Gene expression profiling of trimethoprim resistant Escherichia coli
Ontology highlight
ABSTRACT:
ORGANISM(S): Escherichia coli str. K-12 substr. MG1655
SUBMITTER: Amrisha Bhosle
PROVIDER: E-MTAB-6536 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Transcriptional profiling of E. coli MG1655 to Trimethoprim in i) LB media, ii) M9 minimal media and iii) M9 minimal media with supplements to study the association of gene expression with corresponding lethal and non-lethal growth conditions. Supplementation conditions in M9 media included addition of 50 microgram/ml of adenine, methionine, glycine or thymine in various combinations. For all growth conditions, TMP was added to E. coli in mid-log phase and samples were taken at regular intervals from 10 minutes to 120 minutes post treatment. 1 Biological replicate per time point.
2011-10-03 | E-GEOD-32562 | biostudies-arrayexpress
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2021-03-18 | GSE169069 | GEO
Project description:Alzheimer's disease (AD) is one of the most common neurodegenerative diseases. So far, there is no effective treatment for this condition. Tetramethylpyrazine (TMP) is an alkaloid extracted from traditional Chinese medicine chuanxiong, which is mainly used in the treatment of ischemic stroke some related diseases. In this study, we studied the potential effects of TMP on AD progression by using two AD mouse models. 8-month-old 3xTg-AD mice received TMP treatment (10mg/kg/d) for 1 month, and 4-month-old APP/PS1-AD mice received TMP treatment (10mg/kg/d) for 2 months. The behavioral tests by step-down passive avoidance test (SDA), new object recognition (NOR) and Morris water maze (MWM) showed that TMP significantly improved the learning and memory impairment of two AD transgenic mice. In addition, TMP reduced Aß levels and tau phosphorylation. Venny analysis showed that 116 differentially expressed proteins were commonly changed in 3xTg mice vs WT mice and TMP treated mice vs untreated mice. The same, 130 differentially expressed proteins were commonly changed in APP/PS1 mice vs WT mice and TMP treated mice vs untreated mice. The functions of the common proteins modified by TMP in the two models were mainly related to mitochondrial function, synaptic function, cytoskeleton, GTP binding, ATP binding. Mitochondrial omics analysis revealed 21 and 20 differentially expressed mitochondrial proteins modified by TMP in 3xTg-AD mice and APP/PS1 mice, respectively. These differential proteins were located in mitochondrial inner membrane, mitochondrial outer membrane, mitochondrial gap and mitochondrial matrix, and the function of some proteins is closely related to oxidative phosphorylation of (OXPHOS). Western-blot further validated that TMP changed the expression of OXPHOS complex proteins (sdhb, ndufa10, uqcrfs1, cox5b, atp5a) in the hippocampus of the two AD mice. Taken together, our study demonstrated that TMP improved the cognitive impairment and AD-like pathology, and modified hippocampal proteome in the two AD mice models. The improvement of the behavioral and pathology might be associated with modification of mitochondrial protein profile by TMP. Our study suggested that TMP had the potential for the treatment of AD.
2021-09-09 | PXD022862 | Pride
Project description:Alzheimer's disease (AD) is one of the most common neurodegenerative diseases. So far, there is no effective treatment for this condition. Tetramethylpyrazine (TMP) is an alkaloid extracted from traditional Chinese medicine chuanxiong, which is mainly used in the treatment of ischemic stroke some related diseases. In this study, we studied the potential effects of TMP on AD progression by using two AD mouse models. 8-month-old 3xTg-AD mice received TMP treatment (10mg/kg/d) for 1 month, and 4-month-old APP/PS1-AD mice received TMP treatment (10mg/kg/d) for 2 months. The behavioral tests by step-down passive avoidance test (SDA), new object recognition (NOR) and Morris water maze (MWM) showed that TMP significantly improved the learning and memory impairment of two AD transgenic mice. In addition, TMP reduced Aß levels and tau phosphorylation. Venny analysis showed that 116 differentially expressed proteins were commonly changed in 3xTg mice vs WT mice and TMP treated mice vs untreated mice. The same, 130 differentially expressed proteins were commonly changed in APP/PS1 mice vs WT mice and TMP treated mice vs untreated mice. The functions of the common proteins modified by TMP in the two models were mainly related to mitochondrial function, synaptic function, cytoskeleton, GTP binding, ATP binding. Mitochondrial omics analysis revealed 21 and 20 differentially expressed mitochondrial proteins modified by TMP in 3xTg-AD mice and APP/PS1 mice, respectively. These differential proteins were located in mitochondrial inner membrane, mitochondrial outer membrane, mitochondrial gap and mitochondrial matrix, and the function of some proteins is closely related to oxidative phosphorylation of (OXPHOS). Western-blot further validated that TMP changed the expression of OXPHOS complex proteins (sdhb, ndufa10, uqcrfs1, cox5b, atp5a) in the hippocampus of the two AD mice. Taken together, our study demonstrated that TMP improved the cognitive impairment and AD-like pathology, and modified hippocampal proteome in the two AD mice models. The improvement of the behavioral and pathology might be associated with modification of mitochondrial protein profile by TMP. Our study suggested that TMP had the potential for the treatment of AD.
