Alexis Ascah, Ph.D.
Affiliations: | 2010 | Université de Montréal, Montréal, Canada |
Area:
PharmacologyGoogle:
"Alexis Ascah"Parents
Sign in to add mentor| Yan Burelle | grad student | 2010 | Université de Montréal | |
| (Vulnerabilite cardiaque au stress au cours du remodelage ventriculaire pathologique: Role de la mitochondrie et du pore de permeabilite transitionnelle (PTP).) | ||||
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| Accardi MV, Troncy E, Abtout S, et al. (2016) Rat cardiovascular telemetry: Marginal distribution applied to positive control drugs. Journal of Pharmacological and Toxicological Methods. 81: 120-127 |
| Daussin FN, Godin R, Ascah A, et al. (2011) Cyclophilin-D is dispensable for atrophy and mitochondrial apoptotic signalling in denervated muscle. The Journal of Physiology. 589: 855-61 |
| Ascah A, Khairallah M, Daussin F, et al. (2011) Stress-induced opening of the permeability transition pore in the dystrophin-deficient heart is attenuated by acute treatment with sildenafil. American Journal of Physiology. Heart and Circulatory Physiology. 300: H144-53 |
| Godin R, Ascah A, Daussin FN. (2010) Intensity-dependent activation of intracellular signalling pathways in skeletal muscle: Role of fibre type recruitment during exercise Journal of Physiology. 588: 4073-4074 |
| Oliver-Dussault C, Ascah A, Marcil M, et al. (2010) Early predictors of cardiac decompensation in experimental volume overload. Molecular and Cellular Biochemistry. 338: 271-82 |
| Burelle Y, Khairallah M, Ascah A, et al. (2010) Alterations in mitochondrial function as a harbinger of cardiomyopathy: lessons from the dystrophic heart. Journal of Molecular and Cellular Cardiology. 48: 310-21 |
| Matas J, Young NT, Bourcier-Lucas C, et al. (2009) Increased expression and intramitochondrial translocation of cyclophilin-D associates with increased vulnerability of the permeability transition pore to stress-induced opening during compensated ventricular hypertrophy. Journal of Molecular and Cellular Cardiology. 46: 420-30 |
| Picard M, Csukly K, Robillard ME, et al. (2008) Resistance to Ca2+-induced opening of the permeability transition pore differs in mitochondria from glycolytic and oxidative muscles. American Journal of Physiology. Regulatory, Integrative and Comparative Physiology. 295: R659-68 |
| Marcil M, Ascah A, Matas J, et al. (2006) Compensated volume overload increases the vulnerability of heart mitochondria without affecting their functions in the absence of stress. Journal of Molecular and Cellular Cardiology. 41: 998-1009 |
| Ciminelli M, Ascah A, Bourduas K, et al. (2006) Short term training attenuates opening of the mitochondrial permeability transition pore without affecting myocardial function following ischemia-reperfusion. Molecular and Cellular Biochemistry. 291: 39-47 |