{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Jiang M"],"funding":["Guanghzou Science and Technology Project","NSFC Project","National Key Research and Development Program of China"],"pagination":["e02086-20"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7683393"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["11(6)"],"pubmed_abstract":["Sodium-translocating NADH:quinone oxidoreductase (Na<sup>+</sup>-NQR) functions as a unique redox-driven sodium pump, generating membrane potential, which is related to aminoglycoside antibiotic resistance. However, whether it modulates other metabolisms to confer antibiotic resistance is unknown. The present study showed that loss of <i>nqrA</i> or <i>nqrF</i> led to differential metabolomes with elevated resistance to aminoglycoside antibiotics. Decreased alanine, aspartate, and glutamate metabolism and depressed abundance of alanine were characterized as the most impacted pathway and crucial biomarker, respectively. Further data showed that higher viability was detected in Δ<i>nqrA</i> and Δ<i>nqrF</i> mutant strains than their parent strain ATCC 33787 in the presence of gentamicin but "],"journal":["mBio"],"pubmed_title":["Na<sup>+</sup>-NQR Confers Aminoglycoside Resistance via the Regulation of l-Alanine Metabolism."],"pmcid":["PMC7683393"],"funding_grant_id":["201904020042","31770045","31822058","2018YFD0900504"],"pubmed_authors":["Li H","Yang J","Chen ZG","Peng B","Kuang SF","Lai SS","Peng XX","Jiang M","Zhang S"],"additional_accession":[]},"is_claimable":false,"name":"Na<sup>+</sup>-NQR Confers Aminoglycoside Resistance via the Regulation of l-Alanine Metabolism.","description":"Sodium-translocating NADH:quinone oxidoreductase (Na<sup>+</sup>-NQR) functions as a unique redox-driven sodium pump, generating membrane potential, which is related to aminoglycoside antibiotic resistance. However, whether it modulates other metabolisms to confer antibiotic resistance is unknown. The present study showed that loss of <i>nqrA</i> or <i>nqrF</i> led to differential metabolomes with elevated resistance to aminoglycoside antibiotics. Decreased alanine, aspartate, and glutamate metabolism and depressed abundance of alanine were characterized as the most impacted pathway and crucial biomarker, respectively. Further data showed that higher viability was detected in Δ<i>nqrA</i> and Δ<i>nqrF</i> mutant strains than their parent strain ATCC 33787 in the presence of gentamicin but ","dates":{"release":"2020-01-01T00:00:00Z","publication":"2020 Nov","modification":"2026-06-09T07:00:57.851Z","creation":"2026-06-09T03:12:13.648Z"},"accession":"S-EPMC7683393","cross_references":{"pubmed":["33203750"],"doi":["10.1128/mBio.02086-20"]}}