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        <rdfs:label xml:lang="en">has part</rdfs:label>
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        <rdfs:label xml:lang="en">attenuated disposition</rdfs:label>
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    <Class rdf:about="http://purl.obolibrary.org/obo/IDO_0101321">
        <rdfs:label xml:lang="en">B. suis virB5 mutant</rdfs:label>
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        <rdfs:label>B. suis 1330 virB5 mutant</rdfs:label>
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        <ns3:IAO_0000119>PMID: 10510235</ns3:IAO_0000119>
        <ns3:IAO_0000115>A mutant of strain Brucella suis 1330 that lacks an intact gene virB5.</ns3:IAO_0000115>
        <ns3:IAO_0000117>YH</ns3:IAO_0000117>
        <rdfs:seeAlso>UniProtKB accession: Q9RPY0</rdfs:seeAlso>
        <rdfs:seeAlso>NCBIGene: 1164502</rdfs:seeAlso>
        <rdfs:comment>The gene virB5 from the strain Brucella suis 1330 is a virulence gene.</rdfs:comment>
        <rdfs:comment>Information about the mutated molecule: MUTATION: A comparison of the VirB8 and  VirB5  contents after induction of the B suis wild type and of virB5  and virB12 mutants further confirmed that the  virB5  and virB12 genes belong to the same operon [Ref6467:O&#39;Callaghan et al., 1999].  Smooth strains of Brucella unable to replicate (ie, killed B suis or the avirulent mutant B suis  virB5) exhibit delayed phagosome-lysosome fusion [Ref6467:O&#39;Callaghan et al., 1999].  Polar mutations in the operon upstream of virB5 exert a greater effect on the expression of virB5  than they do on the expression of the downstream gene virB12. It indicates that in B abortus , regulatory elements other than the virB promoter may influence VirB12 protein levels [Ref6467:O&#39;Callaghan et al., 1999].  Four independent mutants in virB5, virB9 or virB10 were highly attenuated in an in vitro infection model with human macrophages [Ref6467:O&#39;Callaghan et al., 1999].</rdfs:comment>
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