy, which is a canonical downstream mediator of TGF beta signaling.
2020-02-20 | GSE145250 | GEO
Project description:Global expression profile of human osteoblast treated with recombinant TGF-beta compared to human osteoblast treated with growth media alone Dye-swap design with 6 biological replicates. Three arrays performed with TGF-beta treated samples on channel 1 and media-alone treated on channel 2; three arrays performed with TGF-beta treated samples on channel 2 and media-alone on channel 1.
2010-09-29 | E-GEOD-17843 | biostudies-arrayexpress
Project description:TGF-betas have complex roles in tumorigenesis, with context-dependent effects that can either suppress or promote tumor progression. We have previously shown that TGF-beta has tumor suppressor activity in the MCF10Ca1h (M3) human breast cancer xenograft model. To identify potential molecular players in the tumor suppressor responses, we performed global gene expression analyses. To determine which genes were regulated by TGF-beta in this tumor model in vivo, we performed gene expression arrays on tumors derived from xenografts of M3 cells with and without expression of a dominant negative TGF-beta receptor to block activity of endogenous TGF-beta.
2015-01-01 | GSE34276 | GEO
Project description:circRNAs profile were examined upon TGF-beta treatment in A549 cells
2018-09-04 | GSE119145 | GEO
Project description:Very little is known about how intervertebral disc (IVD) is formed or maintained. Members of the TGF-beta superfamily are secreted signaling proteins that regulate many aspects of development including cellular differentiation. We recently showed that deletion of Tgfbr2 in Col2a expressing tissue results in alterations in development of IVD annulus fibrosus. The results suggested TGF-beta has an important role in regulating development of the axial skeleton, however, the mechanistic basis of TGF-beta action in these specialized joints is not known. To understand the mechanism of TGF-beta action in IVD development, we undertook a global analysis of gene expression comparing gene expression profiles in sclerotome cultures treated with TGF-beta or BMP4. As expected, treatment with BMP4 resulted in up-regulation of cartilage marker genes including Acan, Sox 5, Sox6, and Sox9. In contrast, treatment with TGF-beta1 did not regulate expression of cartilage markers but instead resulted in up-regulation of many IVD markers including Fmod and Adamtsl2. We propose TGF-beta has two functions in IVD development: 1) to prevent chondrocyte differentiation in the presumptive IVD and 2) to promote differentiation of annulus fibrosus from sclerotome. We have identified genes that are enriched in the IVD and regulated by TGF-beta that warrant further investigation as regulators of IVD development. Nine samples were analyzed. Three biological replicates of untreated sclerotome grown in micromass culture. Three biological replicates of cells treated with 50 ng/ml BMP4 for 8 hours and three biological replicates of cells treated with 5 ng/ ml TGF-beta1 for 8 hours.
2010-04-09 | E-GEOD-18648 | biostudies-arrayexpress
Project description:Our group is interested in epithelial-to-mesenchymal transition (EMT), in particular, TGF-beta induced EMT. TGF-beta signalling has been shown to be an important factor in the induction of EMT and it has been demonstrated that adding TGF-beta to epithelial cells in culture is a convenient way to study the process of EMT. In response to TGF-beta, Smad2 and 3 are activated, and form complexes with Smad4, which then regulate transcription of target genes through interactions with other DNA binding transcription factors. In the induction of EMT, the activated Smads mediate transcriptional regulation through three families of transcription factors, resulting in repression of epithelial marker gene expression and activation of mesenchymal gene expression (Xu J, et al. 2009) <br></br> Also investigated in this study is the role of H2A.Z in EMT. H2A.Z is an evolutionary conserved and a metazoan essential histone variant of the H2A class. Mice deficient in H2A.Z die during early development but the reason for this is unknown (Faast et al. 2001). Previously, our laboratory showed that the loss of H2A.Z in Xenpous laevis impaired cell movement required for the formation of the mesoderm and neural crest (Ridgway et al. 2004). Given that mesoderm formation is critically dependent upon EMT, we therefore wondered whether H2A.Z might be a chromatin regulator of EMT. We transfected MDCK cells with a lentiviral vector to express a construct encoding an shRNA targeting canine H2A.Z as we wanted to test the hypothesis that H2A.Z is involved in the maintenance of cellular identity and that its loss might trigger de-differentiation. <br></br> In order to investigate changes in histone variant H2A.Z occupancy associated with TGF-beta induced epithelial-to-mesenchymal transition (EMT) we performed H2A.Z ChIP-Seq in untreated and TGFb-treated MDCK cells. The MDCK cell line has been extensively used as a model system for EMT because they convert fully from the epithelial to the mesenchymal state in response to TGF-beta. <br></br>Please note that RNA-seq data generated in conjunction to this ChIP-seq data set were also deposited at ArrayExpress under accession number E-MTAB-5628 ( https://www.ebi.ac.uk/arrayexpress/experiments/E-MTAB-5628 ).
2017-10-23 | E-MTAB-5637 | biostudies-arrayexpress