Publication:
Antizyme Inhibitor 2-Deficient Mice Exhibit Altered Brain Polyamine Levels and Reduced Locomotor Activity

dc.contributor.authorNuñez Sánchez, María Ángeles
dc.contributor.authorLópez García, Carlos
dc.contributor.authorLópez Contreras, Andrés Joaquín
dc.contributor.authorRamos-Molina, Bruno
dc.contributor.authorPeñafiel, Rafael
dc.contributor.authorLambertos Escudero, Ana
dc.contributor.departmentBioquímica y Biología Molecular B e Inmunología
dc.date.accessioned2025-01-22T08:59:44Z
dc.date.available2025-01-22T08:59:44Z
dc.date.issued2023-12-21
dc.description© 2022 by the authors This document is the published version of a published work that appeared in final form in Biomolecules This document is made available under the CC-BY 4.0 license http://creativecommons.org/licenses/by/4.0 To access the final edited and published work see: https://doi.org/10.3390/biom13010014
dc.description.abstractAlterations in the neural polyamine system are known to be associated with different brain pathological conditions. In addition, the regulation of enzymes involved in polyamine metabolism such as ornithine decarboxylase (ODC), antizymes (AZs), and antizyme inhibitors (AZINs) is critical during brain development. However, while most studies focus on ODC and AZs, less is known about AZIN expression and function in the brain. Thus, our aim was to analyze the expression pattern of AZIN2 during postnatal development, its brain distribution, and its possible implication in phenotypical alterations. Methods: The expression pattern of Azin2 and other genes related to polyamine metabolism was analyzed by RT-qPCR. beta-D-galactosidase staining was used to determine the anatomical distribution of AZIN2 in a Azin2 knockout model containing the beta Geo marker. Brain polyamine content was determined by HPLC. The Rota-Rod and Pole functional tests were used to evaluate motor skills in Azin2-lacking mice. Results: Our results showed that expression of genes codifying for AZs and AZINs showed a similar increasing pattern over time that coincided with a decrease in ODC activity and putrescine levels. The analysis of AZIN2 distribution demonstrated that it is strongly expressed in the cerebellum and distributed along the neuron body and dendrites. The ablation of Azin2 showed a decrease in putrescine levels and is related to reduced motor skills. Conclusions: Our study revealed that AZIN2 expression in the brain is particularly limited to the cerebellum. In addition, the ablation of Azin2 leads to a reduction in putrescine that relates to alterations in motor function, suggesting the role of AZIN2 in the functioning of dopaminergic neurons.es
dc.formatapplication/pdfes
dc.format.extent15es
dc.identifier.citationBiomolecules 13 (1)
dc.identifier.doihttps://doi.org/10.3390/biom13010014
dc.identifier.issn2218-273X
dc.identifier.urihttp://hdl.handle.net/10201/149025
dc.languageenges
dc.publisherMDPIes
dc.relationSpanish Government SAF2011-29051es
dc.relation.publisherversionhttps://www.mdpi.com/2218-273X/13/1/14
dc.rightsinfo:eu-repo/semantics/openAccesses
dc.titleAntizyme Inhibitor 2-Deficient Mice Exhibit Altered Brain Polyamine Levels and Reduced Locomotor Activityes
dc.typeinfo:eu-repo/semantics/articlees
dspace.entity.typePublicationes
relation.isAuthorOfPublication5d0e7a0e-9ee6-41f7-8b88-142f6d773781
relation.isAuthorOfPublication.latestForDiscovery5d0e7a0e-9ee6-41f7-8b88-142f6d773781
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