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Cpd-1 Null Mice Display a Subtle Neurological Phenotype
BACKGROUND: CPD1 (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 exp...
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Formato: | Texto |
Lenguaje: | English |
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Public Library of Science
2010
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2936576/ https://www.ncbi.nlm.nih.gov/pubmed/20844742 http://dx.doi.org/10.1371/journal.pone.0012649 |
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author | Kular, Rupinder K. Gogliotti, Rocky G. Opal, Puneet |
author_facet | Kular, Rupinder K. Gogliotti, Rocky G. Opal, Puneet |
author_sort | Kular, Rupinder K. |
collection | PubMed |
description | BACKGROUND: CPD1 (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 FINDINGS: We 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/SIGNIFICANCE: CPD1 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. |
format | Text |
id | pubmed-2936576 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2010 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-29365762010-09-15 Cpd-1 Null Mice Display a Subtle Neurological Phenotype Kular, Rupinder K. Gogliotti, Rocky G. Opal, Puneet PLoS One Research Article BACKGROUND: CPD1 (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 FINDINGS: We 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/SIGNIFICANCE: CPD1 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. Public Library of Science 2010-09-09 /pmc/articles/PMC2936576/ /pubmed/20844742 http://dx.doi.org/10.1371/journal.pone.0012649 Text en Kular et al. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited. |
spellingShingle | Research Article Kular, Rupinder K. Gogliotti, Rocky G. Opal, Puneet Cpd-1 Null Mice Display a Subtle Neurological Phenotype |
title | Cpd-1 Null Mice Display a Subtle Neurological Phenotype |
title_full | Cpd-1 Null Mice Display a Subtle Neurological Phenotype |
title_fullStr | Cpd-1 Null Mice Display a Subtle Neurological Phenotype |
title_full_unstemmed | Cpd-1 Null Mice Display a Subtle Neurological Phenotype |
title_short | Cpd-1 Null Mice Display a Subtle Neurological Phenotype |
title_sort | cpd-1 null mice display a subtle neurological phenotype |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2936576/ https://www.ncbi.nlm.nih.gov/pubmed/20844742 http://dx.doi.org/10.1371/journal.pone.0012649 |
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