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
| PRJNA211860 | ENA
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: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:DHX15 is an ATP-dependent RNA helicase involved in pre-mRNA splicing. We have recently reported that DHX15 is a downstream substrate for Akt1, which plays a significant role in vascular biology. Therefore, we aimed to explore the regulatory function of DHX15 over the vasculature, and the endothelial cell biology in different contexts: development, metabolism, ischemia and tumor growth. Methods: Deficient DHX15 mice and zebrafish were generated using transcription activator-like effector nuclease (TALEN) and Crispr/cas9 gene edition. Lymphatic functionality was evaluated by lymphangiography and magnetic resonance imaging. Mouse-induced tumor and metastasis model were generated by injection of syngeneic LLC1 tumor cells. DHX15 gene silencing in mouse liver endothelial cells (LEC) was performed by the lentiviral transduction of shRNA (Dharmacon). The changes in the transcriptome and the proteome resulting from the shRNA transduction were investigated by RNAseq and mass spectrometry, respectively. Results: Homozygous DHX15 gene deficiency was lethal in mouse and zebrafish embryos. DHX15-/- zebrafish also showed an undeveloped parachordal line, which leads to the formation of lymphatic structures in the trunk during the development. DHX15+/- mice and zebrafish were viable, although DHX15+/- gene deficiency triggered lower vascular network density and impaired lymphatic function postnatally in mice. Whole transcriptome and proteome analysis of DHX15 silenced LEC revealed differential expression of enzymes involved in the glycolysis and the gluconeogenesis pathways. The functional validation of these results demonstrated an uncoupling of the glycolysis with the oxidation of pyruvate into the mitochondria and lower activity of the Complex I in the mitochondrial membrane, resulting in lower cellular ATP production. Noteworthy, heterozygous DHX15 deficiency partially inhibited primary tumor growth and reduced lung metastasis after injection of syngeneic LLC1 tumor cells, compared to wild-type mice
2021-11-04 | PXD018104 | Pride
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