TânIa M. Stevanin
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
TânIa M. Stevanin has a total of 5 co-authors. Here are the top co-authors by number of shared publications:
- James W. B. Moir
Department of Biology
2 shared publications - Robert Charles Read
NIHR Southampton Biomedical Research Centre, University Hospital Southampton NHS Foundation Trust, Southampton, UK; Faculty of Medicine and Institute for Life Sciences, University of Southampton, Southampton, UK
2 shared publications Jay R. Laver
1 shared publicationMuna F. Anjum
Department of Molecular Biology and Biotechnology, University of Sheffield, Western Bank, Sheffield S10 2TN
1 shared publicationRobert K. Poole
1 shared publication
Latest Publications
- 1 July 2007
- Published by Elsevier in Microbes and Infection
- Vol. 9 (8) , 981-987
Metabolism of nitric oxide by Neisseria meningitidis modifies release of NO-regulated cytokines and chemokines by human macrophages
- 1 July 2007
- Published by Elsevier in Microbes and Infection
- Vol. 9 (8) , 981-987
Metabolism of nitric oxide by Neisseria meningitidis modifies release of NO-regulated cytokines and chemokines by human macrophages
- Open Access
- 1 June 2002
- Published by American Society for Microbiology in Journal of Bacteriology
- Vol. 184 (11) , 2987-2993
Nitric Oxide Metabolism in Neisseria meningitidis
Neisseria meningitidis , the causative agent of meningococcal disease in humans, is likely to be exposed to nitrosative stress during natural colonization and disease. The genome of N. meningitidis includes the genes aniA and norB , predicted to encode nitrite reductase and nitric oxide (NO) reductase, respectively. These gene products should allow the bacterium to denitrify nitrite to nitrous oxide. We show that N. meningitidis can support growth microaerobically by the denitrification of nitrite via NO and that norB is required for anaerobic growth with nitrite. NorB and, to a lesser extent, the cycP gene product cytochrome c ′ are able to counteract toxicity due to exogenously added NO. Expression of these genes by N. meningitidis during colonization and disease may confer protection against exogenous or endogenous nitrosative stress.
- 1 June 2002
- Published by American Society for Microbiology in Journal of Bacteriology
- Vol. 184 (11) , 2987-2993
Open AccessNitric Oxide Metabolism in Neisseria meningitidis
Neisseria meningitidis , the causative agent of meningococcal disease in humans, is likely to be exposed to nitrosative stress during natural colonization and disease. The genome of N. meningitidis includes the genes aniA and norB , predicted to encode nitrite reductase and nitric oxide (NO) reductase, respectively. These gene products should allow the bacterium to denitrify nitrite to nitrous oxide. We show that N. meningitidis can support growth microaerobically by the denitrification of nitrite via NO and that norB is required for anaerobic growth with nitrite. NorB and, to a lesser extent, the cycP gene product cytochrome c ′ are able to counteract toxicity due to exogenously added NO. Expression of these genes by N. meningitidis during colonization and disease may confer protection against exogenous or endogenous nitrosative stress.