Increased oxidative stress and CaMKIIactivity contribute to electro‐mechanical defects in cardiomyocytes from a murine model of Huntington's disease-Reference-Cited by-同舟云学术

Increased oxidative stress and CaMKIIactivity contribute to electro‐mechanical defects in cardiomyocytes from a murine model of Huntington's disease

Published:2018-12-20 Issue:1 Volume:286 Page:110-123
ISSN:1742-464X
Container-title:The FEBS Journal
language:en
Short-container-title:FEBS J

Author:

Joviano‐Santos Julliane Vasconcelos¹,Santos‐Miranda Artur²,Botelho Ana Flávia Machado³,Jesus Itamar Couto Guedes⁴,Andrade Jéssica Neves¹,Oliveira Barreto Tatiane²,Magalhães‐Gomes Matheus Proença S.¹,Valadão Priscila Aparecida Costa¹,Cruz Jader dos Santos²,Melo Marília Martins³,Guatimosim Silvia⁴,Guatimosim Cristina¹

Affiliation:

1. Department of Morphology Instituto de Ciências Biológicas Universidade Federal de Minas Gerais Belo Horizonte Brazil

2. Department of Biochemistry and Immunology Instituto de Ciências Biológicas Universidade Federal de Minas Gerais Belo Horizonte Brazil

3. Department of Veterinary Clinic and Surgery Escola de Veterinária Universidade Federal de Minas Gerais Belo Horizonte Brazil

4. Department of Physiology Instituto de Ciências Biológicas Universidade Federal de Minas Gerais Belo Horizonte Brazil

Funder

Fundação de Amparo à Pesquisa do Estado de Minas Gerais

Conselho Nacional de Desenvolvimento Científico e Tecnológico

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior

Publisher

Wiley

Subject

Cell Biology,Molecular Biology,Biochemistry

Link

https://onlinelibrary.wiley.com/doi/pdf/10.1111/febs.14706

Reference37 articles.

1. Neuropathological diagnosis and CAG repeat expansion in Huntington's disease.

2. Pathogenic Mechanisms in Huntington's Disease

3. A novel gene containing a trinucleotide repeat that is expanded and unstable on Huntington's disease chromosomes

4. Formation of Polyglutamine Inclusions in a Wide Range of Non-CNS Tissues in the HdhQ150 Knock-In Mouse Model of Huntington's Disease

5. Huntington's disease: from molecular pathogenesis to clinical treatment

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