Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Ptk2 ablation in a Trp53fl/fl, Ptenfl/fl, Rb1fl/fl mouse brain tumor model

ABSTRACT: Ptk2 ablation in a Trp53fl/fl, Ptenfl/fl, Rb1fl/fl mouse brain tumor model

PROVIDER: PRJNA1047561 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Ptk2 ablation in a Trp53fl/fl, Ptenfl/fl, Rb1fl/fl mouse brain tumor model

Project description:Ptk2 was identified as a targetable genetic vulnerability in glioblastoma (GBM) cells. Our objective was to test the effect of Ptk2 deletion on survival and tumor phenotype in a mouse model of GBM. At P0, mice carrying Trp53fl/fl (Trp53tm1Brn, JAX #008462), Ptenfl/fl (Ptentm1Hwu/J, JAX #006440), Rb1fl/fl and R26-LSL-Cas9-GFP (JAX #026175) alleles were subjected to stereotactic injection to deliver lentiviral particles expressing Cre and either Ptk2-targeting or control gRNAs to the NSCs residing in the lateral subventricular zone. This injection initiates a GBM tumor in the mice. At time of sacrifice, tumor tissue was harvested and RNA was extracted for sequencing.

2024-08-10 | GSE249154 | GEO

Brain tumor model phenotype study

Project description:This experiment aims at assessing the molecular difference at the transcriptome level of invasive and angiogenic phenotype samples from a rat brain tumor model.

2012-07-31 | E-MTAB-1185 | biostudies-arrayexpress

Single cell RNA sequencing of mouse brain hematopoietic cells after brain ischemia model

Project description:We performed scRNA-seq of brain CD45+ hematopoietic cells from the brain of Cd300a-fl/fl and Cd300a-fl/fl Lys2-Cre mice 0, 1 and 3 hrs after the reperfusion of middle cerebral artery occlusion (MCAO).

2021-12-22 | GSE154396 | GEO

Ablation of placental REST deregulates fetal brain metabolism and impacts gene expression of the offspring brain at the postnatal and adult stages (snRNA-seq)

Project description:The Repressor Element-1 Silencing Transcription (REST) factor is a transcriptional repressor. The aim of this study is to characterize role of REST in placental influences on offspring brain. REST was ablated in mouse placenta by mating mouse carrying floxed (FL) alleles of REST with mouse that expresses Cre recombinase under the control of the promoter of placenta-specific gene Gcm1 (glial cells missing 1). To investigate placental influence on gene expression of adult offspring brain cells, single-nuclei RNA-seq was performed. Data analysis showed that ablation of placental REST significantly impacted specific pathways in choroid plexus and ependymal cells of the offspring brain.

2024-04-19 | GSE237181 | GEO

RNA sequencing in islets from Rip-Cre CDK8fl/fl and CDK8fl/fl mice with or without metabolic stress.

Project description:mRNA of pancreatic islets from Rip-Cre CDK8fl/fl and CDK8fl/fl mice were sequenced to investigate the consequence of genetic CDK8 ablation on genome wide transcript levels. Additionally, Rip-Cre CDK8fl/fl and CDK8fl/fl mice were stressed with STZ and then islets from those mice were sequenced to describe the transcriptome-wide regulation of beta-cells under stress condition.

2019-08-30 | E-MTAB-8201 | biostudies-arrayexpress

Atp4b-Cre;Cdh1(fl/fl);Kras(LSL-G12D/+);Trp53(fl/fl);Rosa26(LSL-YFP/LSL-YFP) mouse stomach vs. Atp4b-Cre;Cdh1(fl/+);Kras(LSL-G12D/+);Trp53(fl/fl);Rosa26(LSL-YFP/LSL-YFP) mouse stomach microarray

Project description:We wished to investigate the role of E-cadherin loss in our mouse parietal cell/pre-parietal cell E-cadherin knock-out, p53 knock-out, oncogenic Kras induced model of gastric cancer. As such, we isolated RNA from stomach tissue from our E-cadherin knock-out model (Atp4b-Cre;Cdh1(fl/fl);Kras(LSL-G12D/+);Trp53(fl/fl);Rosa26(LSL-YFP/LSL-YFP)) and our E-cadherin heterozygous model (Atp4b-Cre;Cdh1(fl/+);Kras(LSL-G12D/+);Trp53(fl/fl);Rosa26(LSL-YFP/LSL-YFP)). We then performed a microarray on this stomach tissue from four independent mice of each genotype. Differentially expressed genes were identified and gene set overlap analysis was used to identify pathways enriched in one model over the other.

2018-05-01 | E-MTAB-5833 | biostudies-arrayexpress

Transcriptional profiling of E14.5 control and Tbr2 fl/fl;Foxg1::Cre cortices

Project description:The abscence of TBR2 gene in human leads to microcephaly. This condition is mimicked by the specific ablation of the murine gene in developing cerebral cortex. Herein we compared gene expression in control and Tbr2 cKO in E14.5 cerebral cortices. This approach represents a useful tool to identify the molecular mechanisms at the basis of the phenotype. 6 samples, 3x Tbr2 +/+;Foxg1::Cre (control) and 3x Tbr2 fl/fl;Foxg1::Cre

2016-09-08 | E-GEOD-63619 | biostudies-arrayexpress

Single Cell RNA Sequencing of WT and Cdh5-cre Myct1 fl/fl Endothelium

Project description:Edothelial cells were FACS sorted as CD31+CD45- population from PYMT-BO1 transplant tumor bearing WT and Cdh-cre Myct1 fl/fl mice on Day 14 post tumor transplantation

2021-09-10 | GSE157879 | GEO

Ablation of Cdh1 and Trp53 in the uterus reveals novel mechanisms controlling tumor microenvironment in endometrial cancer.

Project description:Because TP53 mutation and CDH1 inactivation are the most common abnormalities found in human type II endometrial carcinomas, the contribution of dysfunctional TRP53 and CDH1 in the tumor microenvironment to induce type II endometrial cancer was characterized using mouse as a model. The results of our analysis revealed that conditional deletion of Cdh1 and Trp53 in the uterus regulated most of the genes categorized by their involvement in inflammatory responses, immune cell trafficking, cellular movement, cell-to-cell signaling and interaction and cellular growth and proliferation. A direct comparison of mouse uteri (n=3) from control, single ablation of Cdh1 or Trp53, and ablation of both Cdh1 and Trp53 at 2 months of age.

2014-06-23 | E-GEOD-48131 | biostudies-arrayexpress

Acinetobacter sp. FL strain:FL

Project description:Acinetobacter sp. FL strain:FL Genome sequencing

| PRJNA1131933 | ENA