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dc.contributor.authorSchneider, Rafael de Oliveirapt_BR
dc.contributor.authorFogaça, Natully de Souza Süffertpt_BR
dc.contributor.authorSilva, Lívia Kmetzsch Rosa ept_BR
dc.contributor.authorSchrank, Augustopt_BR
dc.contributor.authorVainstein, Marilene Henningpt_BR
dc.contributor.authorStaats, Charley Christianpt_BR
dc.date.accessioned2021-08-06T04:43:06Zpt_BR
dc.date.issued2012pt_BR
dc.identifier.issn1932-6203pt_BR
dc.identifier.urihttp://hdl.handle.net/10183/225336pt_BR
dc.description.abstractZinc homeostasis is essential for fungal growth, as this metal is a critical structural component of several proteins, including transcription factors. The fungal pathogen Cryptococcus gattii obtains zinc from the stringent zinc-limiting milieu of the host during the infection process. To characterize the zinc metabolism in C. gattii and its relationship to fungal virulence, the zinc finger protein Zap1 was functionally characterized. The C. gattii ZAP1 gene is an ortholog of the master regulatory genes zafA and ZAP1 that are found in Aspergillus fumigatus and Saccharomyces cerevisiae, respectively. There is some evidence to support an association between Zap1 and zinc metabolism in C. gattii: (i) ZAP1 expression is highly induced during zinc deprivation, (ii) ZAP1 knockouts demonstrate impaired growth in zinc-limiting conditions, (iii) Zap1 regulates the expression of ZIP zinc transporters and distinct zinc-binding proteins and (iv) Zap1 regulates the labile pool of intracellular zinc. In addition, the deletion of ZAP1 reduces C. gattii virulence in a murine model of cryptococcosis infection. Based on these observations, we postulate that proper zinc metabolism plays a crucial role in cryptococcal virulence.en
dc.format.mimetypeapplication/pdfpt_BR
dc.language.isoengpt_BR
dc.relation.ispartofPLoS ONE. San Francisco. Vol. 7, no. 8 (Aug. 2012), e43773, 11 p.pt_BR
dc.rightsOpen Accessen
dc.subjectGlioblastomapt_BR
dc.subjectCiclo celularpt_BR
dc.titleZap1 regulates zinc homeostasis and modulates virulence in Cryptococcus gattiipt_BR
dc.typeArtigo de periódicopt_BR
dc.identifier.nrb000862892pt_BR
dc.type.originEstrangeiropt_BR


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