Foxa2 and H2A.Z Mediate Nucleosome Depletion during Embryonic Stem Cell Differentiation - gene expression
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Li Zhaoyu
PROVIDER: E-MTAB-1308 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:RNAs were extracted from 10 week adult control and FoxA1/A2 Pdx1CreERT2 mice. FoxA1 and FoxA2 are ablated in adult mouse Beta cells by tamoxifen adminstration. We aim to study the roles of FoxA1 and FoxA2 on islet gene expression when they are knocked down.
2010-06-23 | E-MTAB-219 | biostudies-arrayexpress
Project description:The inability of the beta-cell to meet the demand for insulin brought about by insulin resistance leads to type 2 diabetes. In adults, beta-cell replication is one of the mechanisms thought to cause the expansion of beta-cell mass. Efforts to treat diabetes require knowledge of the pathways that drive facultative beta-cell proliferation in vivo. A robust physiological stimulus of beta-cell expansion is pregnancy, and identifying the mechanisms underlying this stimulus may provide therapeutic leads for the treatment of type 2 diabetes. The peak in beta-cell proliferation during pregnancy occurs on day 14.5 of gestation in mice. Using advanced genomic approaches, we globally characterize the gene expression signature of pancreatic islets on day 14.5 of gestation during pregnancy. We identify a total of 1,907 genes as differentially expressed in the islet during pregnancy. We demonstrate that the islet's ability to compensate for relative insulin deficiency during metabolic stress is associated with the induction of both proliferative and survival pathways. A comparison of the genes induced in three different models of islet expansion suggests that diverse mechanisms can be recruited to expand islet mass. The identification of many novel genes involved in islet expansion during pregnancy provides an important resource for diabetes researchers to further investigate how these factors contribute to the maintenance of not only islet mass, but ultimately beta-cell mass.
2010-06-26 | E-MTAB-120 | biostudies-arrayexpress
Project description:We determine the mechanisms that control global nucleosome dynamics during embryonic stem (ES) cell differentiation into endoderm
2012-12-24 | E-MTAB-1302 | biostudies-arrayexpress
Project description:Embryonic stem (ES) cells were differentiated in culture to midbrain dopaminergic (mDA) progenitors and subjected to ChIP-seq analysis to resolve genome-wide binding sites of forkhead box protein A2 (Foxa2). Foxa2 was found to directly regulate multiple lineage pathways to specify midbrain dopaminergic and floor plate progenitor identity.
2012-07-01 | E-MTAB-1137 | biostudies-arrayexpress
Project description:In each cell type the expression of genes is regulated by the action of a large number of transcription factors, but so far we have only a rudimentary knowledge of the location of the gene regulatory elements where they bind. This can now be addressed with genome-wide ChIP experiments. In a previous ChIP-chip study of USF1 and USF2 we found evidence also of binding of GABP, FOXA2 and HNF4a within the enriched regions. Here we have applied ChIP-seq for these transcription factors and identified 3064 peaks of enrichment for GABP, 7266 for FOXA2 and 18783 for HNF4a. HNF4a and FOXA2 binding was found in at least half of the regions previously identified as bound by USF2 but not USF1, showing that they frequently bind the same regulatory elements. GABP peaks were found at transcription start sites whereas 94 % of FOXA2 and 90 % of HNF4a peaks were located at other positions. We developed a method based on the high resolution achieved by ChIP-seq to accurately define TFBS within peaks, and found the predicted sites to have an elevated conservation level compared to peak centers; however the majority of bindings were not evolutionary conserved. An unexpected interaction between HNF4a and GABP was seen at TSS, with as many as 1/3 of the HNF4a positive promoters being bound also by GABP, and co-immunoprecipitations show that these factors are in the same complex in the nucleus.
