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GSE8729
Saccharomyces cerevisiae
4 Downloadable Samples
Affymetrix Yeast Genome S98 Array (ygs98)
Description
Rsp5 is an essential and multi-functional E3 ubiquitin ligase in Saccharomyces cerevisiae. We previously isolated the Ala401Glu rsp5 mutant, which is hypersensitive to various stresses. To understand the function of Rsp5 in stress responses, suppressor genes whose overexpression allows rsp5A401E cells to grow at high temperature were screened. The KIN28 and POG1 genes, encoding a subunit of the transcription factor TFIIH and a putative transcriptional activator, respectively, were identified as multicopy suppressors of not only high temperature but also LiCl stresses. The overexpression of Kin28 and Pog1 in rsp5A401E cells caused an increase in the transcriptional level of some stress proteins when exposed to temperature up-shift. DNA microarray analysis under LiCl stress revealed that the transcriptional level of some proteasome components was increased in rsp5A401E cells overexpressing Kin28 or Pog1. These results suggest that the overexpression of Kin28 and Pog1 enhances the protein refolding and degradation pathways in rsp5A401E cells.
Publication Title
Overexpression of two transcriptional factors, Kin28 and Pog1, suppresses the stress sensitivity caused by the rsp5 mutation in Saccharomyces cerevisiae.
Sample Metadata Fields
No sample metadata fields
View Samples- Caenorhabditis elegans
- 4 Downloadable Samples
- Affymetrix C. elegans Genome Array (celegans)
Description
MAP kinases are integral to the mechanisms by which cells respond to a wide variety of environmental stresses. In Caenorhabditis elegans, the KGB-1 JNK signaling pathway regulates the response to heavy metal stress. The deletion mutants of this cascade show hypersensitivity to heavy metals like copper or cadmium. However, factors that function downstream of KGB-1 pathway are not well characterized.
Publication Title
The Caenorhabditis elegans JNK signaling pathway activates expression of stress response genes by derepressing the Fos/HDAC repressor complex.
Sample Metadata Fields
Age
View Samples- Mus musculus
- 22 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Polycomb repressive complexes (PRCs) are important chromatin regulators of ES cell function. RYBP binds Polycomb H2A monoubiquitin ligases Ring1A and Ring1B, and has been suggested to participate in localizing Polycomb complexes to their targets. Moreover, constitutive inactivation of RYBP precludes ES cell formation. Here we have used ES cells conditionally deficient in RYBP to investigate RYBP function. Chromosome immunoprecipitation on a chip (ChIP-chip) of RYBP and microarray experiments were performed using wild type and knocked-out ES cells.
Publication Title
RYBP represses endogenous retroviruses and preimplantation- and germ line-specific genes in mouse embryonic stem cells.
Sample Metadata Fields
Specimen part, Disease
View Samples- Mus musculus
- 16 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
We used microarrays to investigate a global change in gene expression by conditional depletion of Rybp in mouse ES cells.
Publication Title
RYBP represses endogenous retroviruses and preimplantation- and germ line-specific genes in mouse embryonic stem cells.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Gene expression change by Yaf2 KD in wild type or RYBP KO ES cells.
Publication Title
RYBP represses endogenous retroviruses and preimplantation- and germ line-specific genes in mouse embryonic stem cells.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 72 Downloadable Samples
Illumina HiSeq 2500
Description
Circadian clock oscillation emerges in mouse embryo in the later developmental stages. Although circadian clock development is closely correlated with cellular differentiation, the mechanisms of its emergence during mammalian development are not well understood. Here, we demonstrate an essential role of the post-transcriptional regulation of Clock subsequent to the cellular differentiation for the emergence of robust circadian clock oscillation in mouse fetal hearts and mESCs (mouse embryonic stem cells). In mouse fetal hearts, no apparent oscillation of cell-autonomous molecular clock was detectable in around embryonic day (E) 10 whereas robust oscillation was clearly visible in E18 heart. Temporal RNA-seq analysis using mouse fetal hearts reveals much fewer rhythmic genes in E10-12 hearts (63, no clock genes) than E17-19 (483 genes), indicating the lack of functional circadian clocks in E10 mouse fetal hearts. In both mESCs and E10 embryos, CLOCK protein was absent despite the expression of Clock mRNA, which we showed was at least partially due to miRNA-mediated translational suppression of CLOCK. The CLOCK protein is required for the robust molecular oscillation in differentiated cells, and the post-transcriptional regulation of Clock plays a key role in setting the timing for the emergence of the circadian clock oscillation during mammalian development.
Publication Title
Involvement of posttranscriptional regulation of <i>Clock</i> in the emergence of circadian clock oscillation during mouse development.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 50 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
This study focus on the expression signature between tumor and adjacent normal tissues.
Publication Title
Protein arginine methyltransferase 5 is a potential oncoprotein that upregulates G1 cyclins/cyclin-dependent kinases and the phosphoinositide 3-kinase/AKT signaling cascade.
Sample Metadata Fields
Age
View Samples- Mus musculus
- 24 Downloadable Samples
- Illumina MouseRef-8 v2.0 expression beadchip
Description
Low Klf4 expression reproducibly gives rise to a homogeneous population of partially reprogrammed iPSCs. Upregulation of Klf4 allows these cells to resume reprogramming, indicating that they are paused iPSCs that remain on the path towards pluripotency. Paused iPSCs with different Klf4 expression levels remain at distinct intermediate stages of reprogramming.
Publication Title
Manipulation of KLF4 expression generates iPSCs paused at successive stages of reprogramming.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 16 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Since the initial discovery that OCT4, SOX2, KLF4 and c-MYC overexpression sufficed for the induction of pluripotency in somatic cells, methodologies replacing the original factors have enhanced our understanding of the reprogramming process. However, unlike in mouse, OCT4 has not been replaced successfully during reprogramming of human cells. Here we report on a strategy to do so. Through a combination of transcriptome and bioinformatic analysis we have identified factors previously characterized as being lineage specifiers that are able to replace OCT4 and SOX2 in the reprogramming of human fibroblasts. Our results show that is possible to replace OCT4 and SOX2 simultaneously with alternative lineage specifiers in the reprogramming of human cells. At a broader level, they also support a model in which counteracting lineage specification networks underlie the induction of pluripotency,
Publication Title
Reprogramming of human fibroblasts to pluripotency with lineage specifiers.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 18 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
We explored the relationship between Myc activity and PI3K signaling in ESCs. Our data demonstrate that Myc and PI3K signaling function cooperatively for supporting pluripotent property of ESCs. Moreover, our data demonstrate that exposure of ESCs to 2i condition render both Myc and PI3K dispensable for preserving ESC status.
Publication Title
Functional compensation between Myc and PI3K signaling supports self-renewal of embryonic stem cells.
Sample Metadata Fields
Sex, Specimen part
View Samples