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dc.provenanceFacultad de Ciencias Exactas y Naturales de la UBA-
dc.contributorNikel, P.I.-
dc.contributor<div class="autor_fcen" id="2305">De Almeida, A.</div>-
dc.contributor<div class="autor_fcen" id="6704">Pettinari, M.J.</div>-
dc.contributor<div class="autor_fcen" id="5666">Méndez, B.S.</div>-
dc.creatorNikel, P.I.-
dc.creator<div class="autor_fcen" id="2305">De Almeida, A.</div>-
dc.creator<div class="autor_fcen" id="6704">Pettinari, M.J.</div>-
dc.creator<div class="autor_fcen" id="5666">Méndez, B.S.</div>-
dc.date.accessioned2018-05-04T21:59:06Z-
dc.date.accessioned2018-05-28T15:47:42Z-
dc.date.available2018-05-04T21:59:06Z-
dc.date.available2018-05-28T15:47:42Z-
dc.date.issued2008-
dc.identifier.urihttp://10.0.0.11:8080/jspui/handle/bnmm/68342-
dc.descriptionStrains derived from HfrH carrying the arcA2 null mutation exhibit a higher respiratory rate, enhanced glucose consumption, and a more-reduced intracellular redox state than arcA deletion mutants of a different lineage. The phenotype of the arcA2 mutants was due to the presence of a creC constitutive mutation introduced by P1 transduction. Copyright © 2008, American Society for Microbiology. All Rights Reserved.-
dc.descriptionFil:De Almeida, A. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina.-
dc.descriptionFil:Pettinari, M.J. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina.-
dc.descriptionFil:Méndez, B.S. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina.-
dc.formatapplication/pdf-
dc.languageeng-
dc.rightsinfo:eu-repo/semantics/openAccess-
dc.rightshttp://creativecommons.org/licenses/by/2.5/ar-
dc.sourceJ. Bacteriol. 2008;190(9):3404-3407-
dc.source.urihttp://digital.bl.fcen.uba.ar/Download/paper/paper_00219193_v190_n9_p3404_Nikel.pdf-
dc.subjectglucose-
dc.subjectarcA gene-
dc.subjectarcA2 gene-
dc.subjectarticle-
dc.subjectbacterial gene-
dc.subjectbacterial strain-
dc.subjectCreBC gene-
dc.subjectdeletion mutant-
dc.subjectEscherichia coli-
dc.subjectgene mutation-
dc.subjectglucose intake-
dc.subjectmutant-
dc.subjectnonhuman-
dc.subjectoxidation reduction state-
dc.subjectphenotype-
dc.subjectpriority journal-
dc.subjectAmino Acid Sequence-
dc.subjectBacterial Outer Membrane Proteins-
dc.subjectBacterial Proteins-
dc.subjectBacteriophage P1-
dc.subjectBase Sequence-
dc.subjectCytochrome b Group-
dc.subjectCytochromes-
dc.subjectElectron Transport Chain Complex Proteins-
dc.subjectEscherichia coli-
dc.subjectEscherichia coli Proteins-
dc.subjectGene Deletion-
dc.subjectGlucose-
dc.subjectMolecular Sequence Data-
dc.subjectMutation-
dc.subjectOxidation-Reduction-
dc.subjectOxidoreductases-
dc.subjectOxygen-
dc.subjectOxygen Consumption-
dc.subjectPhenotype-
dc.subjectProtein Kinases-
dc.subjectRepressor Proteins-
dc.subjectArca-
dc.subjectEscherichia coli-
dc.titleThe legacy of HfrH: Mutations in the two-component system CreBC are responsible for the unusual phenotype of an Escherichia coli arcA mutant-
dc.typeinfo:eu-repo/semantics/article-
dc.typeinfo:ar-repo/semantics/artículo-
dc.typeinfo:eu-repo/semantics/publishedVersion-
Aparece en las colecciones: FCEN - Facultad de Ciencias Exactas y Naturales. UBA

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