Ontology highlight
ABSTRACT:
PROVIDER: PRJNA181199 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Mouse P0 cerebellum: Smarca5 conditional KO mice (cKO) versus wild type controls
| PRJNA181200 | ENA
Project description:Mouse P10 cerebellum: Smarca5 conditional KO mice (cKO) versus wild type controls
| PRJNA181201 | ENA
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:Here we utilized a conditional knock-out mouse model to investigate the role of Smarca5, an ISWI subfamily chromatin remodeling ATPase, during thymocyte development using hCD2-iCre transgene. We did transcriptional profiling of FACS-sorted CD4/CD8 double-positive thymocytes as this thymic population was persistent yet strongly underrepresented in adult 6-week mutant thymi. Controls included age-matched CD4/CD8 double-positive thymocytes from wild-type and tumor suppressor protein Trp53-null mice. For comparison, the Smarca5/Trp53-double-deficient thymocytes included in the experiment were partially rescued upon loss of Trp53.
2019-04-01 | E-MTAB-7758 | biostudies-arrayexpress
Project description:Tamoxifen-inducible conditional knockout (CKO) mice were generated to explore the function of Gcn1 in adult mice using the Cre/loxP system. To analyze the function of GCN1 in the intestinal epithelium, we compared the whole cell proteome of jejunum harvested from GCN1 CKO mice with that of wild-type mice.
2022-08-29 | PXD030519 | JPOST Repository
Project description:Tamoxifen-inducible conditional knockout (CKO) mice were generated to explore the function of Gcn1 in adult mice using the Cre/loxP system. To analyze the function of GCN1 in the liver, we compared the whole cell proteome of livers harvested from GCN1 CKO mice with that of wild-type mice.
2023-04-01 | PXD030514 | JPOST Repository
Project description:Tamoxifen-inducible conditional knockout (CKO) mice were generated to explore the function of Gcn1 in adult mice using the Cre/loxP system. To analyze the function of GCN1 in the intestinal epithelium, we compared the whole cell proteome of ileum harvested from GCN1 CKO mice with that of wild-type mice.
2024-03-31 | PXD030518 | JPOST Repository
Project description:Tamoxifen-inducible conditional knockout (CKO) mice were generated to explore the function of Gcn1 in adult mice using the Cre/loxP system. To analyze the function of GCN1 in the intestinal epithelium, we compared the whole cell proteome of duodenum harvested from GCN1 CKO mice with that of wild-type mice.
2024-03-31 | PXD030517 | JPOST Repository
Project description:A microarray study was performed in unstimulated and TCR-stimulated CD4 + T cells and Treg in wild type and conditional Trim28 KO mice to identify genes that are regulated by Trim28. These experiments constitute a portion of the study described below: Paper Abstract: Peripheral T cell activation and differentiation into specialized effectors are regulated by TCR- and cytokine-mediated signals that induce clonal expansion and unique transcriptional factors. These processes may include active chromatin modification by nuclear factors. In search of such molecules, we found Trim28, a component of large nuclear chromatin-regulatory complex is tightly controlled upon TCR stimulation at the level of phosphorylation, and examined global impact of Trim28 loss in especially CD4+ T cells, by generating T cell-specific conditional Trim28 KO mice (CKO). CD4+ T cells from CKO mice showed defective IL-2 production and T cell proliferation associated with defective upregulation of cell-cycle associated proteins. Accordingly, young CKO showed T-lymphopenia. Surprisingly, Trim28 CKO mice eventually accumulated auto-reactive memory-phenotype T cells that produced inflammatory IL-17. CKO mice are also susceptible to induced auto-inflammatory disease with TH-17 dominant immune response. Loss of Trim28 showed aberrant accumulation of TH-17 and FoxP3+ T cells, two key T cells in inflammation vs. tolerance. We found CKO T cells showed a cell-extrinsic promotion of TH-17 and FoxP3+ T cell development by a mechanism involving overproduction of TGF-beta. Our study revealed unexpected roles of Trim28, a global chromatin regulator in both T cell activation and tolerance. Trim28 conditional KO mice and age-matched control mice were sacrificed, and neive CD4+ T cells (CD4+CD62+CD25-) and Treg (CD4+CD62+CD25+) were sorted. Stimulation of naive T cells was done with anti-CD3 and anti-CD28 for 13 hours. We collected quadruplicates for each group.
2012-04-28 | E-GEOD-32224 | biostudies-arrayexpress