Nrf2 ChIP-seq data of Nrf2KO, wild-type and Keap1KO esophagus
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PROVIDER: PRJNA505432 | ENA |
REPOSITORIES: ENA
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Project description:To understand how hyperactive NRF2 causes the esophageal phenotype in mice.
2018-11-15 | GSE122504 | GEO
Project description:Oltipraz is an activator of Nrf2 but is also an activator of other pathways including those mediated by constitutive activated receptor (CAR). To identify genes regulated by oltipraz that were Nrf2-dependent, we compared gene expression after exposure in wild-type and Nrf2-null mice.
2016-08-16 | GSE85222 | GEO
Project description:We hypothesize that gene expression in the Type II cells of Nrf2+/+ and Nrf2-/- mice are divergent thus contributing the cell growth. More specifically, type II cells from Nrf2-/- mice have increased reactive oxygen species that cause the impaired cell growth. In order to test these hypotheses at the gene expression level, we utilized microarray analysis to examine transcriptional differences between Nrf2+/+ and Nrf2-/- cells. Experiment Overall Design: . This study utilizes microarray analysis to test these hypotheses. Three sets of type II cells were isolated from lungs from both Nrf2+/+ and Nrf2-/- mice and grown for 5 days. RNA was isolated and used for global gene expression profiling (Affymetrix Mouse 430 2.0 array). Statistically significant gene expression was determined as a minimum 6 counts of 9 pairwise comparisons, minimum 1.5-fold change, and p < 0.05. Further, Absolute | FC - FC SEM | >= 1.5.
2008-06-15 | E-GEOD-7810 | biostudies-arrayexpress
Project description:Oltipraz is an activator of Nrf2 but is also an activator of other pathways including those mediated by constitutive activated receptor (CAR). To identify genes regulated by oltipraz that were Nrf2-dependent, we compared gene expression after exposure in wild-type and Nrf2-null mice. Wild-type or Nrf2-null mice were treated each day for 4 days with 75 mg/kg/day/day oltipraz in corn oil or corn oil alone. There were 4 biological replicates used for each of the 4 genotype-treatment groups. Gene expression in the livers of the mice was evaluated using Affymetrix mouse exon arrays (MoEx-1_0-st-v1).
2016-08-16 | E-GEOD-85222 | biostudies-arrayexpress
Project description:To assess the role of the transcription factor NFE2 related factor 2 like 2 ( Nrf2) in the development of high-fat diet (HFD)-induced obesity and non-alcoholic HFD-induced fatty liver disease, 8 wild type (WT) and 8 Nrf2 knock-out (Nrf2-KO) C57BL6J male mice (obtained from Riken BRC, Tsukuba, Japan and originally developed by Prof. M. Yamamoto) were fed an HFD (60 kcal % fat) for 180 days. Whole genome microarray expression profiling was performed in pooled liver samples of WT and Nrf2-KO mice to identify genes that are differentially expressed between WT and Nrf2-KO mice under the stress conditions of HFD-induced obesity. Liver samples were taken from 8 wild type (WT) and 8 Nrf2 knock-out (Nrf2-KO) male mice on high-fat diet (60 kcal % fat) for 180 days. Total RNA was isolated from pooled liver samples from WT or Nrf2-KO mice to produce 4 samples each using the guanidinium thiocyanate method.
2011-11-30 | E-GEOD-33575 | biostudies-arrayexpress
Project description:Nrf2 is a transcription factor that binds to antioxidant response elements of the regulatory region of a number of antioxidant genes. A mutation in the Nrf2 gene increases susceptibility to hyperoxic lung injury. This project examines expression differences between wild type and Nrf2 knock out mice with the hope of providing insight to the downstream effector genes regulated by Nrf2.
