Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15216500.fastq.gz | Fastqsanger.gz | |||
| SRR15216501.fastq.gz | Fastqsanger.gz | |||
| SRR15216502.fastq.gz | Fastqsanger.gz | |||
| SRR15216503.fastq.gz | Fastqsanger.gz | |||
| SRR15216504.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Rothia mucilaginosa strain:IE | isolate:IE Raw sequence reads
| PRJNA672880 | ENA
Project description:Infective endocarditis (IE) has high mortality, partly due to delayed diagnosis and treatment. Currently, no biomarker can identify IE in patients with fever and clinical picture of infection. To find putative biomarkers we analyzed serum levels of two proteins found in cardiac valves, osteoprotegerin and fibulin-1 among 689 and 696 patients on clinical suspicion of IE, respectively. In addition, proteomic analyses were performed in 24 patients with bacteremia, 12 patients with definite IE and 12 patients with excluded IE.
2020-02-26 | PXD010149 | Pride
Project description:IE-0392 Genome sequencing
| PRJNA793986 | ENA
Project description:Epigenetic modulation of herpes simplex virus (HSV) immediate early (IE) genes is a critical regulatory parameter governing lytic infection, latency, and viral reactivation. Multiple factors, including epigenetic complexes associated with the cellular transcriptional coactivator HCF-1, modulate the state of HSV-1 chromatin. As an approach to identify novel epigenetic factors that regulate the initial stage of HSV-1 infection, an epigenetic chemical probe library was screened for their impact on viral IE gene expression. This screen identified several epigenetic inhibitors that modulated IE expression. Notably, UNC0379, an inhibitor of the histone H4K20 mono-methyltransferase SETD8, potently repressed HSV-1 infection in vitro and in vivo. Furthermore, SETD8 inhibition suppressed HSV-1 reactivation in a mouse ganglia explant model. Importantly, these results correlated with enhanced heterochromatin suppression and decreased accessibility of HSV-1 chromatin. Reduced IE transcription was concomitant with disruption in recruitment of HCF-1 and RNA polymerase II (RNAPII). These results are consistent with the established roles of SETD8 in promoting chromatin accessibility through H4K20me1 deposition and regulating transcriptional elongation, suggesting that SETD8 may facilitate multiple steps in regulation of HSV-1 IE gene expression.
2025-11-10 | GSE302607 | GEO
Project description:Epigenetic modulation of herpes simplex virus (HSV) immediate early (IE) genes is a critical regulatory parameter governing lytic infection, latency, and viral reactivation. Multiple factors, including epigenetic complexes associated with the cellular transcriptional coactivator HCF-1, modulate the state of HSV-1 chromatin. As an approach to identify novel epigenetic factors that regulate the initial stage of HSV-1 infection, an epigenetic chemical probe library was screened for their impact on viral IE gene expression. This screen identified several epigenetic inhibitors that modulated IE expression. Notably, UNC0379, an inhibitor of the histone H4K20 mono-methyltransferase SETD8, potently repressed HSV-1 infection in vitro and in vivo. Furthermore, SETD8 inhibition suppressed HSV-1 reactivation in a mouse ganglia explant model. Importantly, these results correlated with enhanced heterochromatin suppression and decreased accessibility of HSV-1 chromatin. Reduced IE transcription was concomitant with disruption in recruitment of HCF-1 and RNA polymerase II (RNAPII). These results are consistent with the established roles of SETD8 in promoting chromatin accessibility through H4K20me1 deposition and regulating transcriptional elongation, suggesting that SETD8 may facilitate multiple steps in regulation of HSV-1 IE gene expression.
2025-11-10 | GSE302606 | GEO
Project description:Background—Diagnosis and pronostic assessment are challenging in infective endocarditis (IE). To investigate the host response during IE and identify potential biomarkers, we determined the circulating gene expression profile through a whole genome microarray analysis. Methods and Results—A transcriptomic case-control study was performed on blood samples from patients with native valve IE (n=39), excluded IE after an initial suspicion (n=10) at patient’s admission, and age-matched healthy controls (n=10). The whole genome microarray analysis showed that patients with IE exhibited a specific transcriptional program with a predominance of gene categories associated with cell activation, innate immune and inflammatory responses. These categories were organized in a dense network from which arose numerous subnetworks including major histocompatibily complex and natural killer cell network, type 1 interferon pathway and intracellular traffic. Quantitative real-time RT-PCR performed on a selection of highly modulated genes showed that the expression of the gene encoding S100 calcium binding protein A11 (S100A11) was significantly increased in patients with IE in comparison with controls (P<0.001) and patients with excluded IE (P<0.05). Interestingly, the upregulated expression of S100A11 gene was more pronounced in staphylococcal IE than in streptococcal IE (P<0.01). These results were confirmed by serum concentrations of the S100A11 protein. Finally, we showed that, in patients with IE, the upregulation of aquaporin-9 gene (AQP9) was significantly related to the occurrence of acute heart failure (P=0.02). Conclusions— Using transcriptional signatures of blood samples, we identified S100A11 as a potential diagnostic marker of IE. In addition, the determination of AQP9 may improve the prognostic assessment of IE.
