Mitochondrial energy metabolism in neurodegeneration associated with methylmalonic acidemia (2011)
- Authors:
- Autor USP: KOWALTOWSKI, ALICIA JULIANA - IQ
- Unidade: IQ
- DOI: 10.1007/s10863-011-9330-2
- Subjects: SISTEMA NERVOSO CENTRAL; MITOCÔNDRIAS; BIOQUÍMICA
- Language: Inglês
- Imprenta:
- Source:
- Título do periódico: Journal of Bioenergetics and Biomembranes
- ISSN: 0145-479X
- Volume/Número/Paginação/Ano: v. 43, n. 1, p. 39-46, 2011
- Este periódico é de assinatura
- Este artigo NÃO é de acesso aberto
- Cor do Acesso Aberto: closed
-
ABNT
MELO, Daniela R et al. Mitochondrial energy metabolism in neurodegeneration associated with methylmalonic acidemia. Journal of Bioenergetics and Biomembranes, v. 43, n. 1, p. 39-46, 2011Tradução . . Disponível em: https://doi.org/10.1007/s10863-011-9330-2. Acesso em: 18 set. 2024. -
APA
Melo, D. R., Kowaltowski, A. J., Wajner, M., & Castilho, R. F. (2011). Mitochondrial energy metabolism in neurodegeneration associated with methylmalonic acidemia. Journal of Bioenergetics and Biomembranes, 43( 1), 39-46. doi:10.1007/s10863-011-9330-2 -
NLM
Melo DR, Kowaltowski AJ, Wajner M, Castilho RF. Mitochondrial energy metabolism in neurodegeneration associated with methylmalonic acidemia [Internet]. Journal of Bioenergetics and Biomembranes. 2011 ; 43( 1): 39-46.[citado 2024 set. 18 ] Available from: https://doi.org/10.1007/s10863-011-9330-2 -
Vancouver
Melo DR, Kowaltowski AJ, Wajner M, Castilho RF. Mitochondrial energy metabolism in neurodegeneration associated with methylmalonic acidemia [Internet]. Journal of Bioenergetics and Biomembranes. 2011 ; 43( 1): 39-46.[citado 2024 set. 18 ] Available from: https://doi.org/10.1007/s10863-011-9330-2 - Caloric restriction protects mice against isoproterenol-induced cardiac hypertrophy by mechanisms that involve mitochondrial ATP sensitive potassium channel and modulation of redox state
- Bioenergetic consequences of opening the ATP-sensitive `K POT. +´ channel of heart mitochondria
- Mechanisms by which opening the mitochondrial ATP- sensitive 'K POT. +' channel protects the ischemic heart
- Effect of Bcl-2 overexpression on mitochondrial structure and function
- Mitochondrial ATP-sensitive 'K POT. +' channel opening decreases reactive oxygen species generation
- Mitochondrial channels that regulate cell viability
- Mitochondrial permeability transition is delayed by ATP-sensitive 'K POT. +' channel ('Mitok IND. ATP') opening
- Protection against ischemic brain injury by inhibition of mitochondrial oxidative stress
- ATP-sensitive K+ channel (mitoKATP) opening protects against cellular damage preventing mitochondrial permeability transition
- Diet, mitochondria and energy metabolism
Informações sobre o DOI: 10.1007/s10863-011-9330-2 (Fonte: oaDOI API)
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