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Data on protein abundance alteration induced by chronic exercise in mdx mice model of Duchenne muscular dystrophy and potential modulation by apocynin and taurine
Here we present original data related to the research paper entitled “Proteome analysis in dystrophic mdx mouse muscle reveals a drastic alteration of Key Metabolic and Contractile Proteins after chronic exercise and the potential modulation by anti-oxidant compounds” (Gamberi et al., 2018) [1]. The...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Elsevier
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5996268/ https://www.ncbi.nlm.nih.gov/pubmed/29900212 http://dx.doi.org/10.1016/j.dib.2018.03.037 |
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author | Gamberi, Tania Fiaschi, Tania Valocchia, Elisa Modesti, Alessandra Mantuano, Paola Rolland, Jean-Francois Sanarica, Francesca De Luca, Annamaria Magherini, Francesca |
author_facet | Gamberi, Tania Fiaschi, Tania Valocchia, Elisa Modesti, Alessandra Mantuano, Paola Rolland, Jean-Francois Sanarica, Francesca De Luca, Annamaria Magherini, Francesca |
author_sort | Gamberi, Tania |
collection | PubMed |
description | Here we present original data related to the research paper entitled “Proteome analysis in dystrophic mdx mouse muscle reveals a drastic alteration of Key Metabolic and Contractile Proteins after chronic exercise and the potential modulation by anti-oxidant compounds” (Gamberi et al., 2018) [1]. The dystrophin-deficient mdx mouse is the most common animal model for Duchenne muscular dystrophy. The mdx mice phenotype of the disorder is milder than in human sufferers and it can be worsened by chronic treadmill exercise. Apocynin and taurine are two antioxidant compounds proved to be beneficial on some pathology related parameters (Schröder and Schoser, 2009) [2]. This article reports the detailed proteomic data on protein abundance alterations, in tibialis anterior muscle of mdx mice, induced by chronic exercise protocol. A selected group of mdx mice was also treated with apocynin and taurine during this protocol. Detailed MS data, comparison between mdx vs wild type, exercised mdx vs wild type, and complete analysis of spot variation are provided. Furthermore, in wild type mice subjected to the same exercise protocol, the abundance of key proteins, resulted modified in exercised mdx, were analyzed by western blot. |
format | Online Article Text |
id | pubmed-5996268 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Elsevier |
record_format | MEDLINE/PubMed |
spelling | pubmed-59962682018-06-13 Data on protein abundance alteration induced by chronic exercise in mdx mice model of Duchenne muscular dystrophy and potential modulation by apocynin and taurine Gamberi, Tania Fiaschi, Tania Valocchia, Elisa Modesti, Alessandra Mantuano, Paola Rolland, Jean-Francois Sanarica, Francesca De Luca, Annamaria Magherini, Francesca Data Brief Proteomics and Biochemistry Here we present original data related to the research paper entitled “Proteome analysis in dystrophic mdx mouse muscle reveals a drastic alteration of Key Metabolic and Contractile Proteins after chronic exercise and the potential modulation by anti-oxidant compounds” (Gamberi et al., 2018) [1]. The dystrophin-deficient mdx mouse is the most common animal model for Duchenne muscular dystrophy. The mdx mice phenotype of the disorder is milder than in human sufferers and it can be worsened by chronic treadmill exercise. Apocynin and taurine are two antioxidant compounds proved to be beneficial on some pathology related parameters (Schröder and Schoser, 2009) [2]. This article reports the detailed proteomic data on protein abundance alterations, in tibialis anterior muscle of mdx mice, induced by chronic exercise protocol. A selected group of mdx mice was also treated with apocynin and taurine during this protocol. Detailed MS data, comparison between mdx vs wild type, exercised mdx vs wild type, and complete analysis of spot variation are provided. Furthermore, in wild type mice subjected to the same exercise protocol, the abundance of key proteins, resulted modified in exercised mdx, were analyzed by western blot. Elsevier 2018-03-19 /pmc/articles/PMC5996268/ /pubmed/29900212 http://dx.doi.org/10.1016/j.dib.2018.03.037 Text en © 2018 The Authors http://creativecommons.org/licenses/by/4.0/ This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Proteomics and Biochemistry Gamberi, Tania Fiaschi, Tania Valocchia, Elisa Modesti, Alessandra Mantuano, Paola Rolland, Jean-Francois Sanarica, Francesca De Luca, Annamaria Magherini, Francesca Data on protein abundance alteration induced by chronic exercise in mdx mice model of Duchenne muscular dystrophy and potential modulation by apocynin and taurine |
title | Data on protein abundance alteration induced by chronic exercise in mdx mice model of Duchenne muscular dystrophy and potential modulation by apocynin and taurine |
title_full | Data on protein abundance alteration induced by chronic exercise in mdx mice model of Duchenne muscular dystrophy and potential modulation by apocynin and taurine |
title_fullStr | Data on protein abundance alteration induced by chronic exercise in mdx mice model of Duchenne muscular dystrophy and potential modulation by apocynin and taurine |
title_full_unstemmed | Data on protein abundance alteration induced by chronic exercise in mdx mice model of Duchenne muscular dystrophy and potential modulation by apocynin and taurine |
title_short | Data on protein abundance alteration induced by chronic exercise in mdx mice model of Duchenne muscular dystrophy and potential modulation by apocynin and taurine |
title_sort | data on protein abundance alteration induced by chronic exercise in mdx mice model of duchenne muscular dystrophy and potential modulation by apocynin and taurine |
topic | Proteomics and Biochemistry |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5996268/ https://www.ncbi.nlm.nih.gov/pubmed/29900212 http://dx.doi.org/10.1016/j.dib.2018.03.037 |
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