Evidence that cis-4 decenoic acid acts as an uncoupler of oxidative phosphorylation by opening pores in mitochondrial membrane (2008)
- Authors:
- Autor USP: KOWALTOWSKI, ALICIA JULIANA - IQ
- Unidade: IQ
- Subjects: BIOQUÍMICA; MITOCÔNDRIAS
- Language: Inglês
- Imprenta:
- Source:
- Título do periódico: Journal of Inherited Metabolic Disease
- ISSN: 1387-2362
- Volume/Número/Paginação/Ano: v. 31, suppl. 1, p. 36 res. 139-P, 2008
- Conference titles: Annual Symposium of the Society for the Study of Inborn Errors of Metabolism
-
ABNT
SCHUCK, Patricia Fernanda et al. Evidence that cis-4 decenoic acid acts as an uncoupler of oxidative phosphorylation by opening pores in mitochondrial membrane. Journal of Inherited Metabolic Disease. London: Instituto de Química, Universidade de São Paulo. . Acesso em: 20 maio 2024. , 2008 -
APA
Schuck, P. F., Ferreira, G. da C., Tahara, E. B., Kowaltowski, A. J., & Wajner, M. (2008). Evidence that cis-4 decenoic acid acts as an uncoupler of oxidative phosphorylation by opening pores in mitochondrial membrane. Journal of Inherited Metabolic Disease. London: Instituto de Química, Universidade de São Paulo. -
NLM
Schuck PF, Ferreira G da C, Tahara EB, Kowaltowski AJ, Wajner M. Evidence that cis-4 decenoic acid acts as an uncoupler of oxidative phosphorylation by opening pores in mitochondrial membrane. Journal of Inherited Metabolic Disease. 2008 ; 31 36 res. 139-P.[citado 2024 maio 20 ] -
Vancouver
Schuck PF, Ferreira G da C, Tahara EB, Kowaltowski AJ, Wajner M. Evidence that cis-4 decenoic acid acts as an uncoupler of oxidative phosphorylation by opening pores in mitochondrial membrane. Journal of Inherited Metabolic Disease. 2008 ; 31 36 res. 139-P.[citado 2024 maio 20 ] - 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
How to cite
A citação é gerada automaticamente e pode não estar totalmente de acordo com as normas
