E-MTAB-6399
Ontology highlight
ABSTRACT:
PROVIDER: E-MTAB-6399 | ExpressionAtlas | 2018-05-29
REPOSITORIES: ExpressionAtlas
Similar Datasets
Project description:To investigate the role of SHP2 (Ptpn11) in pancreatic carcinogenesis, murine pancreatic whole tissue RNA samples of 9 week old mice with the genotypes Ptf1a-Cre;LSL-KrasG12D (ID-labels Kxxx) and Ptf1a-Cre;LSL-KrasG12D;Ptpn11fl/fl (ID-labels Mxxxx) were analyzed by microarray.
2018-03-30 | E-MTAB-6399 | biostudies-arrayexpress
Project description:To study the role of the gap junction coupled astrocytic network, we generated inducible double knockouts to selectively delete Cx30 and Cx43 from astrocytes in adult mice. Mice carrying loxP-flanked Gjb6 (Cx30fl/fl mice) (Boulay et al., 2013) and Gja1 (Cx43fl/fl mice) (Theis et al., 2003) alleles were crossbred with mice expressing the tamoxifen-sensitive Cre-recombinase CreERT2 under the endogenous GLAST(Slc1a3)-promoter (Mori et al., 2006). Adult, 8-10 week old mice (Cx30fl/fl:Cx43fl/fl:GLASTCreERT2/+, termed cKO) and littermate control mice (Cx30fl/fl:Cx43fl/fl:GLAST+/+) were injected with tamoxifen for 5 consecutive days and hippocampi were isolated for subsequent TMT-based proteomics analysis 90 days after tamoxifen treatment, to study the consequences of astrocyte decoupling and connexin deletion.
2022-03-14 | PXD031136 | Pride
Project description:Goal of the experiment: Analysis of gene expression changes in the cortex, striatum, hippocampus, hypothalamus, Drd2-MSNs and Drd1-MSNs of mice with a postnatal, neuron-specific ablation of GLP or G9a as compared to control mice. For microarray analysis, hippocampus, hypothalamus, cortex and striatum of Camk2a-Cre; GLPfl/fl, Camk2a-Cre; G9afl/fl and age (10-14 week old) and sex matched littermate controls were used for total RNA purification. Four biological replicates were performed for each experiment. Polyribosome associated mRNAs from five, age (10-14 week old) and sex matched Drd1-Cre; Drd1-bacTRAP; G9afl/fl, or Drd2-Cre; Drd2-bacTRAP; G9afl/fl and Drd1-bacTRAP; G9afl/fl or Drd2-bacTRAP; G9afl/fl control mice were used. Three biological replicates were performed for each experiment.
2009-12-10 | E-GEOD-19402 | biostudies-arrayexpress
Project description:Liver-specific depletion of HDAC3 leads to liver steatosis (fatty liver), suggesting disregulation of lipid metabolism. This is correlated with changes in lipid metabolic gene expression. Livers depleted of HDAC3 were removed from 12 week old male HDAC3 fl/fl mice (loxP sites flanking exon 4 to 7 of the HDAC3 gene encoding the catalytic domain of HDAC3) one week after the injection of AAV2/8-Tbg-Cre virus. Livers from the HDAC3 fl/fl mice injected with AAV2/8-Tbg-GFP were used as normal controls.
