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GSE41147
Mus musculus
9 Downloadable Samples
Illumina MouseWG-6 v2.0 expression beadchip
Description
We previously showed that pre-exposure of the cornea to TLR5 ligand flagellin induces profound mucosal innate protection against pathogenic microbes by reprogramming gene expression. To date, there was no genome-wide cDNA array to detect full scale of flagellin mediated reprogramming of gene expression in mucosal surface epithelial cells. Taking advantage of readily accessible, easily procurable epithelial cell population, this study is the first report to use genome-wide cDNA microarray approach to document genes associated with flagellin-induced protection against Pseudomonas aeruginosa infection in corneal epithelial cells (CECs).
Publication Title
Genome-wide transcriptional analysis of differentially expressed genes in flagellin-pretreated mouse corneal epithelial cells in response to Pseudomonas aeruginosa: involvement of S100A8/A9.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 68 Downloadable Samples
IlluminaHiSeq2500
Description
The aim of our study was to discover a miR marker panel prognostic of 5-year survival in OSCC patients that may be utilized in parallel with the current clinical covariates. We assessed differential expression of miRNAs genome-wide via deep sequencing in 20 tumor tissue samples. We also attempted to identify deregulated miR expression signatures that may serve as the prognostic marker of cancer survival. Selected miR marker-based panel then may serve as a guide for selection of appropriate follow-up chemo/radiation treatment, significantly improving the clinical management of OSCC and the overall survival rate. Overall design: Identify miRs differentially expressed in the poor prognosis group compared to the good prognosis group
Publication Title
Prognostic value of miR-375 and miR-214-3p in early stage oral squamous cell carcinoma.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 133 Downloadable Samples
- NextSeq 500
Description
The mammalian genome contains thousands of loci that transcribe long noncoding RNAs (lncRNAs), some of which are known to play critical roles in diverse cellular processes through a variety of mechanisms. While some lncRNA loci encode RNAs that act non-locally (in trans), emerging evidence indicates that many lncRNA loci act locally (in cis) to regulate expression of nearby genes—for example, through functions of the lncRNA promoter, transcription, or transcript itself. Despite their potentially important roles, it remains challenging to identify functional lncRNA loci and distinguish among these and other mechanisms. To address these challenges, we developed a genome-scale CRISPR-Cas9 activation screen targeting more than 10,000 lncRNA transcriptional start sites (TSSs) to identify noncoding loci that influence a phenotype of interest. We found 11 novel lncRNA loci that, upon recruitment of an activator, each mediate BRAF inhibitor resistance in melanoma. Most candidate loci appear to regulate nearby genes. Detailed analysis of one candidate, termed EMICERI, revealed that its transcriptional activation results in dosage-dependent activation of four neighboring protein-coding genes, one of which confers the resistance phenotype. Our screening and characterization approach provides a CRISPR toolkit to systematically discover functions of noncoding loci and elucidate their diverse roles in gene regulation and cellular function. Overall design: RNA-seq on A375 cells overexpressing candidate lncRNA or protein-coding gene.
Publication Title
Genome-scale activation screen identifies a lncRNA locus regulating a gene neighbourhood.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Homo sapiens
- 3 Downloadable Samples
Description
RNA-seq and ATAC-seq data to understand how gene regulation and chromatin accessibility correlates with function enrichment in CRISPR screen for melanoma drug resistance
Publication Title
Genome-scale activation screen identifies a lncRNA locus regulating a gene neighbourhood.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 12 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Comparative analysis of gene expression in bone marrow-derived macrophages (BMDM) from trsp knockout mice (Trspfl/fl-LysM-Cre+/-) and Control (Trspfl/fl-LysM-Cre-/-) mice.
Publication Title
Selenoproteins regulate macrophage invasiveness and extracellular matrix-related gene expression.
Sample Metadata Fields
Sex, Treatment
View Samples- Pseudomonas aeruginosa pao1
- 2 Downloadable Samples
- Affymetrix Pseudomonas aeruginosa Array (paeg1a)
Description
Pseudomonas aeruginosa undergoes cell elongation and forms robust biofilms during anaerobic respiratory growth using nitrate (NO3-) as an alternative electron acceptor. Understanding the mechanism of cell shape change induced upon anaerobiosis is crucial to the development of effective treatments against P. aeruginosa biofilm infection. Anaerobic growth of PAO1 reached higher cell density in the presence of vitamin B12, an essential coenzyme of class II ribonucleotide reductase. In addition, cell morphology returned to a normal rod shape. These results suggest that vitamin B12, the production of which was suppressed during anaerobic growth, can restore cellular machineries for DNA replication and therefore facilitate better anaerobic growth of P. aeruginosa with normal cell division.
