Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1084738 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We report on the identification of nitric-oxide regulated H3K9/14ac sites in Arabidopsis. For this purpose liquid grown Arabidopsis seedlings were treated with the natural NO-donor S-nitrosoglutathione (GSNO), GSNO in combination with the NO-scavenger cPTIO, GSH (control) or TSA (positive control). Material was crosslinked and harvested 3h and 16h after onset of the treatments. Then, quantitative analysis of the H3K9/14ac patterns across these treatment was performed using DiffBind. By comparison of the GSNO and GSNO/cPTIO treatment, NO-regulated H3K9/14ac sites were identified. These sites were then annotated to the nearest TSS. GO enrichment analysis revealed that NO affects H3K9/14ac at many stress-responsive and photosynthetic genes.
2017-03-07 | GSE82075 | GEO
Project description:Chromatin immunoprecipitation followed by massive parallel sequencing (ChIP-Seq) in HGC27 cells using anti-ARGLU1 antibody
2021-06-30 | GSE174158 | GEO
Project description:Temporal dynamics of histone modification H3K9/14ac, H3K27ac, H3K4me3, H3K27me3, and H3K36me3 after wounding in Arabidopsis thaliana.
| PRJEB34113 | ENA
Project description:In a previous study, we found that wound-induced transcriptional expression is strongly correlated with an increase of the level of acetylation of the N-tails of histone 3. To investigate if the increase in histone acetylation is a prerequisite for the induction of wound-induced gene expression, we performed in another experiment the transcriptional profiling of wounded roots with and without treatment with γ-butyrolactone (MB3), a chemical inhibitor of GNAT-MYST family of histone acetyltransferase. In this experiment, to test whether the transcriptional changes we observed in presence of MB3 can be correlated with changes in the epigenetic landscape, we assessed by ChIP-sequencing the impact of MB3 on the enrichment levels of histone marks H3K4me3, H3K27me3, H3K27ac and H3K9/14ac, using H3 as a normalization reference.
2019-11-27 | E-MTAB-8265 | biostudies-arrayexpress
Project description:Liver fibrosis is an urgent clinical problem without effective treatment. Herein, we conduct a high-content screening on a natural “privileged” diterpenoid library to identify a potent anti-liver fibrosis lead DP. Leveraging photoaffinity labeling approach, apolipoprotein L2 (APOL2), an ER-rich protein, is identified as the direct target of DP. APOL2 is mainly expressed in activated hepatic stellate cells (HSCs) and could activate HSCs to synthesize ECM proteins. It can be induced by TGF-b1 and be antagonized by DP. Mechanistically, upon TGF-b1 stimulation, APOL2 binds ER Ca2+ pump SERCA2 to trigger ER stress, elevating its downstream PERK-HES1 axis to promote liver fibrosis, mildly dependent on the canonical TGF-b/Smad signaling. As a result, ablation of APOL2 significantly alleviates TGF-b1-stimulated HSCs activation, and abolishes anti-fibrosis effect of DP. Our findings not only define APOL2 as a novel therapeutic target for liver fibrosis, but also highlight DP as a promising lead for treatment of this symptom.
2023-12-17 | GSE250087 | GEO
Project description:TGF-b1-stimulation induces an epithelial dedifferentiation-process, throughout which epithelial cell sheets disintegrate and gradually switch into fibroblastic-appearing cells (EMT-like transition). Several transcription factors, some of them being TGF-b1-responsive, are functionally involved in such a switch and affect epithelial differentiation and plasticity. We used microarray-based gene expression profiling of mammary epithelial cells that actively undergo TGF-b1-induced epithelial dedifferentiation. Further, we determined gene expression changes in Basonuclin-1 knock-down cells in conjunction with TGF-b1-stimulation in order to determine a possible effect of Bnc1 on TGF-b1-responsive genes. Cells were transfected with non-silencing (control) siRNA or siRNA against Basonuclin-1 (Bnc1) for 24hrs. Subsequently, cells were treated with 5ng/ml TGF-b1 or left untreated for additional 24hrs. The experiments were performed as independent biological triplicate.