2012-03-12 | GSE29161 | GEO
Project description:Herpes simplex virus 1 (HSV-1) transcribes its genome in a highly coordinated temporal cascade, utilizing the host RNA polymerase II (Pol II). Repression of transcription precedes the cascade's progression in a process requiring viral immediate early (IE) genes, in a phenomenon termed Transient Immediate Early gene Mediated Repression (TIEMR). Given that components of promyelocytic leukaemia nuclear bodies (PML-NBs) are known to rapidly engage incoming HSV-1 genomes, we investigated their potential role in TIEMR regulation. Using siRNA knockdown of PML-NB constituents (PML, DAXX, and ATRX), we unexpectedly observed that ATRX depletion resulted in a significant reduction in nascent viral transcription on viral IE promoters at 1.5 hours post-infection (hpi). ChIP-Seq analysis indicated ATRX is associated with both highly transcriptionally active and transcriptionally restricted regions, indicating that ATRX has diverse functions in the viral genome. We show here that ATRX association with active transcription on IE genes is correlated to the presence of G-quadruplexes (G4s). Drug stabilization of G4s mimicked the effects of ATRX knockdown, significantly reducing transcription initiation on IE genes. These findings suggest that ATRX promotes transcriptional initiation of HSV-1 IE genes by preventing G4 formation. In sum, our results reveal a previously unrecognized pro-transcriptional role for ATRX early in HSV-1 infection.
2025-08-26 | GSE293672 | GEO
Project description:BackgroundM-bM-^@M-^TDiagnosis and pronostic assessment are challenging in infective endocarditis (IE). To investigate the host response during IE and identify potential biomarkers, we determined the circulating gene expression profile through a whole genome microarray analysis. Methods and ResultsM-bM-^@M-^TA transcriptomic case-control study was performed on blood samples from patients with native valve IE (n=39), excluded IE after an initial suspicion (n=10) at patientM-bM-^@M-^Ys admission, and age-matched healthy controls (n=10). The whole genome microarray analysis showed that patients with IE exhibited a specific transcriptional program with a predominance of gene categories associated with cell activation, innate immune and inflammatory responses. These categories were organized in a dense network from which arose numerous subnetworks including major histocompatibily complex and natural killer cell network, type 1 interferon pathway and intracellular traffic. Quantitative real-time RT-PCR performed on a selection of highly modulated genes showed that the expression of the gene encoding S100 calcium binding protein A11 (S100A11) was significantly increased in patients with IE in comparison with controls (P<0.001) and patients with excluded IE (P<0.05). Interestingly, the upregulated expression of S100A11 gene was more pronounced in staphylococcal IE than in streptococcal IE (P<0.01). These results were confirmed by serum concentrations of the S100A11 protein. Finally, we showed that, in patients with IE, the upregulation of aquaporin-9 gene (AQP9) was significantly related to the occurrence of acute heart failure (P=0.02). ConclusionsM-bM-^@M-^T Using transcriptional signatures of blood samples, we identified S100A11 as a potential diagnostic marker of IE. In addition, the determination of AQP9 may improve the prognostic assessment of IE. The transcriptomic case-control study was performed in 39 consecutive patients with native valve IE (IE group) diagnosed by a multidisciplinary team who applied the modified Duke criteria,12 10 patients admitted for a suspicion of IE but with a final excluded IE diagnosis. Ten IE patients and five controls were arbitrary selected and investigated with microarrays.
2012-03-12 | E-GEOD-29161 | biostudies-arrayexpress
Project description:The goal of the present study was to determine whether loss of the insulin receptor alters the molecular landscape of the intestinal mucosa, using intestinal-epithelial insulin receptor knockout (IE-irKO) mice and both genetic (IRfl/fl and Villin-cre) controls. Quantitative proteomic analysis by Liquid Chromatography Mass Spectrometry (LC-MS) was deployed on jejunal and colonic mucosa from mice fed a chow- or Western diet (WD). Jejunal mucosa from IE-irKO mice demonstrated alterations in all intestinal cell linages, Paneth, goblet, absorptive and enteroendocrine cells, whereas only goblet and absorptive cells were affected in the colon. There was also a significant effect of the WD on the gut proteome. A significant reduction was detected in Paneth cell proteins with anti-microbial activity, including lysozyme C-1, angiogenin-4, cryptdin-related sequence1C-3 and -2, a-defensin 17 and intelectin-1a. The key protein expressed by goblet cells, mucin-2, was also reduced in the IE-irKO mice. Proteins involved in lipid metabolism, including aldose reductase-related protein 1, 15-hydroxyprostaglandin dehydrogenase [NAD(+)], apolipoprotein A-II and pyruvate dehydrogenase kinase isozyme 4, were increased in the mucosa of WD-fed IE-irKO mice as compared to controls. In contrast, expression of the nutrient-responsive gut hormones, glucose-dependent insulinotropic polypeptide and neurotensin, was reduced in the jejunal mucosa of IE-irKO mice, and there was a reduction in proteins of the P-type ATPases and the solute carrier-transporter family in the colon of WD-fed IE-irKO mice. In conclusion, IE-irKO mice display a distinct molecular phenotype, suggesting a biological role of insulin and its receptor in determining differentiated cell-specificity in the intestinal epithelium.
2017-08-18 | PXD005932 | Pride
Project description:We investigated the role of the chromatin remodeling protein ATRX on chromatin accessibility of HCMV genomes during the IE phase of lytic infections
2024-08-28 | GSE262839 | GEO