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GSE74156
Mus musculus
6 Downloadable Samples
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
An integrated systems biology approach identifies positive cofactor 4 as a factor that increases reprogramming efficiency.
Sample Metadata Fields
Sex, Specimen part
View Samples- Mus musculus
- 6 Downloadable Samples
Description
Multipotent spermatogonial stem cells (mSSCs) derived from SSCs are a potential new source of individualized pluripotent cells in regenerate medicine such as ESCs. We hypothesized that the culture-induced reprogramming of SSCs was mediated by a mechanism different from that of iPS, and was due to up-regulation of specific pluripotency-related genes during cultivation. Through a comparative analysis of expression profile data, we try to find cell reprogramming candidate factors from mouse spermatogonial stem cells. We used microarrays to analyze the gene expression profiles of culture-induced reprogramming converting unipotent spermatogonial stem cells to pluripotent spermatogonial stem cells.
Publication Title
An integrated systems biology approach identifies positive cofactor 4 as a factor that increases reprogramming efficiency.
Sample Metadata Fields
Sex, Specimen part
View Samples- Mus musculus
- 26 Downloadable Samples
Description
The transcription factor Nkx2.5 is required for specification of pharyngeal arch second heart field (SHF) progenitors that contribute to outflow tract (OFT) and right ventricle (RV) formation. Multiple sets of microarray data were analyzed to identify genes that are candidate targets of Nkx2.5 in the second heart field. These sets are: 1) publicly available data for cardiothoracic tissue from E9.5 Nkx2.5 wild-type, heterozygous and homozygous embryos; 2) an analysis of mouse E10.5 pharyngeal arch tissue; 3) an analysis of mouse E12.5 heart tissue; and 4) a temporal analysis of the cardiogenic cell line P19CL6. This combined analysis identified 11 genes (Lrrn1, Elovl2, Safb, Slc39a6, Khdrbs1, Hoxb4, Fez1, Ccdc117, Jarid2, Nrcam, and Enpp3) expressed in SHF-containing pharyngeal arch tissue whose regulation is dependent on Nkx2.5 expression.
Publication Title
Jarid2 is among a set of genes differentially regulated by Nkx2.5 during outflow tract morphogenesis.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Mus musculus
- 16 Downloadable Samples
Description
Pluripotent P19CL6 embryonic carcinoma cells can be differentiated to a cardiac lineage by culture in the presence of DMSO. The goal of this study was to characterize temporal gene expression patterns associated with cardiogenic differentiation. Gene expression analysis was conducted on differentiating P19CL6 cells at several time points following induction with 1% DMSO. Samples were processed for analysis by Affymetrix GeneChip.
Publication Title
Jarid2 is among a set of genes differentially regulated by Nkx2.5 during outflow tract morphogenesis.
Sample Metadata Fields
Cell line
View Samples- Mus musculus
- 4 Downloadable Samples
Description
We have generated transgenic mice expressing constitutively activated aryl hydrocarbon receptor (CA-AhR) to examine the biological consequences of AhR activation..
Publication Title
A novel role for the dioxin receptor in fatty acid metabolism and hepatic steatosis.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus, Rattus norvegicus
- 6 Downloadable Samples
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Transcription factor <i>TFCP2L1</i> patterns cells in the mouse kidney collecting ducts.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 6 Downloadable Samples
Description
Gene expression analysis of mouse kidney after conditional inactivation of transcription factor Tfcp2l1
Publication Title
Transcription factor <i>TFCP2L1</i> patterns cells in the mouse kidney collecting ducts.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 8 Downloadable Samples
Description
To examine the role of SPS1 in mammals, we generated a Sps1 knockout mouse and found that systemic SPS1 deficiency was embryonic lethal. Embryos were clearly underdeveloped by E8.5 and virtually reabsorbed by E14.5. Removal of Sps1 specifically in hepatocytes using Albumin-cre preserved viability, but significantly affected expression of a large number of mRNAs involved in cancer, embryonic development and the glutathione system. Particularly notable was the extreme deficiency of glutaredoxin 1 (GLRX1) and glutathione-S-transferase omega 1. To assess these phenotypes at the cellular level, we targeted the removal of SPS1 in F9 cells, a mouse embryonal carcinoma cell line, which recapitulated changes in the glutathione system proteins. We further found that several malignant characteristics of SPS1-deficient F9 cells were reversed, suggesting that SPS1 has a role in supporting and/or sustaining cancer. In addition, the increased ROS levels observed in F9 SPS1/GLRX1 deficient cells were reversed and became more like those in F9 SPS1 sufficient cells by overexpressing mouse or human GLRX1. The results suggest that SPS1 is an essential mammalian enzyme with roles in regulating redox homeostasis and controlling cell growth.
Publication Title
Selenophosphate synthetase 1 is an essential protein with roles in regulation of redox homoeostasis in mammals.
Sample Metadata Fields
Sex, Specimen part
View Samples- Mus musculus
- 6 Downloadable Samples
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Derivation of haploid embryonic stem cells from mouse embryos.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 6 Downloadable Samples
Description
Twist1, a basic helix-loop-helix transcription factor, is expressed in mesenchymal precursor populations during embryogenesis and in metastatic cancer cells. In the developing heart, Twist1 is highly expressed in endocardial cushion (ECC) valve mesenchymal cells and is down regulated during valve differentiation and remodeling. Previous studies demonstrated that Twist1 promotes cell proliferation, migration, and expression of primitive ECM molecules in ECC mesenchymal cells. Furthermore, Twist1 expression is induced in human pediatric and adult diseased heart valves. However, the Twist1 downstream target genes that mediate increased cell proliferation and migration during early heart valve development remain largely unknown. Candidate gene and global gene profiling approaches were used to identify direct transcriptional targets of Twist1 during heart valve development. Candidate target genes were analyzed for evolutionarily conserved regions (ECRs) containing E-box consensus sequences that are potential Twist1 binding sequences. ECRs containing conserved E-box sequences were identified for Twist1 responsive genes Tbx20, Cdh11, Sema3C, Rab39b, and Gadd45a. Twist1 binding to these sequences in vivo was determined by chromatin immunoprecipitation assays, and binding was detected in ECCs but not late stage remodeling valves. In addition identified Twist1 target genes are highly expressed in ECCs and have reduced expression during heart valve remodeling in vivo which is consistent with the expression pattern of Twist1. Together these analyses identify multiple new genes involved in cell proliferation and migration that are differentially expressed in the developing heart valves, are responsive to Twist1 transcriptional function, and contain Twist1 responsive regulatory sequences.
Publication Title
Twist1 directly regulates genes that promote cell proliferation and migration in developing heart valves.
Sample Metadata Fields
Cell line
View Samples