Mice forestomach
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA210843 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR941141.fastq.gz | Fastqsanger.gz | |||
| SRR941142.fastq.gz | Fastqsanger.gz | |||
| SRR941143.fastq.gz | Fastqsanger.gz | |||
| SRR941144.fastq.gz | Fastqsanger.gz | |||
| SRR941145.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 11 |
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Project description:mice forestomach Transcriptome or Gene expression
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Project description:Gene expression was compared between wild type forestomach and hindstomach epithelial cells at embryonic day E14.5. Gene expression was compared between GATA4 knock out hindstomach epithelial cells and wild type hindstomach epithelial cells at embryonic day E14.5. Gene expression was compared between GATA4 knock in forestomach epithelial cells and wild type forestomach epithelial cells at embryonic day E14.5.
2020-08-17 | GSE156307 | GEO
Project description:Whole forestomach of mice treated with 20% ethanol for 4 weeks; Whole forestomach of mice treated with 15% ethanol for 40 weeks; negative control (0% alcohol treated mice)
2017-12-21 | GSE75373 | GEO
Project description:Differentially expressed genes in SOX2 KO vs control forestomach organoids In this dataset, we include expression data from SOX2 KO forestomach organoid and control forestomach organoid
2025-06-06 | GSE297930 | GEO
Project description:Loss of p120ctn results in dysplasia and invasive cancer in the mouse esophagus and squamous forestomach. We used microarray expression analysis to identify gene expression changes in pre-tumorigenic esophagus samples and in tumors of the squamous forestomach.
2010-02-10 | GSE20240 | GEO
Project description:Mouse forestomach fibroblasts were isolated from a wild-type (wt), a FSP-Cre;TGFBR2 lox/lox (TGFBR2cKO) mouse, and a FSP-Cre;TGFBR2 lox/lox; Smad4 lox/lox (TGFBR2/SMAD4 cKO) mouse and expanded in vitro. The cells were then harvested and processed for RNA purification. While wt and TGFBR2/SMAD4 cKO mice are healthy, the TGFBR2cKO mouse presents with forestomach cancer.
2020-11-01 | GSE106442 | GEO
Project description:Commensal (symbiont) bacteria form communities in various regions of the bodies of vertebrates. Phylogenetic analysis of gut communities is advanced, but the relationships, especially at the trophic level, between commensals that share gut habitats of monogastric animals have not been investigated to any extent. Lactobacillus reuteri strain 100-23 and Lactobacillus johnsonii strain 100-33 cohabit in the forestomach of mice. According to the niche exclusion principle, this should not be possible because both strains utilise the two main fermentable carbohydrates present in the stomach digesta: glucose and maltose. We show, based on gene transcription analysis, in vitro physiological assays, and in vivo experiments that the two strains can co-exist in the forestomach habitat because L. reuteri 100-23 transports maltose into its cells more efficiently than does L. johnsonii 100-33. Conversely, strain 100-33 transports glucose more efficiently than 100-23. As a result, 100-23 shows a preference for growth using maltose, whereas 100-33 prefers glucose. Mutation of the maltose phosphorylase gene (malA) of strain 100-23 prevented its growth on maltose-containing culture medium, and resulted in the numerical dominance of 100-33 in the forestomach. The fundamental niche of L. reuteri 100-23 in the mouse forestomach can be defined in terms of glucose and maltose fermentation. Its realised niche when L. johnsonii 100-33 is present is maltose fermentation. Hence nutritional adaptations provided niche differentiation that enabled cohabitation by the two strains through resource partitioning in the mouse forestomach. This real life, trophic phenomenon conforms to a mathematical model. Analysis of the microarray data was obtained from two independent biological replicates. A dye swap was included in the analysis
2010-12-11 | E-GEOD-24472 | biostudies-arrayexpress
Project description:Commensal (symbiont) bacteria form communities in various regions of the bodies of vertebrates. Phylogenetic analysis of gut communities is advanced, but the relationships, especially at the trophic level, between commensals that share gut habitats of monogastric animals have not been investigated to any extent. Lactobacillus reuteri strain 100-23 and Lactobacillus johnsonii strain 100-33 cohabit in the forestomach of mice. According to the niche exclusion principle, this should not be possible because both strains utilise the two main fermentable carbohydrates present in the stomach digesta: glucose and maltose. We show, based on gene transcription analysis, in vitro physiological assays, and in vivo experiments that the two strains can co-exist in the forestomach habitat because L. reuteri 100-23 transports maltose into its cells more efficiently than does L. johnsonii 100-33. Conversely, strain 100-33 transports glucose more efficiently than 100-23. As a result, 100-23 shows a preference for growth using maltose, whereas 100-33 prefers glucose. Mutation of the maltose phosphorylase gene (malA) of strain 100-23 prevented its growth on maltose-containing culture medium, and resulted in the numerical dominance of 100-33 in the forestomach. The fundamental niche of L. reuteri 100-23 in the mouse forestomach can be defined in terms of glucose and maltose fermentation. Its realised niche when L. johnsonii 100-33 is present is maltose fermentation. Hence nutritional adaptations provided niche differentiation that enabled cohabitation by the two strains through resource partitioning in the mouse forestomach. This real life, trophic phenomenon conforms to a mathematical model.
2010-12-11 | GSE24472 | GEO
Project description:Mice were applied with 125mg/day/kg body weight for 5 days while control mice were applied with corn oil. The microRNA expression profiles of 3 target organs (lung, spleen and forestomach) and 3 non-target organs (liver, colon and glandular stomach) were compared to look for the difference between the target and the non-target organs.
2014-06-30 | E-MTAB-2407 | biostudies-arrayexpress
Project description:Specific deletion of Tgfbr2 in FSP1+ fibroblasts (Tgfbr2fspKO) induced development of SCC in forestomach with 100% penetrance. Tgfbr2fspKO mice die by 7 weeks with a median survival of 38 days (Log rank p<0.001). Examination of Tgfbr2fspKO forestomach between embryonic day 16 (E16) and 5 weeks of age suggested that hyperplasia began during week 3 and was followed by dysplasia, carcinoma in situ, and invasive squamous cell carcinoma (SCC). The aim of this study was to elucidate genetic aberrations in the tumor associated stroma and SCC tumor using array comparative genomic hybridization (CGH) analysis. Laser capture micro-dissection was performed using formalin-fixed, paraffin-embedded, 5 week old Tgfbr2fspKO forestomach tissues. Genetic loss of cyclin-dependent kinase inhibitor, Cdkn2a/ p16Ink4A was found in laser captured epithelia of all three Tgfbr2fspKO forestomachs. Surprisingly, no genetic change was seen in the tumor associated stroma. Examination of human esophageal SCC showed a down-regulation of TGFβ receptor 2 (TβRII) in the stromal fibroblasts as well as increased inflammation and DNA damage. Published literature showed that loss of Cdkn2a/p16Ink4A tumor suppressor is the common event in human ESCCs. Our study suggests anti-inflammation may be a new therapeutic option in treating human SCCs with down-regulation of TβRII in the stroma.
2012-12-06 | GSE42773 | GEO