Publication Title
Vitamin B12-mediated restoration of defective anaerobic growth leads to reduced biofilm formation in Pseudomonas aeruginosa.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 15 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
Many cancer cells require more glycolytic adenosine triphosphate production due to a mitochondrial respiratory defect. However, the roles of mitochondrial defects in cancer development and progression remain unclear. To address the role of transcriptomic regulation by mitochondrial defects in liver cancer cells, we performed gene expression profiling for three different cell models of mitochondrial defects: cells with chemical respiratory inhibition (rotenone, thenoyltrifluoroacetone, antimycin A, and oligomycin), cells with mitochondrial DNA depletion (Rho0), and liver cancer cells harboring mitochondrial defects (SNU354 and SNU423). By comparing gene expression in the three models, we identified 10 common mitochondrial defectrelated genes that may be responsible for retrograde signaling from cancer cell mitochondria to the intracellular transcriptome. The concomitant expression of the 10 common mitochondrial defect genes is significantly associated with poor prognostic outcomes in liver cancers, suggesting their functional and clinical relevance. Among the common mitochondrial defect genes, we found that nuclear protein 1 (NUPR1) is one of the key transcription regulators. Knockdown of NUPR1 suppressed liver cancer cell invasion, which was mediated in a Ca2+ signalingdependent manner. In addition, by performing an NUPR1-centric network analysis and promoter binding assay, granulin was identified as a key downstream effector of NUPR1. We also report association of the NUPR1granulin pathway with mitochondrial defectderived glycolytic activation in human liver cancer. Conclusion: Mitochondrial respiratory defects and subsequent retrograde signaling, particularly the NUPR1granulin pathway, play pivotal roles in liver cancer progression.
Publication Title
Identification of a mitochondrial defect gene signature reveals NUPR1 as a key regulator of liver cancer progression.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 4 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
We developed transcriptome expression assisted non-directed proteome profiling (TEAnDPP) method to investigate host-pathogen interaction. Analysis of HCV replicon induced host-cell metabolism perturbation at gene expression level. Gene enrichment analysis on DEG revealed disulfide formation related genes were significantly enriched. Based on this observation, we addminitrated thiol reactive chemical probes to visualize reactive thiol profile in live cell, and observed unique reactivity profile. Using SILAC-based quantitative profiling method, we identified 26 proteins that are labeled by iodoacetamide probes. Among these proteins, we discovered t-plastin was upregulated in APC140 cells, and its knock-down experiment showed significant HCV replication inhibition effect. In short, TEAnDPP strategy demonstrated its usefulness in host-pathogen interaction study for HCV infection.
Publication Title
Chemical proteomic identification of T-plastin as a novel host cell response factor in HCV infection.
Sample Metadata Fields
Cell line
View Samples- Homo sapiens
- 9 Downloadable Samples
- Affymetrix Human Gene 2.0 ST Array (hugene20st)
Description
End-stage renal disease (ESRD) is the final stage of chronic kidney disease, which is increasingly prevalent worldwide and is associated with the progression of cardiovascular disease (CVD). Indoxyl sulfate (IS) and p-cresyl sulfate (PCS), major uremic toxins, are major risk factors involved in the pathology of CVD via adverse effects on endothelial cells and immune cells. Thus, transcriptomic overview of uremic toxin-mediated genes in immune cells of ESRD patients is critical, but not yet fully known. We investigated the alteration of gene expressions and biological pathways mediated by major uremic toxins, in ESRD patients monocytes, via microarray analysis.
Publication Title
Indoxyl Sulfate-Mediated Metabolic Alteration of Transcriptome Signatures in Monocytes of Patients with End-Stage Renal Disease (ESRD).
Sample Metadata Fields
Specimen part, Disease, Disease stage, Treatment
View Samples- Homo sapiens
- 6 Downloadable Samples
- Affymetrix Human Gene 2.0 ST Array (hugene20st)
Description
End-stage renal disease (ESRD) is the final stage of chronic kidney disease, which is increasingly prevalent worldwide and is associated with the progression of cardiovascular disease (CVD). Despite accumulating evidence that monocytes/macrophages play a pivotal role in the pathogenesis of CVDs in ESRD patients, the current knowledge of transcriptomic signatures of monocytes or macrophages in ESRD patients is very lacking. Therefore, we investigated the transcriptome profiling of monocyte separated from patients with ESRD and HC.
Publication Title
Indoxyl Sulfate-Mediated Metabolic Alteration of Transcriptome Signatures in Monocytes of Patients with End-Stage Renal Disease (ESRD).
Sample Metadata Fields
Specimen part, Disease, Disease stage
View Samples