Erratum: Targeted Disruption of the Mouse <i>Npal3</i> Gene Leads to Deficits in Behavior, Increased IgE Levels, and Impaired Lung Function

The non-imprinted in Prader-Willi/Angelman syndrome (NIPA) proteins are highly conserved receptors or transporters. Translocation of <i>NIPA</i> genes were found in patients with Prader-Willi syndrome, and loss-of-function of the <i>NIPA1</i> gene was identified in hereditary spastic paraplegia. The family of NIPA-like domain containing (NPAL) proteins is closely related to the NIPA proteins, but to date nothing is known about their function. Here, we could demonstrate that both human <i>NPAL3 </i>and mouse <i>Npal3 </i>are ubiquitously expressed and encode highly conserved proteins. To further elucidate the function of the <i>Npal3</i> gene, knockout <i>(Npal3</i><sup>–/–</sup><i>)</i> mice were generated. Intensive phenotypic analyses revealed that disruption of the <i>Npal3</i> gene results in a pleiotropic phenotype. The function of the nervous system was impaired in both mutant males and females which could be demonstrated in behavioral tests. In addition, in <i>Npal3 </i>mutants the number of NK cells was decreased and changes in IgM, IgG<sub>2</sub>, and IgA were observed, indicating that the immune system is also affected. Interestingly, increased IgE levels as well as impaired lung functions were observed in mutant males but not in mutant females. It should be noted that the human <i>NPAL3</i> gene is located at 1p36.12→p35.1, and atopic diseases were previously linked to this genomic region. Thus, the <i>Npal3</i><sup>–/–</sup> mice could serve as a valuable model system for studying atopic diseases.