{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T20:27:18Z","timestamp":1792787238580,"version":"4.5.0"},"reference-count":40,"publisher":"American Society for Microbiology","issue":"6","license":[{"start":{"date-parts":[[2020,11,17]],"date-time":"2020-11-17T00:00:00Z","timestamp":1605571200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2020,12,22]],"date-time":"2020-12-22T00:00:00Z","timestamp":1608595200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"name":"Guanghzou Science and Technology Project","award":["201904020042"],"award-info":[{"award-number":["201904020042"]}]},{"name":"National Key Research and Development Program of China","award":["2018YFD0900504"],"award-info":[{"award-number":["2018YFD0900504"]}]},{"name":"NSFC Project","award":["31822058"],"award-info":[{"award-number":["31822058"]}]},{"name":"NSFC Project","award":["31770045"],"award-info":[{"award-number":["31770045"]}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["mBio"],"published-print":{"date-parts":[[2020,12,22]]},"abstract":"<jats:p>\n                    The Na\n                    <jats:sup>+<\/jats:sup>\n                    -NQR complex functions as a unique redox-driven sodium pump, generating membrane potential directly. However, whether it mediates generation of membrane potential indirectly is unknown. The present study shows that the Na\n                    <jats:sup>+<\/jats:sup>\n                    -NQR complex impacts membrane potential through other antiporter families Atp and Mnh. It proceeds by ATP and then cAMP\/CRP regulon, which inhibits\n                    <jats:sc>l-<\/jats:sc>\n                    alanine catabolism and promotes\n                    <jats:sc>l-<\/jats:sc>\n                    alanine anabolism. When the Na\n                    <jats:sup>+<\/jats:sup>\n                    -NQR complex is reduced as in antibiotic-resistant bacteria,\n                    <jats:sc>l-<\/jats:sc>\n                    alanine is depressed, which is related to the antibiotic resistance phenotypes. However, exogenous\n                    <jats:sc>l-<\/jats:sc>\n                    alanine reverts the phenotype and promotes antibiotic-mediated killing. These findings suggest a novel mechanism by which the Na\n                    <jats:sup>+<\/jats:sup>\n                    -NQR system regulates antibiotic resistance via\n                    <jats:sc>l-<\/jats:sc>\n                    alanine metabolism in a cAMP\/CRP complex-dependent manner.\n                  <\/jats:p>","DOI":"10.1128\/mbio.02086-20","type":"journal-article","created":{"date-parts":[[2020,11,16]],"date-time":"2020-11-16T08:59:50Z","timestamp":1605517190000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":57,"title":["Na\n                    <sup>+<\/sup>\n                    -NQR Confers Aminoglycoside Resistance via the Regulation of\n                    <scp>l-<\/scp>\n                    Alanine Metabolism"],"prefix":"10.1128","volume":"11","author":[{"given":"Ming","family":"Jiang","sequence":"first","affiliation":[{"name":"The Third Affiliated Hospital, Sun Yat-sen University, University 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