{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T14:13:25Z","timestamp":1790777605331,"version":"4.1.0"},"reference-count":17,"publisher":"American Society for Microbiology","issue":"4","license":[{"start":{"date-parts":[[2000,4,1]],"date-time":"2000-04-01T00:00:00Z","timestamp":954547200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Antimicrob Agents Chemother"],"published-print":{"date-parts":[[2000,4]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    A clinical isolate of\n                    <jats:italic>Helicobacter pylori<\/jats:italic>\n                    that developed resistance to rifabutin during therapy carried an\n                    <jats:italic>rpoB<\/jats:italic>\n                    gene that retained a wild-type cluster region sequence but had acquired a novel codon 149 (V149F) mutation. In transformation experiments, the mutation was shown to confer high-level rifabutin resistance. The equivalent mutation (V176F) was present in several resistant isolates of\n                    <jats:italic>Mycobacterium tuberculosis<\/jats:italic>\n                    .\n                  <\/jats:p>","DOI":"10.1128\/aac.44.4.1075-1077.2000","type":"journal-article","created":{"date-parts":[[2002,7,27]],"date-time":"2002-07-27T05:56:57Z","timestamp":1027749417000},"page":"1075-1077","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":128,"title":["Mutations in the Beginning of the\n                    <i>rpoB<\/i>\n                    Gene Can Induce Resistance to Rifamycins in both\n                    <i>Helicobacter pylori<\/i>\n                    and\n                    <i>Mycobacterium tuberculosis<\/i>"],"prefix":"10.1128","volume":"44","author":[{"given":"Markus","family":"Heep","sequence":"first","affiliation":[{"name":"<!--label omitted: 1-->Institute for Medical Microbiology, Regensburg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ulrich","family":"Rieger","sequence":"additional","affiliation":[{"name":"<!--label omitted: 1-->Institute for Medical Microbiology, Regensburg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniela","family":"Beck","sequence":"additional","affiliation":[{"name":"<!--label omitted: 1-->Institute for Medical Microbiology, Regensburg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Norbert","family":"Lehn","sequence":"additional","affiliation":[{"name":"<!--label omitted: 1-->Institute for Medical Microbiology, Regensburg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1128\/AAC.43.5.1072"},{"key":"e_1_3_2_3_2","first-page":"117","article-title":"H. pylori DNA fingerprinting using the arbitrarily primed PCR (AP-PCR) or random amplified polymorphic DNA (RAPD) method.","volume":"8","author":"Berg D. 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