2021-09-09 | PXD022840 | Pride
Project description:HEK293 cells were selected and subcloned for doxycyclin (DOX) and trimethoprim (TMP) inducible dCas9GFP and a guide RNA molecule targeting an EGA enriched Alu-motif (EEA-g1). Cells were treated with DOX and TMP for three days to induce dCas9GFP expression and ATAC-seq samples were collected from treated and non-treated cells to analyse the effect of targeting the motif with dCas9.
2018-06-07 | E-MTAB-6195 | biostudies-arrayexpress
Project description:The response of antibiotic adapted resistant mutants of B. cenocepacia J2315 to antibiotic stress was investigated using expression profiling of three biological replicates and comparing the profiles to the J2315 parent control grown without antibiotics.<br>A reference design was used with Cy3 labeled genomic DNA of B. cenocepacia J2315 as common reference. Three test conditions with three biological replicates each were compared to three replicates of the control condition.<br>Test conditions: J2315-A grown in the presence of 250 ug per ml amikacin, J2315-M grown in the presence of 8 ug per ml meropenem and J2315-T grown in the presence of 60 ug per ml trimethoprim and 300 ug per ml sulfamethoxazole.<br>Control condition: J2315 parent strain grown without antibiotics.
2010-08-12 | E-MEXP-2708 | biostudies-arrayexpress
Project description:Temporal control of proteins in cells and living animals is crucial to improving the understanding of protein function in the post-genomic era. In addition, technologies that offer such control for engineered proteins could be used in therapeutic applications. Since regulation of proteins at a genomic or transcriptional level can be irreversible or a slow process, these tools may not be useful in settings where rapid temporal control is required to achieve immediate knockdown effects. PRoteolysis-TArgeting Chimeras (PROTACs) have emerged as a strategy to achieve rapid, post-translational control of protein abundance via recruitment of an E3 ligase to the target protein of interest. Here, we developed several PROTAC molecules by covalently linking the antibiotic trimethoprim (TMP) to pomalidomide, a small molecule ligand of the E3 ligase Cereblon. These molecules induce degradation of various proteins of interest (POIs) genetically fused to E. coli dihydrofolate reductase (eDHFR), the molecular target of TMP. We demonstrate that various eDHFR-tagged proteins, from fluorescent proteins to transcription factors and membrane-associated proteins, can be downregulated to 95% of maximum expression with our lead PROTAC molecule 7c. The data suggest that TMP-based PROTACs induce maximal degradation of POIs at drug concentrations that minimally affect the expression of immunomodulatory imide drug (IMiD)-sensitive neosubstrates. Finally, we show the ability to achieve multiplexed regulation with another known degron-PROTAC pair, and the formidable strength of our system for reversible protein regulation in a rodent model of metastatic cancer. Altogether, TMP PROTACs are a robust approach for selective and reversible degradation of eDHFR-tagged protein and have a strong potential for translation to in vivo models as well as dual degradation strategies with existing technologies.
2023-12-06 | PXD045052 | Pride
Project description:We present a DNA array-based method for the genome-wide analysis of Psoralen photobinding in Saccharomyces cerevisiae cells. PB was found reduced in subtelomeric regions and increased in the subset of genes with smallest nucleosomal density. The analysis includes 3 repeats of the wild type strain (JCW25) at 30ºC and 3 more at 37ºC, 3 repeats of the double top1 (delta) top2ts mutant at 37ºC and 3 repeats of naked genomic DNA treated with trimethyl psoralen (TMP) in the same way to be used as a control of unspecific binding.
2010-06-24 | E-GEOD-16758 | biostudies-arrayexpress
Project description:Purpose: Determine new therapeutic targets for a refractory drug-induced hypersensitivity syndrome/DRESS using single cell transcriptomic analysis. Methods: Skin cells were dissociated from skin biopsies of a patient with DRESS and 5 healthy volunteers using enzymatic digestion, then viable skin cells were sorted using flow cytometry. Peripheral blood mononuclear cells (PBMCs) were isolated from peripheral blood using Ficoll-paque density separation. PBMCs were cultured with or without medications for 4 days. In detail, 200,000 PBMCs were cultivated in 200ul of RPMI-1640 supplemented with 10% human AB serum with (PBMC_T4_BACT) or without (PBMC_T4_CTRL) 48 ug/mL sulfamethoxazole/trimethoprim (SMX-TMP). For the in vitro therapeutic experiments, PBMCs were cultured in the presence of SMX-TMP with (DRESS_Day4_TOFA) or without (DRESS_Day4_BACT) tofacitinib. The patient was treated with 10mg/d of tofacitinib, a JAK3 inhibitor. The freshly isolated PBMCs were collected again two weeks after initiation of intervention (PBMC_POST2W). Single cells from the skin, freshly isolated PBMCs, and culture PBMCs were captured using droplet based single-cell approach (10x Genomics) and library were prepared. Results: The lymphocytes in skin and PBMCs exhibited upregulation of skin-homing chemokine receptors, CCR4 and CCR10, and JAK3 and STAT1. Treatment with tofacitinib dramatically extinguished skin inflammation in a chronic refractory case of DiHS/DRESS. Conclusions: A successful intervention with tofacitinib in a refractory case of DiHS/DRESS was guided by the use of scRNAseq, which demonstrated aberrant activity in the JAK-STAT pathway.
2019-06-17 | GSE132802 | GEO