Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Outer Membrane Target of the Efflux Inhibitor Phe-Arg-β-naphthylamide

ABSTRACT: Proof of an Outer Membrane Target of the Efflux Inhibitor Phe-Arg-β-naphthylamide from Random Mutagenesis

PROVIDER: PRJEB30347 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	ERR2993130_1.fastq.gz	Fastqsanger.gz
	ERR2993130_2.fastq.gz	Fastqsanger.gz
	ERR2993128_1.fastq.gz	Fastqsanger.gz
	ERR2993128_2.fastq.gz	Fastqsanger.gz
	ERR2993129_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 6

Similar Datasets

RNA-seq of wild-type Salmonella Typhimurium SL1344 in the presence and absence of chlorpromazine or Phe-Arg-Beta-Napthylamide

Project description:The aim of this experiment was to determine the changes in transcription caused by inhibition of efflux pumps by the Phe-Arg-Beta-Naptylamide (PABN) and chlorpromazine. Four biological replicates per condition were grown to mid-log phase in MOPS minimal media (OD600) and were exposed to the known efflux inhibitor PABN, and the proposed efflux inhibitor chlorpromazine at 100 µg/ml and 50 µg/ml, respectively. Exposure lasted for two hours. Total RNA was extracted and DNase-treated. The samples were sent to BGI, Hong Kong for sequencing by Illumina Hiseq 4000.

2020-06-01 | E-MTAB-8190 | biostudies-arrayexpress

Proof of an Outer Membrane Target of the Efflux Inhibitor Phe-Arg-β-Naphthylamide from Random Mutagenesis.

Project description:Phe-Arg-β-naphthylamide (PAβN) has been characterized as an efflux pump inhibitor (EPI) acting on the major multidrug resistance efflux transporters of Gram-negative bacteria, such as AcrB in Eschericha coli. In the present study, in vitro random mutagenesis was used to evolve resistance to the sensitizing activity of PAβN with the aim of elucidating its mechanism of action. A strain was obtained that was phenotypically similar to a previously reported mutant from a serial selection approach that had no efflux-associated mutations. We could confirm that acrB mutations in the new mutant were unrelated to PAβN resistance. The next-generation sequencing of the two mutants revealed loss-of-function mutations in lpxM. An engineered lpxM knockout strain showed up to 16-fold decreased PAβN activity with large lipophilic drugs, while its efflux capacity, as well as the efficacy of other EPIs, remained unchanged. LpxM is responsible for the last acylation step in lipopolysaccharide (LPS) synthesis, and lpxM deficiency has been shown to result in penta-acylated instead of hexa-acylated lipid A. Modeling the two lipid A types revealed steric conformational changes due to underacylation. The findings provide evidence of a target site of PAβN in the LPS layer, and prove membrane activity contributing to its drug-sensitizing potency.

| S-EPMC6384556 | biostudies-literature

SLC17 transporters mediate renal excretion of Lac-Phe in mice and humans

Project description:N-lactoyl-phenylalanine (Lac-Phe) is a lactate-derived metabolite that suppresses food intake and body weight. Little is known about the mechanisms that mediate Lac-Phe transport across cell membranes. Here we identify SLC17A1 and SLC17A3, two kidney-restricted plasma membrane-localized solute carriers, as physiologic urine Lac-Phe transporters. In cell culture, SLC17A1/3 exhibit high Lac-Phe efflux activity. In humans, levels of Lac-Phe in urine exhibit a strong genetic association with the SLC17A1-4 locus. Urine Lac-Phe levels are also increased following a Wingate sprint test. In mice, genetic ablation of either SLC17A1 or SLC17A3 reduces urine Lac-Phe levels. Despite these differences, both knockout strains have normal blood Lac-Phe and body weights, demonstrating SLC17-dependent de-coupling of urine and plasma Lac-Phe pools. Together, these data establish SLC17A1/3 family members as the physiologic urine transporters for Lac-Phe and uncover a biochemical pathway for the renal excretion of this signaling metabolite. Our data do not exclude the involvement of other transporters in mediating Lac-Phe transport.

2024-10-17 | PXD054202 | Pride

SLC17 transporters mediate renal excretion of Lac-Phe in mice and humans

2025-01-18 | PXD054049 | Pride

Xanthomonas prunicola strain:Arg-1 | isolate:Arg-1

Project description:Xanthomonas prunicola strain:Arg-1 | isolate:Arg-1 Genome sequencing and assembly

| PRJNA819403 | ENA

NS-PHE-2016-S4

Project description:NS-PHE-2016-S4 Metagenome

| PRJNA656711 | ENA

RNA-seq of wild-type Salmonella Typhimurium SL1344 in the presence and absence of chlorpromazine or Phe-Arg-Beta-Napthylamide

Project description:RNA-seq of wild-type Salmonella Typhimurium SL1344 in the presence and absence of chlorpromazine or Phe-Arg-Beta-Napthylamide

| PRJEB33710 | ENA

Arg C and Linezolid on Th17 cells

Project description:Arg C and Linezolid were added to differentiating Th17 cells for 96h. Cells were harvested and sorted according to proliferation cycle before being lysed and having their RNA extracted.

2020-10-15 | GSE159401 | GEO

NS-NHE-PHE-2016-C

Project description:NS-NHE-PHE-2016-C Metagenome

| PRJNA656705 | ENA

NS-PHE-PGPR-2016-S3

Project description:NS-PHE-PGPR-2016-S3 Metagenome

| PRJNA656696 | ENA