2009-06-09 | E-MTAB-115 | biostudies-arrayexpress
Project description:This study considers the physiological modulation of liver proteins due to the supplementation with fish oils under two different dietary backgrounds: low- or high- fat and sucrose diets, and the effect of their combination with an antioxidant agent (grape polyphenols) which provides reducing power. For this scope, a quantitative proteomics approach based on the Isobaric Tag for relative and Absolute Quantitation methodology (iTRAQ)-coupled to nano-LC-MS/MS and complemented with 2D-DIGE analysis were used for determining the regulation of liver proteins exerted by the supplementation with fish oils, polyphenols or their combination of Wistar Kyoto rats in the two chosen dietary backgrounds. This experimental design was useful to investigate if the behavior of fish oils changes when the dietary background is modified and the possible synergy between fish oils and polyphenols. Results show that the capacity of fish oils, polyphenols or their combination for down or up-regulating liver proteins depends on the dietary context. In the background of low-fat low-sucrose healthy diets, 10 different proteins were altered by the sum of three supplements, in opposite to the 45 altered proteins found in the high-fat high-sucrose unhealthy diets. In both situations, fish oils seemed to be the main force for regulating liver proteins, although the addition of polyphenols was able to modulate some fish oils effects. Moreover, we provide evidence of the effect of fish oils and their combination with grape polyphenols for improving biochemical parameters and for reducing enzymes of hepatic lipogenesis and glycolysis, for enhancing fatty acid beta oxidation and insulin signaling and for the amelioration of endoplasmic reticule stress and protein oxidation when are included in an unhealthy diet.
2017-01-17 | PXD003080 | Pride
Project description:Neuroendocrine (NE) carcinoma and NE differentiation (NED) of human prostate tumor are hallmarks of aggressive human prostate cancer. Here we reveal that HIF-1a cooperation with FoxA2, a transcription factor expressed in NE tissue, is required for determining NE phenotype. Reduced HIF-1a expression, as seen in the E3 ubiquitin ligase Siah2 mutant mice, converted NE tumors to atypical hyperplasia when crossed with the TRAMPTg mice. Significantly, HIF-1a cooperation with FoxA2 enables the trans-activation of select HRE-regulated genes such as Hes6, Plod2 and Jmjd1a, whose expression is notably higher in metastatic prostate adenocarcinomas. Our findings disclose the requirement for spatial and timely regulation of FoxA2 and HIF-1a for NE/NED in prostate tumors. 12 prostate tumor samples were analyzed during normoxia and hypoxia, with different FOX/HIF genotypes. The pivotal samples are represented as duplicates.
2010-07-13 | E-GEOD-18478 | biostudies-arrayexpress
Project description:We performed genome-wide location analysis for Foxa2 to identify its targets in the adult mouse liver. Chromatin isolated from the liver of five adult mice was cross-linked, sheared and immunoprecipitated with a Foxa2-specific antibody. The resulting material, as well as material that was not immunoprecipitated, was uncross-linked, amplified, labeled and hybridized to the Mouse Promoter Chip BCBC-5A. Statistical analysis resulted in a set of 107 genes that are bound by Foxa2. Using computational analyses, we showed that Foxa2 containing cis-regulatory modules are dependent on the strength of the Foxa2 consensus site present.
2008-07-04 | E-MTAB-32 | biostudies-arrayexpress
Project description:RNAs were extracted from E18.5 control and Cdx2/villin-cre mutant ileums. We aim to identify the gene network changes in the mutant epithelia. We are especially interested in genes related with proliferation, apoptosis and cell differentiation.
2010-06-23 | E-MTAB-218 | biostudies-arrayexpress
Project description:The experimental data indicate that during a persistent infection, lymphocytic choriomeningitis virus (LCMV) may both directly or indirectly modulate the regulatory cellular processes and alter the cellular functions that are not critical for the survival, but are needed for the homeostasis in the organism. Two-dimensional differential in-gel electrophoresis (2D-DIGE) and MALDI-TOF MS/MS analyses were used to determine the cellular proteome response of HeLa cell line to persistent LCMV infection. Quantitative analysis revealed 24 differentially abundant proteins, half of which were up-regulated and the rest down-regulated. Functional categorization showed that LCMV-responsive proteins were mainly involved in metabolism, stress and defense responses. Among identified proteins, significant changes were found for peroxiredoxins, family of antioxidant enzymes. Decreased amount of these antioxidant proteins was accompanied with the elevation of ROS content in infected cells.
2019-11-15 | PXD005205 | Pride