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.
Vitamin B12-mediated restoration of defective anaerobic growth leads to reduced biofilm formation in Pseudomonas aeruginosa.
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View SamplesMany 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.
Identification of a mitochondrial defect gene signature reveals NUPR1 as a key regulator of liver cancer progression.
Specimen part
View SamplesWe 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.
Chemical proteomic identification of T-plastin as a novel host cell response factor in HCV infection.
Cell line
View SamplesEnd-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.
Indoxyl Sulfate-Mediated Metabolic Alteration of Transcriptome Signatures in Monocytes of Patients with End-Stage Renal Disease (ESRD).
Specimen part, Disease, Disease stage, Treatment
View SamplesEnd-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.
Indoxyl Sulfate-Mediated Metabolic Alteration of Transcriptome Signatures in Monocytes of Patients with End-Stage Renal Disease (ESRD).
Specimen part, Disease, Disease stage
View SamplesWe isolated Farage cells expressing the cell surface marker SLAMF1. LMP1 and its target gene CCL22 were highly expressed in SLAMF1high Farage cells. These cells survived longer following treatment with a combination of cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP). Genes associated with interferon-alpha, allograft rejection, NF-kB, STAT3 and 5 were also overexpressed in the surviving Farage cells.
LMP1+SLAMF1high cells are associated with drug resistance in Epstein-Barr virus-positive Farage cells.
Specimen part, Treatment, Time
View SamplesIn this study, we have investigated the role of secondhand smoke (SHS) in the development of metabolic liver disease by characterizing the global regulation of genes and molecular pathways in SHS-exposed mice after termination of exposure (SHS 4M) and following one-month recovery in clean air (SHS 4M +1M RECOVERY).
Secondhand Smoke Induces Liver Steatosis through Deregulation of Genes Involved in Hepatic Lipid Metabolism.
Sex
View SamplesThe cochlear duct is tonotopically organized, such that the basal cochlea responds more sensitively to high frequency sounds and the apical cochlea to low frequency sounds. In effort to understand how the tonotopic organization is established in mammals, we searched for genes that are differentially expressed along the tonotopic axis during neonatal development.
Developmental gene expression profiling along the tonotopic axis of the mouse cochlea.
Specimen part
View SamplesSHH signaling pathway is activated in many type of cancers. However, the role of its activation in particular type of cancer was poorly understood. The GLI family transcription factor GLI1 is the effector of Shh pathway activation and functions as oncogene. Our goal of research is to identify the GLI1 targets in desmoplastic medulloblastomas.
Defining a role for Sonic hedgehog pathway activation in desmoplastic medulloblastoma by identifying GLI1 target genes.
No sample metadata fields
View SamplesRNA-seq transcriptome analysis identified a functional requirement for zebrafish Rfx4 in the developing neural floor plate and roof plate. Overall design: Embryos derived from an rfx4uw8013/+ incross were sorted by phenotype into mutant and sibling groups. RNA was prepared from each individual embryo at ~ 25 hpf
Zebrafish Rfx4 controls dorsal and ventral midline formation in the neural tube.
No sample metadata fields
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