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GSE7309
Mus musculus
12 Downloadable Samples
Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Preimplantation development is a crucial step for successful implantation and pregnancy. Although both compaction and blastocyst formation have been extensively studied, mechanisms regulating early cell division stages before compaction have remained unclear. Here, we show that ERK MAP kinase function is required for early embryonic cell division and normal cell-cell adhesion before compaction. Our analysis demonstrates that inhibition of ERK activation in the late 2-cell stage embryos leads to a reversible arrest in G2 phase in the 4-cell stage. The G2 arrested, 4-cell stage embryos show weakened cell-cell adhesion as compared to control embryos. Remarkably, microarray analyses show that most of the programmed changes of upregulated and downregulated gene expression during the 4- to 8-cell stages normally proceed in the 4-cell stage-arrested embryos, except for a portion of the genes whose expression profiles closely parallel the stages of embryonic development when arrested in G2 and released to resume development. These parallel genes include the genes encoding intercellular adhesion molecules, whose expression is found to be positively regulated by the ERK pathway. We also show that while ERK inactivation in the 8-cell stage embryos does not lead to cell division arrest, it does cause cell division arrest when cadherin-mediated cell-cell adhesion is disrupted. These results demonstrate an essential role of ERK function in the G2/M transition and the expression of adhesion molecules during the 2-cell to 8-cell stage embryos, and suggest a loose parallelism between the gene expression programs and the developmental stages before compaction.
Publication Title
Requirement for ERK MAP kinase in mouse preimplantation development.
Sample Metadata Fields
No sample metadata fields
View Samples- Gallus gallus
- 2 Downloadable Samples
- Affymetrix Chicken Genome Array (chicken)
Description
PTIP (Pax2 transactivation domain-interacting protein) is a nuclear protein containing six BRCT domains. It has been shown that PTIP affects gene expression by controlling the activity of the transcription factor Pax2 and histone H3 lysine 4 methyltransferase complexes. In addition to its role in transcriptional regulation, PTIP has been implicated in DNA damage response. To ask if the depletion of PTIP affects the expression level of genes encoding DNA damage response factors , we compared the whole transcripts between wild-type and PTIP deficient chicken DT40 B cell lines.
Publication Title
PTIP promotes DNA double-strand break repair through homologous recombination.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Mus musculus
- 12 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
The division rate of hematopoietic stem cells (HSCs) are promoted by estradiol. To identify the mechanism by which estradiol regulates HSCs, we performed gene expresssion profiling of HSCs isolated from mice of both sexes treated with either control vehicle (oil) or estradiol for one week.
Publication Title
Oestrogen increases haematopoietic stem-cell self-renewal in females and during pregnancy.
Sample Metadata Fields
Sex, Specimen part
View Samples- Homo sapiens
- 24 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
The development of T cells has been characterized as taking place over three stages: nave (Tn), central memory (Tcm), and effector memory (Tem) cells.
Publication Title
Polarization diversity of human CD4+ stem cell memory T cells.
Sample Metadata Fields
Sex, Age
View Samples- Mus musculus
- 6 Downloadable Samples
Ion Torrent Proton
Description
Growing evidences are suggesting that extra-long genes in mammals are vulnerable for full-gene length transcription and dysregulation of long genes is a mechanism underlying human genetic disorders. Skeletal muscle expresses Dystrophin which is 2.26 Mbp in length; however, how long-distance transcription is achieved is totally unknown. We had discovered RNA-binding protein SFPQ preferentially binds to long pre-mRNAs and specifically regulates the cluster of neuronal genes > 100 kbp. Here we investigated the roles of SFPQ for long gene expression, target specificities, and also physiological functions in skeletal muscle. Loss of Sfpq selectively downregulated genes >100 kbp including Dystrophin and caused progressive muscle mass reduction and metabolic myopathy characterized by glycogen accumulation and decreased abundance of mitochondrial oxidative phosphorylation complexes. Functional clustering analysis identified metabolic pathway related genes as the targets of SFPQ. These findings indicate target gene specificities and tissue-specific physiological functions of SFPQ in skeletal muscle. Overall design: We analyzed polyA-tailed RNA profiles including transcribing RNAs in gastrocnemius skeletal muscle ( from 3 control and 3 Sfpq-/- P35 male mice) using Ion-proton.
Publication Title
Loss of RNA-Binding Protein Sfpq Causes Long-Gene Transcriptopathy in Skeletal Muscle and Severe Muscle Mass Reduction with Metabolic Myopathy.
Sample Metadata Fields
Sex, Specimen part, Cell line, Subject
View Samples- Mus musculus
- 2 Downloadable Samples
- Ion Torrent Proton
Description
Growing evidences are suggesting that extra-long genes in mammals are vulnerable for full-gene length transcription and dysregulation of long genes is a mechanism underlying human genetic disorders. Skeletal muscle expresses Dystrophin which is 2.26 Mbp in length; however, how long-distance transcription is achieved is totally unknown. We had discovered RNA-binding protein SFPQ preferentially binds to long pre-mRNAs and specifically regulates the cluster of neuronal genes > 100 kbp. Here we investigated the roles of SFPQ for long gene expression, target specificities, and also physiological functions in skeletal muscle. Loss of Sfpq selectively downregulated genes >100 kbp including Dystrophin and caused progressive muscle mass reduction and metabolic myopathy characterized by glycogen accumulation and decreased abundance of mitochondrial oxidative phosphorylation complexes. Functional clustering analysis identified metabolic pathway related genes as the targets of SFPQ. These findings indicate target gene specificities and tissue-specific physiological functions of SFPQ in skeletal muscle. Overall design: We analyzed rRNA-depleted RNA profiles including transcribing RNAs in primary myoblasts obtained from skeletal muscles of 1-month-old SfpqSM-KO (n=1) and control (n=1) mice under differentiated condition using Ion-proton.