2007-12-14 | E-GEOD-495 | biostudies-arrayexpress
Project description:Background. Nuclear erythroid 2 p45-related factor 2 (Nrf2) regulates the expression of antioxidant and detoxification genes and are thought to be important in protection against intracellular pathogens. The aim of this study was to determine the role of Nrf2 in the host defense against Mycobacterium avium complex (MAC) infection in mice. Methods. Wild-type mice and Nrf2-deficient mice were infected with MAC via intranasal inoculation with 1x107 CFU of Mycobacterium avium subsp. hominissuis. At 2 months after infection, the bronchoalveolar lavage fluid, lung tissues were collected, then, comprehensive transcriptome analysis in the lungs was performed by RNA-seq. Results. Nrf2-deficient mice were highly susceptible to MAC, compared with wild-type mice. There was no significant changes between genotypes in the level of oxidative stress. In addition, the expression of genes related to Th1 immunity and the proportion of Th1 cells were not changed between genotypes. Comprehensive transcriptome analysis showed that the expression of Nramp1 was much lower in the infected lungs of Nrf2-deficient mice than those of Wild-type mice. The expression of Nramp1 was also much lower in the infected alveolar macrophages of Nrf2-deficient mice than those of Wild-type mice. The result of electron microscopy showed that many infected alveolar macrophages from Nrf2-deficient mice were found to contain a large number of intracellular MAC bacteria compare to alveolar macrophages from wild-type mice, due to inhibition of phagolysosome fusion. Conclusions. This study identified that the Nramp1 regulated by Nrf2 is essential in defining the outcome of MAC disease. Nrf2 is a critical determinant for host resistance to MAC infection as a regulator for the expression of Nramp1.
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Project description:Barrett's esophagus transcriptome was analysed and compared with Barrett's esophagus primary cell culture and esophageal adenocarcinoma. Keywords: SAGE analysis to compare tissues Barrett's esophagus biopsy was taken from 1 male metaplastic Barrett's esophagus patient. Barrett's esophagus primary cell culture was cultures from a biopsy taken from a Barrett's esophagus patient and cultured for about 4 to 5 weeks. Esophageal adenocarcinoma was taken from a patient known to have cancer and previously Barrett's esophagus
2006-06-28 | E-GEOD-5155 | biostudies-arrayexpress
Project description:Transcriptional profiling of mouse esophageal development. Goal was to globally profile critical genes and signaling pathways during the development of mouse esophagus and determine how Nrf2/Keap1 pathway regulates the morphogenesis of the esophageal epithelium. Mutiple-comparison. WT-E11.5 vs. WT-E15.5 vs. WT-P0 vs. WT-P7; WT-P7 vs. WT-adult; WT-adult vs. Nrf2-/--adult; WT-P7 vs. Nrf2-/--P7 vs. Keap1-/--P7 vs. Nrf2-/-Keap1-/--P7. Biological replicates: 3 replicates for each group.
2011-12-09 | E-GEOD-34278 | biostudies-arrayexpress
Project description:We identified a SNP rs242561, located within a regulatory region of the MAPT gene (encoding microtubule-associated protein Tau). It was consistently occupied by NRF2/sMAF in multiple ChIP-seq experiments, and its strong-binding allele increased transactivation, and accorded higher mRNA levels in cell lines and human brain. To confirm the allele-specific binding, we conducted ChIP tagmentaion sequencing experiment in human lymphoblastoid cell line GM12763 which is heterozygous for rs242561. NRF2 ChIP DNA was isolated from GM12763 cells treated with Sulforaphane (SFN) in triplicates. The region containing rs242561 was amplified using primers, Fwd 5â??-AGCCTTCCCTGTCCTTGATT-3â??, Rev 5â??-GGACCGAGCTTCCAGTCTAA-3â??, and tagmentated using Tn5-based transposition for library construction. Libraries were sequenced on Illumina MiSeq. NRF2 ChIP tagmentation sequencing of a 241bp intron region in MAPT gene using GM12763 treated with sulforaphane
2016-04-14 | E-GEOD-79569 | biostudies-arrayexpress