Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA274044 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The impact of P53 loss on transcriptome changes following loss of Apc in the intestine
| PRJNA288119 | ENA
Project description:Vil-CreERT2 was used to drive loss of APC (Adenomatous polyposis coli) in the murine intestinal epithelium. 4 days post induction, mice were sampled and 1cm of tissue from the proximal intestine was collected into RNA later. This was compared to control (wild-type) intestine. This analysis allows investigation of transcriptional changes following APC loss (and therefore activation of the WNT signalling pathway).
2019-12-31 | GSE112226 | GEO
Project description:Here we investigate the transcription changes in the murine intestine 4 days following loss of APC under the control of Vil-CreErT2 driver. We compare the RNAseq data from epithelial organoids generated from control (APC loss) intestines to organoids generated from lacking VAV2, VAV3 and TIAM1. We show that loss of these GEFs supress the APC WNT driven intestinal phenotype in a RAC-dependent manner.
2019-12-31 | GSE112261 | GEO
Project description:BACKGROUND: p53 is an important tumor suppressor with a known role in the later stages of colorectal cancer, but its relevance to the early stages of neoplastic initiation remains somewhat unclear. Although p53-dependent regulation of Wnt signalling activity is known to occur, the importance of these regulatory mechanisms during the early stages of intestinal neoplasia has not been demonstrated. METHODS: We have conditionally deleted the Adenomatous Polyposis coli gene (Apc) from the adult murine intestine in wild type and p53 deficient environments and subsequently compared the phenotype and transcriptome profiles in both genotypes. RESULTS: Expression of p53 was shown to be elevated following the conditional deletion of Apc in the adult small intestine. Furthermore, p53 status was shown to impact on the transcription profile observed following Apc loss. A number of key Wnt pathway components and targets were altered in the p53 deficient environment. However, the aberrant phenotype observed following loss of Apc (rapid nuclear localisation of beta-catenin, increased levels of DNA damage, nuclear atypia, perturbed cell death, proliferation, differentiation and migration) was not significantly altered by the absence of p53. CONCLUSION: p53 related feedback mechanisms regulating Wnt signalling activity are present in the intestine, and become activated following loss of Apc. However, the physiological Wnt pathway regulation by p53 appears to be overwhelmed by Apc loss and consequently the activity of these regulatory mechanisms is not sufficient to modulate the immediate phenotypes seen following Apc loss. Thus we are able to provide an explanation to the apparent contradiction that, despite having a Wnt regulatory capacity, p53 loss is not associated with early lesion development. Samples were collected from genetically modified mice. Gene recombination was induced using IP administration of beta-napthoflavone.
2015-06-25 | E-GEOD-70262 | biostudies-arrayexpress
Project description:Genome wide expression profiling to determine the overlap of Affymetrix-signals with SOLID sequencing RNA was extracted using the Qiagen RNeasy kit following the manufacturers guidelines, arrays were prepared and hybridized following the Affymetrix protocol. Mus musculus samples from small intestine and colon, to be compared to transcript data aquired with other techniques
2011-01-06 | E-GEOD-19767 | biostudies-arrayexpress
Project description:BACKGROUND: p53 is an important tumor suppressor with a known role in the later stages of colorectal cancer, but its relevance to the early stages of neoplastic initiation remains somewhat unclear. Although p53-dependent regulation of Wnt signalling activity is known to occur, the importance of these regulatory mechanisms during the early stages of intestinal neoplasia has not been demonstrated. METHODS: We have conditionally deleted the Adenomatous Polyposis coli gene (Apc) from the adult murine intestine in wild type and p53 deficient environments and subsequently compared the phenotype and transcriptome profiles in both genotypes. RESULTS: Expression of p53 was shown to be elevated following the conditional deletion of Apc in the adult small intestine. Furthermore, p53 status was shown to impact on the transcription profile observed following Apc loss. A number of key Wnt pathway components and targets were altered in the p53 deficient environment. However, the aberrant phenotype observed following loss of Apc (rapid nuclear localisation of beta-catenin, increased levels of DNA damage, nuclear atypia, perturbed cell death, proliferation, differentiation and migration) was not significantly altered by the absence of p53. CONCLUSION: p53 related feedback mechanisms regulating Wnt signalling activity are present in the intestine, and become activated following loss of Apc. However, the physiological Wnt pathway regulation by p53 appears to be overwhelmed by Apc loss and consequently the activity of these regulatory mechanisms is not sufficient to modulate the immediate phenotypes seen following Apc loss. Thus we are able to provide an explanation to the apparent contradiction that, despite having a Wnt regulatory capacity, p53 loss is not associated with early lesion development.
2015-06-25 | GSE70262 | GEO
Project description:Transcriptional profiling of intestinal changes following APC loss
| PRJNA445299 | ENA
Project description: Not available
| S-EPMC8784167 | biostudies-literature
Project description: Not available
| S-EPMC395764 | biostudies-literature
Project description: Not available
| S-EPMC4490682 | biostudies-literature