Staphylococcus aureus Escherichia coli Klebsiella sp. Proteus cibi
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA636233 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| JABTVG01.dat.gz | Other | |||
| JABTVG01.fasta.gz | Fasta.gz | |||
| JABTVG01.master.dat | Other | |||
| JABTVH01.dat.gz | Other |
Items per page: 5 1 - 5 of 277 |
Similar Datasets
Project description:Alpha-mangostin (α-MG) is a natural xanthone reported to exhibit rapid bactericidal activity against Gram-positive bacteria, and may therefore have potential clinical application in healthcare sectors. This study sought to identify the antibacterial mode of action of α-MG against Staphylococcus epidermidis RP62A through RNA-sequencing technology.
2018-04-19 | GSE113302 | GEO
Project description:Streptococcus agalactiae (Group B Streptococcus, GBS) is a leading cause of early-onset neonatal bacterial infection. Evasion of innate immune defenses is critical to neonatal GBS disease pathogenesis. Effectors of the innate immune system such as antimicrobial peptides, as well as numerous antibiotics, target the peptidoglycan layer of the gram positive bacterial cell wall. The intramembrane-sensing histidine kinase class of two-component regulatory systems has recently been identified as important to the gram-positive response to cell wall stress. We identified and characterized the GBS homolog of LiaR, the response regulator component of the LiaFSR system and constructed site-directed, non-polar deletion mutations in the regulator gene liaR. GBS LiaR deletion mutant strains are more susceptible to cell wall active antibiotics (vancomycin and bacitracin) as well as antimicrobial peptides (colistin, nisin and the human cathelicidin LL-37) compared to isogenic wild-type GBS. LiaR mutant GBS are significantly attenuated in mouse models of both GBS sepsis and GBS pneumonia. To determine the genes regulated by LiaR that account for these defects, transcriptional profiling was performed using DNA microarray analysis, comparing wild-type GBS to LiaR mutant GBS under non-stressed conditions. Two separate RNA samples were extracted for each condition. One flip-dye replicate (2 hybridizations) was obtained for each pair of RNA samples for 4 hybridizations total.
2012-11-18 | E-GEOD-14571 | biostudies-arrayexpress
Project description:Abstract The infection of drug resistant bacteria seriously threats to public health, which makes it more urgent to find novel antibacterial compounds. Compared with traditional development approaches, drug repurposing provides a faster and more effective strategy to find new antimicrobial agents. Here, we screened an FDA-approved small-molecule library upon S. aureus, and identified crizotinib as an antimicrobial agent. We confirmed the antibacterial activities of crizotinib in vitro and in vivo by MIC, growth curve, SEM and mice experiment. At the same time, crizotinib also showed low tendency to develop resistance. Mechanistically, quantitative proteomics, bioinformatics analyses, qRT-PCR and flow cytometry biochemical validation experience confirmed that crizotinib exerted its antibacterial effects by interfering pyrimidine metabolism and disrupting DNA synthesis eventually. Furthermore, our data from drug affinity responsive target stability, bio-layer interferometry and a series of functional assays demonstrated that crizotinib could target PyrG directly in pyrimidine metabolism pathway. Taken together, our results indicated that crizotinib could be a potential antimicrobial agent to treat Gram-positive bacterial infections in the future.
2022-03-10 | PXD029546 | Pride
Project description:To survive during colonization or infection of the human body, microorganisms must defeat antimicrobial peptides, which represent a key component of innate host defense in phagocytes and on epithelia. However, is not known how the clinically important group of Gram-positive bacteria sense antimicrobial peptides to coordinate a directed defensive response. By determining the genome-wide gene regulatory response to human beta defensin 3 in the nosocomial pathogen Staphylococcus epidermidis, we discovered an antimicrobial peptide sensor system that controls major specific resistance mechanisms to antimicrobial peptides and is unrelated to the Gram-negative PhoP/PhoQ system. Keywords: Wild type control vs treated vs mutant
2008-02-26 | GSE7163 | GEO
Project description:To survive during colonization or infection of the human body, microorganisms must defeat antimicrobial peptides, which represent a key component of innate host defense in phagocytes and on epithelia. However, is not known how the clinically important group of Gram-positive bacteria sense antimicrobial peptides to coordinate a directed defensive response. By determining the genome-wide gene regulatory response to human beta defensin 3 in the nosocomial pathogen Staphylococcus epidermidis, we discovered an antimicrobial peptide sensor system that controls major specific resistance mechanisms to antimicrobial peptides and is unrelated to the Gram-negative PhoP/PhoQ system. Wild type untreated in triplicate is compared to wild type treated in triplicate along with three mutants in triplicate with and without treatment of human beta defensin 3, totalling 30 samples
2010-05-26 | E-GEOD-7163 | biostudies-arrayexpress
Project description:A Gram-positive three-component antimicrobial peptide-sensing system
| PRJNA98169 | ENA
Project description:Lactobacillus johnsonii, a Gram-positive, gut bacterium is well studied for its several health-beneficial properties. This
2024-07-15 | GSE271801 | GEO
Project description:Streptococcus agalactiae (Group B Streptococcus, GBS) is a leading cause of early-onset neonatal bacterial infection. Evasion of innate immune defenses is critical to neonatal GBS disease pathogenesis. Effectors of the innate immune system such as antimicrobial peptides, as well as numerous antibiotics, target the peptidoglycan layer of the gram positive bacterial cell wall. The intramembrane-sensing histidine kinase class of two-component regulatory systems has recently been identified as important to the gram-positive response to cell wall stress. We identified and characterized the GBS homolog of LiaR, the response regulator component of the LiaFSR system and constructed site-directed, non-polar deletion mutations in the regulator gene liaR. GBS LiaR deletion mutant strains are more susceptible to cell wall active antibiotics (vancomycin and bacitracin) as well as antimicrobial peptides (colistin, nisin and the human cathelicidin LL-37) compared to isogenic wild-type GBS. LiaR mutant GBS are significantly attenuated in mouse models of both GBS sepsis and GBS pneumonia. To determine the genes regulated by LiaR that account for these defects, transcriptional profiling was performed using DNA microarray analysis, comparing wild-type GBS to LiaR mutant GBS under non-stressed conditions.
2012-11-18 | GSE14571 | GEO