Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA164691 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Transcriptional profiling of adult forestomach epithelium comparing K5-CreER controsl with K5-CreER;Rosa26Sox2/Sox2 mutants. Two doses of tamoxifen were given and four weeks later the epithelal sheets were harvested for RNA extraction. Goal was to determine the effects of Sox2 overexpression on epithelial phenotypic changes. Two-condition experiment, wildtype Vs Sox2 overexpression mutant. Biological replicates: 3 control replicates, 3 mutant replicates.
2012-05-08 | E-GEOD-37857 | biostudies-arrayexpress
Project description:Transcriptional profiling of adult forestomach epithelium comparing K5-CreER controsl with K5-CreER;Rosa26Sox2/Sox2 mutants. Two doses of tamoxifen were given and four weeks later the epithelal sheets were harvested for RNA extraction. Goal was to determine the effects of Sox2 overexpression on epithelial phenotypic changes.
2012-05-09 | GSE37857 | GEO
Project description:RNA-seq of neuronal SOX2-ablated murine suprachiasmatic nuclei against wild-type littermate controls
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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.
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Project description:Trancriptome profiling of murine overexpression of p65/RelA mutants
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Project description:RNA-seq of human glioblastoma cell lines with overexpression of SOX2, SFRP2
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Project description:Cancer originates as the progressive accumulation of genetic mutations in proto-oncogenes and tumor suppressors. However, the early events underlying tumor initiation remain largely elusive, mostly due to the general lack of information regarding the cells-of-origin responsible for tumor formation as well as the precise impacts of genetic insults on tumor initiation in vivo. Here, we demonstrate that Sox2-positive (Sox2+) adult stem cells are responsible for epithelial squamous tumor formation. Conditional expression of oncogenic Kras (KrasG12D) and knockout of p53 (also known as Trp53) in Sox2+ cells quickly and specifically resulted in the formation of squamous tumors in the forestomach and esophagus. GFP-based lineage tracing experiments demonstrated that Sox2+ cells are the cells-of-origin of squamous tumors in the esophagus and forestomach. Of note, our data showed that p53 deletion alone did not suffice for tumor initiation. On the contrary, tumor initiation was observed upon KrasG12D activation whereas p53 deletion further contributed to the malignancy of the generated tumors, pointing out distinct roles for Kras activation and p53 deletion in squamous tumor formation and progression, to which a multihit carcinogenesis model can be applied. Global gene expression analysis revealed secreting factors upregulated in the generated tumors induced by oncogenic Kras, which contribute to tumor progression. Taken together, these results demonstrate that epithelial squamous tumors can specifically originate as a consequence of defined genetic mutations in a Sox2+ cell population and highlight the connections between proliferative stem cells and tumor development in vivo.
2017-01-01 | GSE66457 | GEO
Project description:RNA-seq of zebrafish sa12692 mutants against WT controls
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