@article {190,
	title = {Inactivation of NADPH oxidase organizer 1 Results in Severe Imbalance.},
	journal = {Current Biology},
	volume = {16},
	year = {2006},
	note = {CAPLUS AN 2006:87961(Journal)},
	month = {2006///},
	pages = {208 - 213},
	publisher = {Cell Press},
	abstract = {Otoconia are biominerals of the vestibular system that are indispensable for the perception of gravity.  Despite their importance, the process of otoconia genesis is largely unknown.  Reactive oxygen species (ROS) have been recognized for their toxic effects in antimicrobial host defense as well as in aging and carcinogenesis.  Enzymes evolved for ROS prodn. belong to the recently discovered NADPH oxidase (Nox) enzyme family.  Here we show that the inactivation of a regulatory subunit, NADPH oxidase organizer 1 (Noxo1), resulted in the severe balance deficit seen in the spontaneous mutant "head slant" (hslt) mice whose phenotype was rescued by Noxo1 transgenes.  Wild-type Noxo1 was expressed in the vestibular and cochlear epithelia and was required for ROS prodn. by an oxidase complex.  In contrast, the hslt mutation of Noxo1 was biochem. inactive and led to an arrest of otoconia genesis, characterized by a complete lack of calcium carbonate mineralization and an accumulation of otoconial protein, otoconin-90/95 (OC-90/95).  These results suggest that ROS generated by a Noxo1-dependent vestibular oxidase are crit. for otoconia formation and may be required for interactions among otoconial components.  Noxo1 mutants implicate a constructive developmental role for ROS, in contrast to their previously described toxic effects. [on SciFinder(R)]},
	keywords = {NADPH oxidase organizer 1 otoconia formation balance deficit},
	isbn = {0960-9822},
	author = {Kiss, Peter J. and Knisz, Judit and Zhang, Yuzhou and Baltrusaitis, Jonas and Sigmund, Curt D. and Thalmann, Ruediger and Smith, Richard J. H. and Verpy, Elisabeth and Banfi, Botond.}
}
