Mus musculus
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-48622
PROVIDER: PRJNA210871 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Transcriptional Profiling of Neuronal APP/APLP2 Double-Conditional Knockout Mice.
2015-07-16 | E-GEOD-48622 | ExpressionAtlas
Project description:Gene expression analysis of 2-month-old APP/APLP2 double-conditional Knockout (N-dCKO) mice and littermate APLP2 knockout controls, APP knockout and wildtype controls.
2013-07-10 | GSE48622 | GEO
Project description:Gene expression analysis of 2-month-old APP/APLP2 double-conditional Knockout (N-dCKO) mice and littermate APLP2 knockout controls, APP knockout and wildtype controls. Mouse hippocampus were dissected for RNA extraction and hybridization on Affymetrix microarrays.
2013-07-10 | E-GEOD-48622 | biostudies-arrayexpress
Project description:Pre-T cells from control and Zfp36l1, Zfp36l2 double conditional knockout mice. [iCLIP]
| PRJNA315111 | ENA
Project description:Despite its key role in Alzheimer pathogenesis, the physiological function(s) of the amyloid precursor protein (APP) and of its proteolytic fragments are still poorly understood. The secreted APPs? ectodomain has been shown to be involved in neuroprotection and synaptic plasticity. The ?-secretase generated APP intracellular domain, AICD, functions as a transcriptional regulator in heterologous reporter assays although its role for endogenous gene regulation has remained controversial. Previously, we have generated APPs? knockin (KI) mice expressing solely the secreted ectodomain APPs?. Here, we generated double mutants (APPs?-DM) by crossing APPs?-KI mice onto an APLP2-deficient background and show that APPs? rescues the postnatal lethality of the majority of APP/APLP2 double knockout mice. Despite normal CNS morphology and unaltered basal synaptic transmission, young APPs?-DM mice already showed pronounced hippocampal dysfunction, impaired spatial learning and a deficit in LTP. To gain further mechanistic insight into which domains/proteolytic fragments are crucial for hippocampal APP/APLP2 mediated functions, we performed a DNA microarray transcriptome profiling of prefrontal cortex and hippocampus of adult APLP2-KO (APLP2-/-) and APPs?-DM mice (APP?/?APLP2-/- mice).Interestingly, this analysis failed to reveal major genotype-related transcriptional differences. Expression differences between cortex and hippocampus were, however, readily detectable. Prefrontal cortices and hippocampi of adult mice (38 - 40 weeks) of the following genotypes were analyzed: APLP2-KO (APLP2-/-) (n=3) and APPs?-DM (APP?/?APLP2-/-) (n=3).
2011-05-10 | E-GEOD-27888 | biostudies-arrayexpress
Project description:RNAseq of pre-T cells from control and Zfp36l1, Zfp36l2 double conditional knockout mice.
| PRJNA315110 | ENA
Project description:YAP1 gene fusions have been observed in a subset of paediatric ependymomas. Here we show that, ectopic expression of active nuclear YAP1 (nlsYAP5SA) in ventricular zone neural progenitor cells using conditionally-induced NEX/NeuroD6-Cre is sufficient to drive brain tumour formation in mice. Neuronal differentiation is inhibited in the hippocampus. Deletion of YAP1’s negative regulators LATS1 and LATS2 kinases in NEX-Cre lineage in double conditional knockout mice also generates similar tumours, which are rescued by deletion of YAP1 and its paralog TAZ. YAP1/TAZ-induced mouse tumours display molecular and ultrastructural characteristics of human ependymoma. RNA sequencing and quantitative proteomics of mouse tumours demonstrate similarities to YAP1-fusion induced supratentorial ependymoma. Finally, we find that transcriptional cofactor HOPX is upregulated in mouse models and in human YAP1-fusion induced ependymoma, supporting their similarity. Our results show that uncontrolled YAP1/TAZ activity in neuronal precursor cells leads to ependymoma-like tumours in mice.
2020-05-26 | PXD018131 | Pride
Project description:Despite its key role in Alzheimer pathogenesis, the physiological function(s) of the amyloid precursor protein (APP) and of its proteolytic fragments are still poorly understood. The secreted APPsα ectodomain has been shown to be involved in neuroprotection and synaptic plasticity. The γ-secretase generated APP intracellular domain, AICD, functions as a transcriptional regulator in heterologous reporter assays although its role for endogenous gene regulation has remained controversial. Previously, we have generated APPsα knockin (KI) mice expressing solely the secreted ectodomain APPsα. Here, we generated double mutants (APPsα-DM) by crossing APPsα-KI mice onto an APLP2-deficient background and show that APPsα rescues the postnatal lethality of the majority of APP/APLP2 double knockout mice. Despite normal CNS morphology and unaltered basal synaptic transmission, young APPsα-DM mice already showed pronounced hippocampal dysfunction, impaired spatial learning and a deficit in LTP. To gain further mechanistic insight into which domains/proteolytic fragments are crucial for hippocampal APP/APLP2 mediated functions, we performed a DNA microarray transcriptome profiling of prefrontal cortex and hippocampus of adult APLP2-KO (APLP2-/-) and APPsα-DM mice (APPα/αAPLP2-/- mice).Interestingly, this analysis failed to reveal major genotype-related transcriptional differences. Expression differences between cortex and hippocampus were, however, readily detectable.
2011-05-10 | GSE27888 | GEO
Project description:RNA-Seq was performed on pancreatic islets from four transgenic mouse strains affecting LKB1 and AMPK. A conditional LKB1 knockout strain was generated. Double conditional knockouts for AMPK alpha1 and AMPK alpha2 were also generated. These conditional strains were crossed with RIP-Cre (driven by rat insulin promoter) or Ins1-Cre mice to generate LKB1 knockout and AMPK double knockout strains.
2014-10-25 | E-MTAB-2791 | biostudies-arrayexpress
Project description:Pre-T cells from control and Zfp36l1, Zfp36l2 double conditional knockout mice
| PRJNA315108 | ENA