Ontology highlight
ABSTRACT:
PROVIDER: PRJNA436619 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6796910.fastq.gz | Fastqsanger.gz | |||
| SRR6796911.fastq.gz | Fastqsanger.gz | |||
| SRR6796912.fastq.gz | Fastqsanger.gz | |||
| SRR6796913.fastq.gz | Fastqsanger.gz | |||
| SRR6796914.fastq.gz | Fastqsanger.gz |
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Project description:Commensal microbe-derived butyrate epigenetically induces colonic regulatory T cells
| PRJDB2824 | ENA
Project description:Background: Humans with metabolic and inflammatory diseases frequently harbor lower levels of butyrate-producing bacteria in their gut. However, it is not known whether variation in the levels of these organisms is causally linked with disease development and whether diet modifies the impact of these bacteria on health. Results: We use germ-free apolipoprotein E-deficient mice colonized with synthetic microbial communities that differ in their capacity to generate butyrate to demonstrate that Roseburia intestinalis interacts with dietary components to (i) impact gene expression in the intestine, directing metabolism away from glycolysis and toward fatty acid utilization, (ii) improve intestinal barrier function, (iii) lower systemic inflammation and (iv) ameliorate atherosclerosis. Furthermore, intestinal administration of butyrate improves gut barrier function and reduces atherosclerosis development. Conclusions: Altogether, our results illustrate how modifiable diet-by-microbiota interactions impact cardiovascular disease, and suggest that interventions aimed at increasing the representation of butyrate-producing bacteria may provide protection against atherosclerosis.
2018-08-29 | GSE119141 | GEO
Project description:To investigate the molecular mechanism how butyrate promoter differentiation of naïve T cells into regulatory T cells Examination of acetylated histone H3 during the differentiation of regulatory T cells in the presence or absence of butyrate
2013-11-20 | E-GEOD-49653 | biostudies-arrayexpress
Project description:In the mammalian intestine, crypts of Leiberkühn house intestinal epithelial stem /progenitor cells at their base. We found that the presence of this structure was supported by the physiologic role of a prominent bacterial metabolite, butyrate. This bacterially-produced short chain fatty acid inhibited intestinal epithelial proliferation at physiologic concentrations. During homeostasis, butyrate did not suppress epithelial stem proliferation because it was metabolized by differentiated colonocytes. Provision of butyrate access to stem/progenitor cells either through mucosal injury or application to a crypt-less host led to inhibition of proliferation. The mechanism was dependent on HDAC inhibition in stem cells and the transcription factor Foxo3. Thus, the mammalian crypt unit structure provides energy for differentiated cells at a distance from the crypt base and this action prevents suppression of stem/progenitor proliferation. In total 4 samples were analyzed from 2 independent experiments. Two samples of colonic stem cells treated with 1mM Butyrate and two samples of colonic stem cells treated with 1mM NaCl (mock) as a control
2016-06-27 | E-GEOD-74601 | biostudies-arrayexpress
Project description:Many repetitive DNA elements are packaged in heterochromatin, but depend on occasional transcription to maintain long-term silencing. The factors that promote transcription of repeat elements in heterochromatin are largely unknown. Here, we show that DOT1L, a histone methyltransferase that modifies lysine 79 of histone H3 (H3K79), is required for transcription of major satellite repeats to maintain pericentromeric heterochromatin (PCH), and that this function is essential for preimplantation development. DOT1L is a transcriptional activator at single-copy genes but does not have a known role in repeat element transcription. We show that H3K79me3 is specifically enriched at repetitive elements, that loss of DOT1L compromises pericentromeric major satellite transcription, and that this function depends on interaction between DOT1L and the chromatin remodeler SMARCA5. DOT1L inhibition causes chromosome breaks and cell cycle defects, and leads to embryonic lethality. Together, our findings uncover a vital new role for DOT1L in transcriptional activation of heterochromatic repeats.
2023-05-26 | PXD028824 | Pride
Project description:RATIONALE: The Epstein Barr virus can cause cancer and lymphoproliferative disorders. Ganciclovir is an antiviral drug that acts against the Epstein Barr virus. Arginine butyrate may make virus cells more sensitive to ganciclovir. Combining ganciclovir and arginine butyrate may kill more Epstein Barr virus cells and tumor cells.
PURPOSE: Phase I trial to study the effectiveness of arginine butyrate plus ganciclovir in treating patients who have cancer or lymphoproliferative disorders that are associated with the Epstein Barr virus.
| 2005372 | ecrin-mdr-crc
Project description:We report the application of H3K9ac- and H4K16ac-based sequencing technology for high-throughput profiling of histone modifications in human granulosa KGN cells. By obtaining over four billion bases of sequence from chromatin immunoprecipitated DNA, we generated genome-wide chromatin-state maps of KGN cells. We find that H3K9ac effectively discriminates genes that are influenced by butyrate treatment. H4K16ac described less influence of genes by butyrate treatment. Finally, we show that butyrate could mediate the H3K9ac to effectively influence genes that related to biological functions ang signalings. This study provides a framework for the application of comprehensive gene profile towards H3K9ac regulation by butyrate in human granulosa KGN cells.
2020-04-29 | GSE149547 | GEO
Project description:Utilizing next-generation sequencing technology, combined with ChIP (Chromatin Immunoprecipitation) technology to analyze histone modification (acetylation) induced by butyrate and to map the epigenomic landscape of normal histone H3, H4 Cells were treated with 10 mM butyrate for 24 hr, The cells were scraped from the flask and homogenized with ice-cold Dounce homogenizer to release the nuclei. The collected nuclei were resuspended in digestion buffer and enzymatic shearing was performed. ChIP with anti H3, H4 and acetyl-H3 and acetyl-H4.
2014-01-24 | E-GEOD-38973 | biostudies-arrayexpress