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        <rdfs:label xml:lang="en">has part</rdfs:label>
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    <!-- http://purl.obolibrary.org/obo/IDO_0100879 -->

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        <rdfs:label xml:lang="en">attenuated disposition</rdfs:label>
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        <rdfs:label>B. melitensis 16M ftcR mutant</rdfs:label>
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        <ns3:IAO_0000119>PMID: 17056750</ns3:IAO_0000119>
        <rdfs:seeAlso>NCBIGene: 1197929</rdfs:seeAlso>
        <rdfs:comment>The gene ftcR from the strain Brucella melitensis bv. 1 str. 16M is a virulence gene.</rdfs:comment>
        <ns3:IAO_0000117>YH</ns3:IAO_0000117>
        <ns3:IAO_0000115>A mutant of strain Brucella melitensis bv. 1 str. 16M that lacks an intact gene ftcR.</ns3:IAO_0000115>
        <rdfs:comment>Information about the mutated molecule: MUTATION: FtcR is required in B melitensis 16M for the transcription of the fliF gene during vegetative and intracellular growth, and for the production of the two structural flagellar components FlgE and FliC during vegetative growth. A ftcR mutant has the same virulence phenotype as previously found with structural flagellar mutants. In HeLa cells and bovine macrophages, no attenuation of the ftcR mutant was observed compared to the WT parental strain. In BALB/c mice, the ftcR mutant was not attenuated after 1 week of infection but was attenuated after 4 weeks of infection. FtcR acts as a flagellar master regulator in B melitensis and perhaps in other related alpha-proteobacteria [Ref6549:Léonard et al., 2007].</rdfs:comment>
        <rdfs:seeAlso>UniProtKB accession: Q8YDL7</rdfs:seeAlso>
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