Publication Title
Loss of RNA-Binding Protein Sfpq Causes Long-Gene Transcriptopathy in Skeletal Muscle and Severe Muscle Mass Reduction with Metabolic Myopathy.
Sample Metadata Fields
Subject
View Samples- Homo sapiens
- 276 Downloadable Samples
- Ion Torrent Proton
Description
We collected and compared samples from the cohort consisted of six groups as follows: methotrexate (MTX) monotherapy, combination therapy of MTX and infliximab (IFX), tocilizumab (TCZ) monotherapy, age- and gender-matched HC, and a small number of synovial fluid samples. In order to reduce variation due to the proportion of cells at each developmental stage, we performed transcriptome analysis after sorting CD4+ and CD8+ T cells according to developmental stage. We created a gene list that was significantly expressed in RA T cells, and revealed that pathways such as mTORC1, IL-2-stat5, Cell cycle and interferon-related genes were significantly enriched among them. Overall design: Examination among healthy controls and patients with rheumatoid arthritis, including before and after treatment
Publication Title
Multi-dimensional analysis identified rheumatoid arthritis-driving pathway in human T cell.
Sample Metadata Fields
Sex, Age, Specimen part, Disease, Subject
View Samples- Homo sapiens
- 22 Downloadable Samples
- Ion Torrent Proton
Description
We compared whole CD4+ and CD8+ T cells from frozen PBMC samples that were collected before and after treatment initiation of each patient with rheumatoid arthritis. Lists consisting of 858 and 950 differentially expressed genes were created from CD4 and CD8, respectively, and these were used for enrichment analysis. As a result, we found that certain pathways were downregulated after TCZ treatment in both CD4+ and CD8+ T cells, including mechanistic target of rapamycin complex 1 (mTORC1) signaling, the IL-2 pathway, and IFN-related genes. Overall design: Examination between before and after tocilizumab treatment of CD4 and CD8 T cell in rheumatoid arthritis patients
Publication Title
Multi-dimensional analysis identified rheumatoid arthritis-driving pathway in human T cell.
Sample Metadata Fields
Sex, Age, Specimen part, Disease, Subject
View Samples- Mus musculus
- 16 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Estrogen clearly prevents osteoporotic bone loss by attenuating bone resorption. The molecular basis of how this is accomplished, however, remains elusive. Here we report a critical role of osteoclastic ERa in mediating estrogen action on bone in females. We selectively ablated ERa in differentiated osteoclasts (ERa dOc/dOc). ERa dOc/dOc females, but not males, exhibited clear trabecular bone loss, similar to the osteoporotic bone phenotype in post-menopausal women. Recovery of bone loss by estrogen treatment of the ovariectomized ERa dOc/dOc females was ineffective in the trabecular areas of the long bones and lumbar vertebral bodies. Osteoclastic apoptosis, induced by estrogen, occurred simultaneously with up-regulation of Fas ligand (FasL) expression in intact trabecular bones of ERa +/+mice, but not in ERa dOc/dOc mice. ERa was also required for similar effects of estrogen and tamoxifen in cultured osteoclasts. These findings suggest that the osteoprotective actions of estrogen and SERMS are mediated at least in part through osteoclastic ERa in trabecular bone; and the life span of mature osteoclasts is regulated through activation of the Fas/FasL system.
Publication Title
Estrogen prevents bone loss via estrogen receptor alpha and induction of Fas ligand in osteoclasts.
Sample Metadata Fields
Sex, Specimen part
View Samples- Homo sapiens
- 2 Downloadable Samples
- Affymetrix Human Gene 2.0 ST Array (hugene20st)
Description
The molecular features of hepatocellular carcinoma arising from non-alcoholic fatty liver disease (NAFLD-HCC) are not well known. In this study, we investigated the mechanism by which NAFLD-HCC survives in a fat-rich environment. We found that caveolin (CAV)-1 was overexpressed in clinical specimens from NAFLD-HCC patients. HepG2, HLE, and HuH-7 HCC cell lines showed decreased proliferation in the presence of the saturated fatty acids palmitic acid and stearic acid, although only HLE cells expressed high levels of CAV-1. HLE cells treated with oleic acid (OA) showed robust proliferation, whereas CAV-null HepG2 cells showed reduced proliferation and increased apoptosis. CAV-1 knockdown in HLE cells attenuated the OA-induced increase in proliferation and enhanced apoptosis. Liquid chromatography-tandem mass spectrometry analysis revealed that the levels of OA-containing ceramide, a pro-apoptotic factor, were higher in HepG2 and CAV-1-deficient HLE cells than in HLE cells, suggesting that CAV-1 inhibits apoptosis by decreasing the level of OA-containing ceramide. These results indicate that CAV-1 is important for NAFLD-HCC survival in fatty acid-rich environments and is a potential therapeutic target.
Publication Title
Role of caveolin-1 in hepatocellular carcinoma arising from non-alcoholic fatty liver disease.
Sample Metadata Fields
Specimen part
View Samples