BMP treatment induces expression of late differenitation genes in primary human keratinocytes. Overall design: RNA-seq analysis after treatment with EGFR inhibitor AG1478 with or without BMP27 or BMP inhibitor DMH1. each treatment and control was performed in triplicate
Single-Cell ID-seq Reveals Dynamic BMP Pathway Activation Upstream of the MAF/MAFB-Program in Epidermal Differentiation.
Specimen part, Subject
View SamplesWe report the effects of silencing SRSF1 or ZMAT2 in human epidermal stem cells on the transcriptome of epidermal stem cells. We found that silencing ZMAT2 or SRSF1 affects global splicing, however, ZMAT2 seems to regulate splicing of a smaller more specific subset of genes. Overall design: RNA-sequencing data following silencing SRSF1 or ZMAT2
Splicing and Chromatin Factors Jointly Regulate Epidermal Differentiation.
Specimen part, Subject, Time
View SamplesWe report the effects of induction of differentiation in human epidermal stem cells on the splicing of the transcriptome. Overall design: RNA-sequencing data following induction of differentiation in human epidermal stem cells
Splicing and Chromatin Factors Jointly Regulate Epidermal Differentiation.
Specimen part, Treatment, Subject
View SamplesWild-type cells were cultured at 30 deg and cells were harvested. Total RNAs were purified from 3 populations.
Mapping of long-range associations throughout the fission yeast genome reveals global genome organization linked to transcriptional regulation.
No sample metadata fields
View SamplesSeveral Toll-like receptors are activated by Listeria monocytogenes infection, resulting in the activation of MyD88 dependent signaling pathway. However, the negative role of MyD88 in gene expresson is unclear.
Beneficial innate signaling interference for antibacterial responses by a Toll-like receptor-mediated enhancement of the MKP-IRF3 axis.
Specimen part
View SamplesHere we characterized the transcriptome and epigenome of control keratinocytes during differentiation. Epigenomic analyses showed that the temporal enrichment of p63 motifs in dynamic enhancers underscores the key role of p63 in orchestrating the enhancer landscape during keratinocyte differentiation. The cooperation between p63 and its co-regulating factors, such as RUNX1, is important for the finetuning of gene expression. Overall design: RNA-Seq, H3K4me3 ChIP-Seq and H3K27me3 ChIP-Seq of keratinocytes during differentiation on day0(proliferation), day2(early differentiation), day4(mid differentiation) and day7(late differentiation). RUNX1 ChIP-Seq of keratinocytes at the proliferation stage(day0).
Mutant p63 Affects Epidermal Cell Identity through Rewiring the Enhancer Landscape.
No sample metadata fields
View SamplesTo explore functionally crucial tumor-suppressive (TS)-miRNAs in hepatocellular carcinoma (HCC), we performed integrative function- and expression-based screenings of TS-miRNAs in six HCC cell lines. The screenings identified seven miRNAs, which showed growth-suppressive activities through the overexpression of each miRNA and were endogenously downregulated in HCC cell lines. Further expression analyses using a large panel of HCC cell lines and primary tumors demonstrated four miRNAs, miR-101, -195, -378 and -497, as candidate TS-miRNAs frequently silenced in HCCs. Among them, two clustered miRNAs miR-195 and miR-497 showed significant growth-suppressive activity with induction of G1 arrest. Comprehensive exploration of their targets using Argonute2-immunoprecipitation-deep-sequencing (Ago2-IP-seq) and genome-wide expression profiling after their overexpression, successfully identified a set of cell-cycle regulators, including CCNE1, CDC25A, CCND3, CDK4, and BTRC. Our results suggest the molecular pathway regulating cell cycle progression to be integrally altered by downregulation of miR-195 and miR-497 expression, leading to aberrant cell proliferation in hepatocarcinogenesis. Identification of miR-195 and miR-497 target genes by sequencing Ago2-binding mRNAs and total mRNAs of miR-195 or miR-497 overexpressed, or non-treated Hep G2 cell. Overall design: Deep sequencing of RNAs in Ago2-IP fraction and mRNAs extracted from miR-195 or miR-497 overexpressed, or non-treated Hep G2 cell.
The tumor-suppressive miR-497-195 cluster targets multiple cell-cycle regulators in hepatocellular carcinoma.
Cell line, Treatment, Subject, Time
View SamplesWe noticed that ThPOK repression is readily abrogated upon in vitro TCR stimulation of peripheral CD8 T cells. This observation prompted us to investigate a role of ThPOK in the CD8 T cell response to an acute viral infection. We observed that clonal expansion is significantly less in both primary and secondary CD8 T cell responses in the absence of functional ThPOK. To approach this mechanism, we carried out a microarray analysis for comparison of gene expression between ThPOKhd/hd and ThPOKwt/wt P14 memory T cells.
ThPOK derepression is required for robust CD8 T cell responses to viral infection.
No sample metadata fields
View SamplesThe Golgi stress response is a homeostatic mechanism that augments the functional capacity of the Golgi apparatus when Golgi function becomes insufficient (Golgi stress). Three response pathways of the Golgi stress response have been identified in mammalian cells, the TFE3, HSP47 and CREB3 pathways, which augment the capacity of specific Golgi functions such as N-glycosylation, anti-apoptotic activity and pro-apoptotic activity, respectively. On the contrary, glycosylation of proteoglycans (PGs) is another important function of the Golgi, although the response pathway upregulating expression of glycosylation enzymes for PGs in response to Golgi stress remains unknown. Here, we found that expression of glycosylation enzymes for PGs was induced upon insufficiency of PG glycosylation capacity in the Golgi (PG-Golgi stress), and that transcriptional induction of genes encoding glycosylation enzymes for PGs was independent of the known Golgi stress response pathways and ER stress response. Promoter analyses of genes encoding these glycosylation enzymes revealed the novel enhancer element PGSE, which regulates their transcriptional induction upon PG-Golgi stress. From these observations, the response pathway we discovered is a novel Golgi stress response pathway, which we have named the PG pathway. Overall design: Three control samples (DMSO-treated) and three 4MU-xyloside-treated samples
PGSE Is a Novel Enhancer Regulating the Proteoglycan Pathway of the Mammalian Golgi Stress Response.
Sex, Specimen part, Cell line, Treatment, Subject
View SamplesGene expression changes between outside and inside of biofilms were investigated. The gene expression was compared between the outside and inside of the biofilms. At the same time, the gene expressions were also compared with exponential phase and stationary phase in planktonic cells. The gene expression analysis showed that the physiological activities were higher at the outside of the biofilms than those at the inside of the biofilms. The genes induced at the ouside of the biofilms included genes involved in the stress responses and adhesions.
Localized expression profiles of rpoS in Escherichia coli biofilms.
No sample metadata fields
View Samples