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Whole esophagi of WT, Nrf2-/- and Keap1-/- mice on C57BL background at E11.5, E15.5, P0 and P7, and esophageal epithelium of adult (8 weeks old) mice

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE34278 | GEO | 2011/12/09

SECONDARY ACCESSION(S): PRJNA149959

REPOSITORIES: GEO

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Whole esophagi of WT, Nrf2-/- and Keap1-/- mice on C57BL background at E11.5, E15.5, P0 and P7, and esophageal epithelium of adult (8 weeks old) mice

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

Single-cell RNA-seq of the esophagus of Keratin5CreERT2::Keap1 floxB/floxB and Keap1 floxB/floxB mice

Project description:We analyzed the esophagus of Keap1 conditional knockout mice. In these mice, there were both Keap1-normal and Keap1-deleted cells in the esophageal epithelium. To compare the gene expression of these cells, we conducted single-cell RNA-seq for the mice esophagus.

2023-02-19 | GSE197558 | GEO

Keap1-dependent gene expression determined in the liver using conditional Keap1 knockout mice vs. genetic control mice

2008-05-01 | GSE11287 | GEO

Differential squamous cell fates elicited by NRF2 gain-of-function versus KEAP1 loss-of-function

Project description:Clinical evidence has revealed that high-level activation of NRF2 caused by somatic mutations in NRF2 is frequently detected in esophageal squamous cell carcinoma (ESCC), whereas that by somatic mutations in KEAP1, a negative regulator of NRF2, is not. Here, we challenged to generate a mouse model of NRF2-activated ESCC using the cancer-derived NRF2L30F mutation and cancer-driver mutant Trp53R172H. Concomitant expression of NRF2L30F and Trp53R172H induced proliferation of squamous cell epithelia and resulted in NRF2-activated ESCC-like lesions. In contrast, while squamous cell-specific deletion of KEAP1 induced similar NRF2 hyper-activation, the loss-of-KEAP1 combined with Trp53R172H did not elicit the proliferation and formation of ESCC-like lesions. Instead, KEAP1-deleted cells disappeared from the esophageal epithelium over time by cell competition. These findings provide insights into the observation that somatic mutations are more frequently observed in NRF2 than in KEAP1, and the mouse model developed here will be instrumental in elucidating the mechanistic basis leading to NRF2-activated ESCC.

2024-03-22 | GSE255927 | GEO

Transcription profiling of mouse liver from conditional Keap1 knockout mice vs. genetic control mice

Project description:To compare hepatic gene expression in conditional Keap1 knockout (Alb-Cre:Keap1(flox/-)) and genetic control mice. Disruption of Keap1-mediated repression of Nrf2 signaling was expected to result in increased expression of Nrf2-regulated genes. Experiment Overall Design: Hepatic gene expression was compared in conditional Keap1 knockout and genetic control mice (Alb-Cre:Keap1(flox/+)) mice. Male 9 week old mice were used, n=3/group.

2008-06-11 | E-GEOD-11287 | biostudies-arrayexpress

Expression data from Keap1 overexpression and Nrf2 knockdown lung cancer cell

Project description:Keap1 overexpressed and Nrf2 depleted CL1-5 cells were used to identify genes regulated by Keap1/Nrf2 axis-dependent gene regulations We used microarrays to detail the global programme of gene expression underlying metastasis and identified distinct classes of Keap1/Nrf2-regulated genes during this process. CL1-5 cells stably expressed Keap1 expressing construct and Nrf2-specific shRNA were analyzed compared to control cells

2015-03-04 | E-GEOD-66473 | biostudies-arrayexpress

Patient-derived KEAP1 superbinder mutants stabilize KEAP1 structure and sequester NRF2 in p62-dependent clusters

Project description:Cancer-derived loss-of-function mutations in the KEAP1 tumor suppressor gene stabilize the NRF2 transcription factor, resulting in a pro-survival gene expression program that alters cellular metabolism and neutralizes oxidative stress. In a previous study of KEAP1 mutations observed in lung cancer, we classified 40% of the mutations as ‘superbinders’ (superbinders). These mutants bind and ubiquitylate NRF2 but do not promote NRF2 degradation. Here, we further investigated the molecular mechanism(s) driving the superbinder phenotype. BioID-based quantitative proteomic analysis of the R320Q and R470C superbinder mutations revealed increased co-complexed NRF2 without significant alteration to other KEAP1-associated proteins, including CUL3, VCP, and several ubiquitin receptors within the proteasome lid. Dynamic simulation modeling and limited proteolysis analyses suggest that superbinder mutations stabilize residues in KEAP1 that contact NRF2. In cells, KEAP1 R320Q and R470C mutants co-localize with NRF2, p62/SQSTM1 and polyubiquitin in spherical clusters that rapidly fuse and dissolve; KEAP1-NRF2 localization to these clusters requires p62. Expression of R320Q and R470C in lung cancer cells provided resistance to the reactive oxygen species-inducing drug bleomycin. We present a model wherein superbinder mutations alter the conformational dynamics of the KEAP1-NRF2 complex to alter the cycling of KEAP1 between open and closed conformations, thus inhibiting NRF2 degradation.

2018-11-07 | PXD008411 | Pride

Barrett's esophagus

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

Gene expression change in Keap1 knockdown (KD) mice in kidneys of ischemia-reperfusion injury (IRI)

Project description:We analyzed differences in IRI kidneys between WT and Keap1 KD mice (= Nrf2-activated mice). To identify Nrf2-target genes or metabolic genes in kidneys, we examined the mRNA expression profile both in normal (uninjured) and IRI kidneys (at day1 after unilateral IRI) from mice We performed microarray analyses using 1) Injured kidneys at day 1 after unilateral IRI, and 2) intact kidneys from mice which did not undergo UIRI. Samples were harvested from Keap1 KD mice and WT mice, n = 2 each,

2016-04-01 | E-GEOD-71647 | biostudies-arrayexpress

Nrf2 sequesters Keap1 preventing podosome disassembly

Project description:Nrf2 is a transcription factor playing an essential role in stress response. A knowledge of the significance of Nrf2 in cell function has not, as yet, reached out beyond transactivation of gene expression. This paper shows that GDF-15 and SDF-1-induced angiogenesis strongly depends on Nrf2 presence, but is not related to its transcriptional activity. We propose, that Nrf2 serves as a protein restraining Keap1, its known transcriptional repressor. Deficiency of Nrf2 protein available for Keap1 leads to overabundance of RhoGAP1, the protein regulating Cdc42 activity, and impairs podosome assembly, thereby indisposing actin rearrangements, preventing migration and angiogenesis. These activities can be rescued by concomitant deletion of RhoGAP1 or Keap1. We suggest that a new Nrf2 function of a Keap1 scavenger implies revising the established murine model of Nrf2 deficiency as a transcriptional knock out (tKO) mouse. The N-terminal fragment of Nrf2, containing Neh2 domain binding Keap1, is present in these animals. Thus, regarding the function of Nrf2 as a protein sequestering Keap1, both published and unpublished data on Nrf2-Keap1 duet may gain new interpretation.

2018-11-28 | PXD009161 | Pride

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