Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Alterations in rdxA and frxA genes and their upstream regions in metronidazole-resistant Helicobacter pylori isolates.

Research in microbiology - 1 Jan 2000

Han Fengchan, Liu Sookyin, Ho Bow, Yan Zhen, Yan Xiaojun

Abstract excerpt

Metronidazole resistance among Helicobacter pylori strains has been related to alterations in gene products having metronidazole nitroreductase activities. RdxA and FrxA proteins are the two major contributing factors. In this investigation, the rdxA and frxA genes and their upstream regions were analyzed in 19 H. pylori isolates, 8 of which were metronidazole-sensitive (MIC < or = 8 microg/mL) and 11 of which...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Anti-Infective Agents
Share to Drug Resistance, Bacterial

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Genes, Bacterial

Share to Helicobacter Infections

Share to Helicobacter pylori

Share to Metronidazole

Share to Microbial Sensitivity Tests

Share to Sequence Alignment

Source

Identifiers

PMID: 17113269
DOI: 10.1016/j.resmic.2006.10.001

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Alterations in rdxA and frxA genes and their upstream regions in metronidazole-resistant Helicobacter pylori isolates.PMID 17113269Read ↗

DNA sequence analysis of rdxA and frxA from 12 pairs of metronidazole-sensitive and -resistant clinical Helicobacter pylori isolates.Semantic proximity Read ↗

Genetic analysis of Helicobacter pylori clinical isolates suggests resistance to metronidazole can occur without the loss of functional rdxA.Semantic proximity Read ↗

The rdxA gene plays a more major role than frxA gene mutation in high-level metronidazole resistance of Helicobacter pylori in Taiwan.Semantic proximity Read ↗

Analysis of allelic variants of rdxA associated with metronidazole resistance in Helicobacter pylori: detection of common genotypes in rdxA by multiplex allele-specific polymerase chain reaction.Semantic proximity Read ↗

Frequent association between alteration of the rdxA gene and metronidazole resistance in French and North African isolates of Helicobacter pylori.Semantic proximity Read ↗

DNA sequence analysis of rdxA and frxA from paired metronidazole-sensitive and -resistant Helicobacter pylori isolates obtained from patients with heteroresistance.Semantic proximity Read ↗

rdxA, frxA, and efflux pump in metronidazole-resistant Helicobacter pylori: Their relation to clinical outcomes.Semantic proximity Read ↗

Search for novel candidate mutations for metronidazole resistance in Helicobacter pylori using next-generation sequencing.Semantic proximity Read ↗

In vitro induction of resistance to metronidazole, and analysis of mutations in rdxA and frxA genes from Helicobacter pylori isolates.Semantic proximity Read ↗

Role of the rdxA and frxA genes in oxygen-dependent metronidazole resistance of Helicobacter pylori.Semantic proximity Read ↗

Mutations in Helicobacter pylori rdxA gene sequences may not contribute to metronidazole resistance.Semantic proximity Read ↗

Analysis of the rdxA gene in high-level metronidazole-resistant clinical isolates confirms a limited use of rdxA mutations as a marker for prediction of metronidazole resistance in Helicobacter pylori.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.