ArticlePloS one2010
Cpd-1 null mice display a subtle neurological phenotype.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- Cracking the ANP32 whips: important functions, unequal requirement, and hints at disease implications.BioEssays : news and reviews in molecular, cellular and developmental biology · 2014Article
- Article
- LANP mediates neuritic pathology in Spinocerebellar ataxia type 1.Neurobiology of disease · 2012Article
- Differential display RT-PCR reveals genes associated with lithium-induced neuritogenesis in SK-N-MC cells.Cellular and molecular neurobiology · 2011Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
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/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.
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Registered trials
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