Mouse cerebellum: Smarca5 conditional KO mice (cKO) versus wild type controls
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE42371 | GEO | 2014/04/30
SECONDARY ACCESSION(S): PRJNA181199
REPOSITORIES: GEO
Similar Datasets
Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
2014-04-30 | E-GEOD-42371 | biostudies-arrayexpress
Project description:Gene expression profiling of mouse cerebellum in which the experimental strain conditionally lack the Smarca5 gene that encodes for the catalytic subunit of multiple chromatin remodeling complexes. Deletion of Smarca5 was restricted to those cells expressing Cre-recombinase driven by the Nestin promoter.
2014-04-30 | GSE42370 | GEO
Project description:Gene expression profiling of mouse cerebellum in which the experimental strain conditionally lack the Smarca5 gene that encodes for the catalytic subunit of multiple chromatin remodeling complexes. Deletion of Smarca5 was restricted to those cells expressing Cre-recombinase driven by the Nestin promoter.
2014-04-30 | GSE42369 | GEO
Project description:Gene expression profiling of mouse cerebellum in which the experimental strain conditionally lack the Smarca5 gene that encodes for the catalytic subunit of multiple chromatin remodeling complexes. Deletion of Smarca5 was restricted to those cells expressing Cre-recombinase driven by the Nestin promoter. Comparison of gene expression in P0 cerebella of Smarca5 cKO mice versus wild type controls. Three samples of each strain were used in a total of 4 replicates.
2014-04-30 | E-GEOD-42369 | biostudies-arrayexpress
Project description:Gene expression profiling of mouse cerebellum in which the experimental strain conditionally lack the Smarca5 gene that encodes for the catalytic subunit of multiple chromatin remodeling complexes. Deletion of Smarca5 was restricted to those cells expressing Cre-recombinase driven by the Nestin promoter. Comparison of gene expression in P10 cerebella of Smarca5 cKO mice versus wild type controls. Three samples of each strain were used in a total of 3 replicates.
2014-04-30 | E-GEOD-42370 | biostudies-arrayexpress
Project description:We previously reported the different motor abilities of D1R knockout (KO), D2R KO and wild-type (WT) mice. To understand the interaction between the cerebellum and the striatal direct and indirect pathways, we examined the expression patterns of immediate early genes (IEG) in the cerebellum of these three genotypes of mice. In the WT naive mice, there was little IEG expression. However, we observed a robust expression of c-fos mRNA in the vermis and hemisphere after running rota-rod tasks. In the vermis, c-fos was expressed throughout the lobules except lobule 7, and also in crus 1 of the ansiform lobule (Crus1), copula of the pyramis (Cop) and most significantly in the flocculus in the hemisphere. jun-B was much less expressed but more preferentially expressed in Purkinje cells. In addition, we observed significant levels of c-fos and jun-B expressions after handling mice, and after the stationary rota-rod task in naive mice. Surprisingly, we observed significant expression of c-fos and jun-B even 30 min after single weighing. Nonetheless, certain additional c-fos and jun-B expressions were observed in three genotypes of the mice that experienced several sessions of motor tasks 24 h after stationary rota-rod task and on days 1 and 5 after rota-rod tasks, but no significant differences in expressions after the running rota-rod tasks were observed among the three genotypes. In addition, there may be some differences 24 h after the stationary rota-rod task between the naive mice and the mice that experienced several sessions of motor tasks.
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2017-11-02 | PXD006460 | Pride
Project description:We compared maximal cold-induced heat production (HPmax) and cold limits between warm (WA; 27°C), moderate cold (MCA; 18°C), or cold acclimated (CA; 5°C) wild-type and uncoupling-protein 1 knockout (UCP1-KO) mice. In wild-type mice, HPmax was successively increased after MCA and CA, and the cold limit was lowered to -8.3°C and -18.0°C, respectively. UCP1-KO mice also increased HPmax in response to MCA and CA, although to a lesser extent. Direct comparison revealed a maximal cold-induced recruitment of heat production by +473 mW and +227 mW in wild-type and UCP1-KO mice, respectively. The increase in cold tolerance of UCP1-KO mice from -0.9°C in MCA to -10.1°C in CA could not be directly related to changes in HPmax, indicating that UCP1-KO mice used the dissipated heat more efficiently than wild-type mice. As judged from respiratory quotients, acutely cold-challenged UCP1-KO mice showed a delayed transition toward lipid oxidation, and 5-h cold exposure revealed diminished physical activity and less variability in the control of metabolic rate. We conclude that BAT is required for maximal adaptive thermogenesis but also allows metabolic flexibility and a rapid switch toward sustained lipid-fuelled thermogenesis as an acute response to cold. In both CA groups, expression of contractile proteins (myosin heavy-chain isoforms) showed minor training effects in skeletal muscles, while cardiac muscle of UCP1-KO mice had novel expression of beta cardiac isoform. Neither respiration nor basal proton conductance of skeletal muscle mitochondria were different between genotypes. In subcutaneous white adipose tissue of UCP1-KO mice, cold exposure increased cytochrome-c oxidase activity and expression of the cell death-inducing DFFA-like effector A by 3.6-fold and 15-fold, respectively, indicating the recruitment of mitochondria-rich brown adipocyte-like cells. Absence of functional BAT leads to remodeling of white adipose tissue, which may significantly contribute to adaptive thermogenesis during cold acclimation.
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Project description:Gene expression profiling of mouse cortices in which the experimental strain lacks Exon 6 of the Snf2l gene which encodes an ATP-binding motif that is critical for chromatin re-modeling
2012-04-10 | GSE34998 | GEO
Project description:The IkB-Kinase (IKK)-NF-kB signaling pathway plays a multifaceted role in Inflammatory Bowel Disease: One the one hand it protects cells from apoptosis, but on the other, it activates transcription of numerous inflammatory cytokines and chemokines. To examine the role of constitutive NF-kB signaling in intestinal epithelium cells (IEC), we generated a mouse model with a tissue-specific knockout of the direct inhibitor of NF-kB, IkBα. We demonstrate that in IκBαIEC-KO mice, constitutive activation of NF-kB in epithelium leads to abnormal intestinal development, enlarged peyer’s patches, loss of Paneth cells, and spontaneous inflammation. We performed expression analysis of IκBαIEC-KO mice compared to wildtype by using the Affymetrix array Clariom S mouse.
2020-03-22 | GSE139251 | GEO