2014-03-01 | E-GEOD-54715 | biostudies-arrayexpress
Project description:The Forkhead family of transcription factors comprises numerous members and is implicated in various cellular functions, including cell growth, apoptosis, migration and differentiation.In this study we identified the Forkhead factor FoxQ1 as increased in expression during TGF-beta1 induced changes in epithelial differentiation, suggesting functional roles of FoxQ1 for epithelial plasticity.The repression of FoxQ1 in mammary epithelial cells led to a change in cell morphology characterized by an increase in cell size, pronounced cell-cell contacts and an increased expression of several junction proteins (e.g. E-cadherin). In addition, FoxQ1 knock-down cells revealed rearrangements in the actin-cytoskeleton and slowed down cell cycle G1-phase progression.Furthermore, repression of FoxQ1 enhanced the migratory capacity of coherent mammary epithelial cells.Gene expression profiling of NM18 cells indicated that FoxQ1 is a relevant downstream mediator of TGF-beta1 induced gene expression changes. This included the differential expression of transcription factors involved in epithelial plasticity, e.g. Ets-1, Zeb1 and Zeb2.In summary, this study has elucidated the functional impact of FoxQ1 on epithelial differentiation Cells treated with 200µM 4sU for 2h, biological replicate 1:2h_co._total1, Cells treated with 200µM 4sU for 2h, biological replicate 2:2h_co._total2, Cells treated with 200µM 4sU for 2h, biological replicate 3 :2h_co._total3, Cells treated with 200µM 4sU for 2h and enriched for 4sU labelled RNA, biological replicate 1: 2h_co._enriched1, Cells treated with 200µM 4sU for 2h and enriched for 4sU labelled RNA, biological replicate 2: 2h_co._enriched2, Cells treated with 200µM 4sU for 2h and enriched for 4sU labelled RNA, biological replicate 3:2h_co._enriched3, Cells treated with 5 ng/ml TGF-b1 and 200µM 4sU for 2h, biological replicate 1:2h_TGFbeta_total1, Cells treated with 5 ng/ml TGF-b1 and 200µM 4sU for 2h, biological replicate 2:2h_TGFbeta_total2, Cells treated with 5 ng/ml TGF-b1 and 200µM 4sU for 2h, biological replicate 3:2h_TGFbeta_total3, Cells treated with 5 ng/ml TGF-b1 and 200µM 4sU for 2h and enriched for 4sU labelled RNA, biological replicate 1:2h_TGFbeta_enriched1, Cells treated with 5 ng/ml TGF-b1 and 200µM 4sU for 2h and enriched for 4sU labelled RNA, biological replicate 2:2h_TGFbeta_enriched2, Cells treated with 5 ng/ml TGF-b1 and 200µM 4sU for 2h and enriched for 4sU labelled RNA, biological replicate 3:2h_TGFbeta_enriched3, FoxQ1 dataset Cells transfected with 25nm scrambled siRNA for 48hrs, biological replicate 1:ns-siRNA 48hrs 1, Cells transfected with 25nm scrambled siRNA for 48hrs, biological replicate 2:ns-siRNA 48hrs 2, Cells transfected with 25nm scrambled siRNA for 48hrs, biological replicate 3:ns-siRNA 48hrs 3, Cells transfected with 25nm scrambled siRNA for 48hrs and treated with TGF-b1 for 40hrs biological replicate 1:ns-siRNA 48hrs TGF-b1 40hrs 1, Cells transfected with 25nm scrambled siRNA for 48hrs and treated with TGF-b1 for 40hrs biological replicate 2:ns-siRNA 48hrs TGF-b1 40hrs 2, Cells transfected with 25nm scrambled siRNA for 48hrs and treated with TGF-b1 for 40hrs biological replicate 3:ns-siRNA 48hrs TGF-b1 40hrs 3, Cells transfected with 25nm FoxQ1 siRNA for 48hrs and treated with TGF-b1 for 40hrs biological replicate 1:FoxQ1 siRNA 48hrs TGF-b1 40hrs 1, Cells transfected with 25nm FoxQ1 siRNA for 48hrs and treated with TGF-b1 for 40hrs biological replicate 2:FoxQ1 siRNA 48hrs TGF-b1 40hrs 2 Cells transfected with 25nm FoxQ1 siRNA for 48hrs and treated with TGF-b1 for 40hrs biological replicate 3:FoxQ1 siRNA 48hrs TGF-b1 40hrs 3
2010-09-01 | E-GEOD-23833 | biostudies-arrayexpress
Project description:TGF-b1-stimulation induces an epithelial dedifferentiation-process, throughout which epithelial cell sheets disintegrate and gradually switch into fibroblastic-appearing cells (EMT-like transition). Several transcription factors, some of them being TGF-b1-responsive, are functionally involved in such a switch and affect epithelial differentiation and plasticity. We used microarray-based gene expression profiling of mammary epithelial cells that actively undergo TGF-b1-induced epithelial dedifferentiation. Further, we determined gene expression changes in Basonuclin-1 knock-down cells in conjunction with TGF-b1-stimulation in order to determine a possible effect of Bnc1 on TGF-b1-responsive genes.
2014-03-01 | GSE54715 | GEO
Project description:The goal is to localize "active" histone marks known to bind BRD4-NUT in the NMC genome. Characterization of the reference epigenome in humans by use of ChIP-Seq in the TC-797 human NMC cell line. ChIP-seq of untreated TC-797 cells using H3K9/14Ac antibodies versus IgG control.
2013-03-05 | E-GEOD-36512 | biostudies-arrayexpress