2011-03-11 | GSE25937 | GEO
Project description:Cancer cachexia syndrome is observed in 80% of patients with advanced-stage cancer, and it is one of the most frequent causes of death. Severe wasting accounts for more than 80% in patients with advanced pancreatic cancer. Here we wanted to define, by using an microarray approach and the Pdx1-cre;LSL-KrasG12D;INK4a/arffl/fl, the pathways involved in muscle, liver and white adipose tissue wasting. The aim of our work was to characterize as extensively as possible the pathways activated by the pancreatic cancer-induced cachectic tissues. For this purpose, we generated and compared genome-wide expression profiles of white adipose tissue, skeletal muscle and liver, from Pdx1-cre;LSL-KrasG12D;INK4a/arffl/fl and LSL-KrasG12D;INK4a/arffl/fl mice at 10 weeks-old. Tissue samples by triplicate was obtained from liver, muscle and adipose tissues in both groups, controls and cachectic mice. Total RNA samples was processed and profiled on Affymetrix Mouse Gene 1.0 ST arrays as previously described (Cano et al, 2012)
2014-01-10 | E-GEOD-51931 | biostudies-arrayexpress
Project description:Purpose: To investigate whether the skeletal retardation observed in NG2-cre/Pot1afl/fl mice affected hematopoiesis. Methods: Whole bone marrow cells mRNA profiles of 2-week-old wild-type (NG2-cre/Pot1awt/wt) and Pot1a knockout (NG2-cre/Pot1afl/fl) mice were generated by deep sequencing, using Illumina NextSeq 500. Results: We compared the relative sizes of these subpopulations between the NG2-cre/Pot1afl/fl and control mice and found a significant reduction in cells of the B-cell lineage in NG2-cre/Pot1afl/fl marrow. Cell subpopulations associated with B-cell differentiation from hematopoietic stem/progenitor cells (HSPCs) were identified according to the expression of established marker genes. Conclusions: Bone marrow microenvironments composed of POT1a-deleted MSPCs impair B-cell development.
2023-09-13 | GSE197721 | GEO
Project description:To investigate the underlying changes during acinar-to-ductal metaplasia induced by different oncogenes and by acute pancreatitis, pancreatic tissue was isolated from 10 week old control wt, KrasG12D, Pi3kCAH1047R and Mek1dd mice and from mice of the same genotypes after induction of acute pancreatitis.
2024-04-06 | E-MTAB-13946 | biostudies-arrayexpress
Project description:6-plex TMT LC-MSMS quantification of proteins in myeloid progenitors (Lineage- Sca1- Kit+ cells) isolated from the bone marrow of 8-12 week old male and female control and Elp3-deficient (Elp3fl/fl vav-iCreT/+) mice. Biological triplicates of each genotype were analyzed, each consisting of 1.10e6 cells from pools of 12-14 control (Elp3fl/fl) or 26-38 (Elp3-deficient) male and female mice.
2021-01-26 | PXD010486 | Pride
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
Project description:Regulation of RNA processing contributes profoundly to tissue development and physiology. The serine-arginine-rich splicing factor 1 (SRSF1) is essential for hepatocyte function and survival. Although SRSF1 is mainly known for its many roles in mRNA metabolism, it is also crucial for maintaining genome stability. We show that acute liver damage in the setting of targeted SRSF1 deletion in mice is primarily mediated by the excessive formation of deleterious RNA–DNA hybrids (R-loops), which induce DNA damage. Combining hepatocyte-specific transcriptome, proteome, and RNA binding analyses, we demonstrate that widespread genotoxic stress following SRSF1 depletion results in global inhibition of mRNA transcription and protein synthesis, leading to impaired metabolism and trafficking of lipids. Accumulation of lipids in SRSF1-deficient hepatocytes is quickly followed by necroptotic cell death, inflammation, and fibrosis, resulting in NASH-like liver pathology. This pathogenesis is recapitulated in SRSF1-depleted human liver cancer cells illustrating a conserved and fundamental role for SRSF1 in preserving genome integrity and tissue homeostasis. This data set contains a proteomic comparison of hepatocytes from wild type vs. acute knockout of SRSF1. The acute knockout was generated by injecting 8-week-old SRSF1 fl/fl mice with a viral vector expressing Cre under the control of the liver-specific thyroxine binding globulin (TBG) promoter (AAV8-TBG-iCre). Controls were generated by injecting AAV8-TBG-GFP viral vector. The hepatocytes were isolated 2 weeks post injection.
2023-03-11 | PXD027035 | Pride