Pseudomonas sp. CFA
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ABSTRACT:
PROVIDER: PRJNA574744 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Pseudomonas sp. CFA Transcriptome or Gene expression
| PRJNA574774 | ENA
Project description:Transcriptional profiling of Arabidopsis thaliana roots comparing inoculated roots with a bacterial strain Antarctic (Pseudomonas sp, Da-bac TI-8) vs untreated roots (control)
2013-03-28 | GSE45559 | GEO
Project description:The whole proteome analysis of the Pseudomonas sp. FIP_A4 strain in presence and absence of fipronil was conducted to evaluate the differentially expressed enzymes that can play role in fipronil degradation.
2024-02-19 | PXD048521 | Pride
Project description:Transcriptional profiling of Arabidopsis thaliana roots comparing inoculated roots with a bacterial strain Antarctic (Pseudomonas sp, Da-bac TI-8) vs untreated roots (control) Two-condition experiment, inoculated roots vs. untreated roots (control). Biological replicates: 4 inoculated roots replicates vs. 4 untreated roots replicates (control)
2013-03-28 | E-GEOD-45559 | biostudies-arrayexpress
Project description:Proteomic analysis of an Antarctic bacterium Pseudomonas sp. Lz4W by tandem mass spectrometry to unveil the process of cold adaptation. Comparative whole proteome analysis was performed at Low and optimum temperature.
2022-03-17 | PXD029741 | Pride
Project description:Enterotoxigeneic Escherichia coli (ETEC) is a leading cause of diarrhoeal infections in young children living in endemic regions in low and middle-income countries and adults travelling to these destinations. CFA/I fimbriae have been identified as the predominant colonisation factor associated with human ETEC infections. Here we used used Transposon-directed insertion-site sequencing (TraDIS) and transcriptomic analysis to identify the essential genome of the prototypical CFA/I expressing ETEC strain H10407 and uncover the survival mechanisms that enhance persistence of ETEC isolates in water and within mammalian hosts. RNA transcription profiles of H10407 were identified under different in vitro growth conditions including aerobic growth in neutral LB media (pH7); aerobic growth in acidic media (pH5); aerobic growth in alkaline media (pH9); anaerobic growth in neutral LB media (pH7); and survival in fresh water. Research work including RNA preparation and bioinformatics and statistical analyses were conducted at the Wellcome Trust Sanger Institute (WTSI) and the Westmead Institute for Medical Research (WIMR), the University of Sydney. The sequencing data was generated in the Bioscience Core Laboratory at King Abdullah University of Science and Technology (KAUST).
2021-04-21 | E-MTAB-9364 | biostudies-arrayexpress
Project description:Although several underlying pathophysiological processes have been explored, the origin and precise pathomechanism of migraine are still being debated. Inflammatory pathways have been suggested to play role in migraine, trigeminal nociceptor sensitisation, thereby causing hyperalgesia and allodynia. The aim of the present study was to investigate gene expression changes in trigeminal ganglia (TRG), central trigeminal nucleus caudalis (TNC) and peripheral blood mononuclear cells (PBMC) evoked by Complete Freund’s Adjuvant (CFA) induced peripheral inflammation. 512 differentially expressed genes were found between CFA-treated and contralateral TRG samples 7 days after CFA injection. The mRNA expression changes of G-protein coupled receptor 39 (Gpr39), kisspeptin-1 receptor (Kiss1r), kisspeptin (Kiss1) and Lkaaear1 were selected for validation. They were most upregulated on day 3 in TRGs of the CFA-treated side. CFA-induced significant orofacial mechanical allodynia in one day with a maximum on day 3. This correlated with patterns of neuronal (Fosb), glial (Iba1), and astrocyte (Gfap) activation markers in both TRG and TNC, and surprisingly in PBMCs. Similar transcriptional changes of Cgrp, the well-known key molecule in migraine pathophysiology, were also revealed. In TNCs, gene expression changes similar to TRGs were observed but Kiss1r transcripts were not significantly altered while Neurod2 was observed only in TNC. These results could indicate the involvement of Gpr39, Kiss1r and synaptic plasticity associated Lkaaear1, Neurod2 genes in the cascade of events resulting in the sensitization underlying migraine headache and the accompanying facial allodynia.
2018-12-14 | GSE111160 | GEO
Project description:Background: We have previously used the rat 4 day Complete Freund's Adjuvant (CFA) model to screen compounds with potential to reduce osteoarthritic pain. The aim of this study was to identify genes altered in this model of osteoarthritic pain and use this information to infer analgesic potential of compounds based on their own gene expression profiles using the Connectivity Map approach. Results: Using microarrays, we identified differentially expressed genes in L4 and L5 dorsal root ganglia (DRG) from rats that had received intraplantar CFA for 4 days compared to matched, untreated control animals. Analysis of these data indicated that the two groups were distinguishable by differences in genes important in immune responses, nerve growth and regeneration. This list of differentially expressed genes defined a “CFA signature”. We used the Connectivity Map approach to identify pharmacologic agents in the Broad Institute Build02 database that had gene expression signatures that were inversely related (‘negatively connected’) with our CFA signature. To test the predictive nature of the Connectivity Map methodology, we tested phenoxybenzamine (an alpha adrenergic receptor antagonist) – one of the most negatively connected compounds identified in this database - for analgesic activity in the CFA model. Our results indicate that at 10mg/kg, phenoxybenzamine demonstrated analgesia comparable to that of Naproxen in this model. Conclusion: Evaluation of phenoxybenzamine-induced analgesia in the current study lends support to the utility of the Connectivity Map approach for identifying compounds with analgesic properties in the CFA model.
2010-10-07 | GSE24431 | GEO