Cpd-1 Null Mice Display a Subtle Neurological Phenotype |
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Authors: | Rupinder K Kular Rocky G Gogliotti Puneet Opal |
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Institution: | 1. Davee Department of Neurology, and Department of Cell and Molecular Biology, Northwestern University Feinberg School of Medicine, Chicago, Illinois, United States of America.; 2. Integrated Graduate Program, Northwestern University Feinberg School of Medicine, Chicago, Illinois, United States of America.;University of Florida, United States of America |
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Abstract: | BackgroundCPD1 (also known as ANP32-E) belongs to a family of evolutionarily conserved acidic proteins with leucine rich repeats implicated in a variety of cellular processes regulating gene expression, vesicular trafficking, intracellular signaling and apoptosis. Because of its spatiotemporal expression pattern, CPD1 has been proposed to play an important role in brain morphogenesis and synaptic development.Methodology/Principal FindingsWe have generated CPD1 knock-out mice that we have subsequently characterized. These mice are viable and fertile. However, they display a subtle neurological clasping phenotype and mild motor deficits.Conclusions/SignificanceCPD1 is not essential for normal development; however, it appears to play a role in the regulation of fine motor functions. The minimal phenotype suggests compensatory biological mechanisms. |
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