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Gene Review:

napA - neutrophil-activating protein A

Helicobacter pylori J99

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High impact information on napA

In addition to using the well-studied bacterial oxidative stress resistance enzymes superoxide dismutase and catalase, H. pylori depends on a family of peroxiredoxins (alkylhydroperoxide reductase, bacterioferritin co-migratory protein and a thiol-peroxidase) that function to detoxify organic peroxides [1].
Transcript abundance in vitro (mid-log phase) ranged from about 0.004 (feoB and hpaA) to 20 (ureAB, napA, and cag25) copies/cell [2].
Among these, expression of the genes for the neutrophil activating protein (napA) and the major flagellin subunit (flaA) were significantly induced [3].
The napA promoter regions of the two types of AhpC mutants were identical, and primer extension analysis revealed their transcription start site to be the same as for the wild type [4].

Anatomical context of napA

The primary aims of this study were to investigate the relationships between H. pylori neutrophil activation and reported variations in HpNAP expression and the napA gene sequence [5].

References

The diverse antioxidant systems of Helicobacter pylori. Wang, G., Alamuri, P., Maier, R.J. Mol. Microbiol. (2006) [Pubmed]
Comparison of Helicobacter pylori virulence gene expression in vitro and in the Rhesus macaque. Boonjakuakul, J.K., Canfield, D.R., Solnick, J.V. Infect. Immun. (2005) [Pubmed]
Gene expression profiling of Helicobacter pylori reveals a growth-phase-dependent switch in virulence gene expression. Thompson, L.J., Merrell, D.S., Neilan, B.A., Mitchell, H., Lee, A., Falkow, S. Infect. Immun. (2003) [Pubmed]
Oxidative-stress resistance mutants of Helicobacter pylori. Olczak, A.A., Olson, J.W., Maier, R.J. J. Bacteriol. (2002) [Pubmed]
The ability of Helicobacter pylori to activate neutrophils is determined by factors other than H. pylori neutrophil-activating protein. Leakey, A., La Brooy, J., Hirst, R. J. Infect. Dis. (2000) [Pubmed]

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