Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA315858 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:p63 ChIP-seq analysis comparing WT, TAp63-null, and DNp63-null primary murine keratinocytes
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Project description:We performed an RNA-seq analysis characterizing expression profiles in primary keratinocytes obtained from E18.5 mice of 3 different genotypes (WT, TAp63-/-, and ΔNp63-/-). We aimed to identify the specific transcriptional target genes regulated by TAp63 and ΔNp63 in physiological conditions.
2018-03-20 | GSE79447 | GEO
Project description:We performed a ChIP-seq analysis characterizing the p63 binding sites in primary keratinocytes obtained from E18.5 mice of 3 different genotypes (WT, TAp63-/-, and ΔNp63-/-). We aimed to identify the specific genomic regions bound by TAp63 and ΔNp63 in physiological conditions.
2018-03-20 | GSE79448 | GEO
Project description:As a member of the p53/p63/p73 family, p63 is a transcriptional regulator that induces apoptosis, cell cycle arrest, or senescence. TAp63 protein, a p53-like master transcriptional regulator, plays an essential role in epithelial development because p63-null mice are born alive but die shortly after birth due to developmental defects. However, its molecular mechanism remains elusive. We identified these phosphorylation sites during a search for the targets of Cyclin G-associated kinase (GAK) in vitro. LCE1C was drastically upregulated by doxycycline-dependent expression of Myc-TAp63 wild-type (WT) proteins, but not non-phosphorylatable Myc-TAp63-T46A/T281A (AA) proteins.
2018-03-22 | GSE94635 | GEO
Project description:By comparing the comprehensive gene expression profiles between human Th17 cells overexpressing TAp63 and those with TAp63 knockdown, FOXP3 was identified as one of the downregulated genes by TAp63
2023-04-10 | GSE181427 | GEO
Project description:We have compared the response to TGFbeta1 in normal and v-rasHa transduced primary mouse keratinocytes using NCI cDNA microarrays. This analysis reveals that Ha-ras alters global TGFbeta1 mediated gene expression in a gene specific manner. The expression pattern of TGFbeta1 immediate early response genes and down regulation of cell cycle control genes is not altered by Ha-ras but the induction of most extracellular matrix genes is blocked. Using Smad3 null keratinocytes, we find that the majority of TGFbeta1 responsive genes in primary keratinocytes are Smad3 dependent, but patterns of transcriptional responses suggest that the ability of Ha-ras to block TGFbeta1 mediated gene expression is not dependent on Smad3. However, the combination of oncogenic ras and loss of Smad3 prevents the TGFbeta1 dependent suppression of genes associated with cell cycle progression and apoptosis observed with either genotype alone. In addition several extracellular matrix genes are super-repressed by TGFbeta1 in the Ha-ras Smad3 null keratinocytes. These data provide a genomic framework for understanding how disruptions of TGFbeta signaling and oncogenic ras cooperate to promote premalignant progression of primary keratinocytes. Keywords: time series design RNA from Balb/c primary and ras keratinocytes treated for 1, 6, 24, and 48 hours with TGFbeta1 at 1ng/ml was compared to RNA from the corresponding untreated controls. For each timepoint sample from primary and ras cells, multiple arrays (including dye swaps) were analyzed. There are 6, 7, 6, and 5 arrays analyzed for RNA from primary keratinocytes treated for 1, 6, 24, and 48 hours as compared to RNA from untreated primary cells, respectively. There are 6, 8, 7, and 5 arrays analyzed for RNA from ras keratinocytes treated for 1, 6, 24, and 48 hours as compared to RNA from untreated ras cells, respectively. There are 50 arrays analyzed for the Balb/c time-course dataset. RNA from Smad3 WT and KO primary and ras keratinocytes treated 48 hours with TGFbeta1 were compared to RNA from its untreated corresponding controls. There are 6 arrays analyzed for the Smad3 WT/KO data set. There are 56 arrays in this series.
2010-06-30 | E-GEOD-3228 | biostudies-arrayexpress
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2012-02-22 | E-GEOD-34963 | biostudies-arrayexpress
Project description:To identify mutant p53 GOF, murine primary osteosarcomas expressing p53R172H or p53R245W over null and p53-null osteosarcomas were processed for bulk sequencing; DEGs were identified in p53R172H and p53R245W expressing tumors by comparing to p53-null tumors; DEGs were used to identify dysregulated pathways and mutant p53 GOF
2023-05-12 | GSE231849 | GEO
Project description:mTOR activation has been known to affect protein synthesis. To identify molecular signatures in transcriptome that could enhance protein synthesis, RNA-seq and quantitative proteomics studies were conducted using WT and TSC1 null MEFs. In this study, we found that the activation of mTOR leads to genome-wide 3'UTR shortening in mRNAs by alternative polyadenylation and activates ubiquitin-mediated proteolysis. The accession number for the RNA-seq data in this study is SRP056624.
2015-06-16 | PXD002006 | Pride
Project description:RNA-Seq analysis of primary human keratinocytes exposed to Cannabidiol
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