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        <rdfs:label xml:lang="en">has part</rdfs:label>
        <rdfs:label>has_part</rdfs:label>
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        <rdfs:label xml:lang="en">has disposition at some time</rdfs:label>
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    <!-- http://purl.obolibrary.org/obo/IDO_0100775 -->

    <Class rdf:about="http://purl.obolibrary.org/obo/IDO_0100775">
        <rdfs:label>B. abortus virB1 mutant</rdfs:label>
    </Class>
    


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        <rdfs:label xml:lang="en">attenuated disposition</rdfs:label>
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    <!-- http://purl.obolibrary.org/obo/IDO_0110284 -->

    <Class rdf:about="http://purl.obolibrary.org/obo/IDO_0110284">
        <rdfs:label>B. melitensis 16M virb1 mutant</rdfs:label>
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        <ns3:IAO_0000119>PMID: 15322008, 10940027, 16113325, 16272371</ns3:IAO_0000119>
        <rdfs:seeAlso>UniProtKB accession: Q8YDZ5</rdfs:seeAlso>
        <ns3:IAO_0000115>A mutant of strain Brucella melitensis bv. 1 str. 16M that lacks an intact gene virb1.</ns3:IAO_0000115>
        <rdfs:seeAlso>NCBIGene: 1197796</rdfs:seeAlso>
        <rdfs:comment>The gene virb1 from the strain Brucella melitensis bv. 1 str. 16M is a virulence gene.</rdfs:comment>
        <ns3:IAO_0000117>YH</ns3:IAO_0000117>
        <rdfs:comment>Information about the mutated molecule: MUTATION: The Brucella abortus virB operon, encoding a type IV secretion system (T4SS), is required for intracellular replication and persistent infection in the mouse model. The products of the first two genes of the virB operon, virB1 and virB2, are predicted to be localized at the bacterial surface. Both mutants were shown to be nonpolar, as demonstrated by their ability to express the downstream gene virB5 during stationary phase of growth in vitro. Both  VirB1  and VirB2 were essential for intracellular replication in J774 macrophages. The nonpolar  virB1 mutant persisted at wild-type levels, showing that the function of  VirB1 is dispensable in the mouse model of persistent infection [Ref6539:den et al., 2004].  A B abortus polar virB1 mutant failed to replicate in HeLa cells, indicating that the virB operon plays a critical role in intracellular multiplication [Ref6540:Sieira et al., 2000].  Polar mutations in the virB1 to virB2 intergenic region or in virB2 reduced the detection of VirB5 to a greater extent than they did that of VirB12. A virB1 mutation  also eliminates the transcription of virB12 in B suis [Ref6470:Sun et al., 2005].   An infection assay with signature-tagged Brucella abortus  mutants demonstrated that mutagenesis of the  virB1 gene causes attenuation of virulence [Ref6471:Höppner et al., 2005].</rdfs:comment>
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        <rdfs:label>attachment mediating protein VIRB1-like protein</rdfs:label>
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