His primary areas of investigation include Mitochondrion, Biochemistry, Internal medicine, Endocrinology and Ischemic preconditioning. His Mitochondrion research is included under the broader classification of Cell biology. The study incorporates disciplines such as Proinflammatory cytokine, Inflammation, Lipopolysaccharide and Immunology in addition to Cell biology.
His work deals with themes such as Parkin, Naltrindole and Antioxidant, which intersect with Endocrinology. Michael N. Sack combines subjects such as Agonist, Oxidative phosphorylation, Cardioprotection and Pharmacology with his study of Ischemic preconditioning. Michael N. Sack has included themes like Receptor, Opioid receptor, DADLE, Insulin and Kinase in his Cardioprotection study.
His primary scientific interests are in Cell biology, Mitochondrion, Internal medicine, Endocrinology and Biochemistry. His studies in Cell biology integrate themes in fields like Autophagy and Molecular biology. His research in Mitochondrion intersects with topics in Oxidative phosphorylation, SIRT3, Sirtuin and Ischemia.
The various areas that Michael N. Sack examines in his Internal medicine study include Diabetes mellitus and Cardiology. His study explores the link between Endocrinology and topics such as Signal transduction that cross with problems in Receptor. His Cardioprotection course of study focuses on Ischemic preconditioning and Diazoxide, Tumor necrosis factor alpha, Phenotype, Adenosine and Respiratory system.
Michael N. Sack mostly deals with Cell biology, Internal medicine, Acetylation, Endocrinology and mTORC1. His Cell biology study integrates concerns from other disciplines, such as Autophagy, Biogenesis, Lysosome, Reperfusion injury and Cell type. His research links Cardiology with Internal medicine.
While the research belongs to areas of Cardiology, Michael N. Sack spends his time largely on the problem of Lung, intersecting his research to questions surrounding Mitochondrion. His Acetylation research is multidisciplinary, incorporating perspectives in Enzyme assay, Reactive oxygen species, SOD2 and Pyruvate dehydrogenase complex. His biological study focuses on Intermittent fasting.
Michael N. Sack mainly investigates Cell biology, Mitochondrion, Cell type, Reperfusion injury and Acetylation. His study in the field of mTORC1, Signal transduction and Regeneration is also linked to topics like Glutaminase. His study in Mitochondrion is interdisciplinary in nature, drawing from both Heart failure, Pathogenesis, Cardiology, Internal medicine and Lung.
The Cell type study combines topics in areas such as Cardiac function curve, Mitogen-activated protein kinase, Reactive oxygen species, Viability assay and Ischemia. The concepts of his Reperfusion injury study are interwoven with issues in Gene knockdown, mTORC2, Glycolysis, Mitochondrial ROS and Programmed cell death. His Acetylation research incorporates elements of Histone, Protein subunit, Intracellular and Cytosol.
This overview was generated by a machine learning system which analysed the scientist’s body of work. If you have any feedback, you can contact us here.
Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)
Daniel J. Klionsky;Kotb Abdelmohsen;Akihisa Abe;Joynal Abedin.
Autophagy (2016)
Erratum to: Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition) (Autophagy, 12, 1, 1-222, 10.1080/15548627.2015.1100356
Daniel J. Klionsky;Kotb Abdelmohsen;Akihisa Abe;Joynal Abedin.
Autophagy (2016)
Mitochondrial reactive oxygen species promote production of proinflammatory cytokines and are elevated in TNFR1-associated periodic syndrome (TRAPS)
Ariel C. Bulua;Anna Simon;Ravikanth Maddipati;Martin Pelletier.
Journal of Experimental Medicine (2011)
Oestrogen and inhibition of oxidation of low-density lipoproteins in postmenopausal women
M. N. Sack;D. J. Rader;R. O. Cannon.
The Lancet (1994)
Fatty Acid Oxidation Enzyme Gene Expression Is Downregulated in the Failing Heart
Michael N. Sack;Toni A. Rader;Sonhee Park;Jean Bastin.
Circulation (1996)
Myocardial Protection by Insulin at Reperfusion Requires Early Administration and Is Mediated via Akt and p70s6 Kinase Cell-Survival Signaling
Anne K. Jonassen;Michael N. Sack;Ole D. Mjøs;Derek M. Yellon.
Circulation Research (2001)
Nitrite augments tolerance to ischemia/reperfusion injury via the modulation of mitochondrial electron transfer
Sruti Shiva;Michael N. Sack;James J. Greer;Mark Duranski.
Journal of Experimental Medicine (2007)
Fatty liver is associated with reduced SIRT3 activity and mitochondrial protein hyperacetylation.
Agnieszka A. Kendrick;Mahua Choudhury;Shaikh M. Rahman;Carrie E. McCurdy.
Biochemical Journal (2011)
Identification of a Novel Role for Sphingolipid Signaling in TNF α and Ischemic Preconditioning Mediated Cardioprotection
Sandrine Lecour;Robert M. Smith;Brian Woodward;Lionel H. Opie.
Journal of Molecular and Cellular Cardiology (2002)
Mitochondrial Function, Biology, and Role in Disease A Scientific Statement From the American Heart Association
Elizabeth Murphy;Hossein Ardehali;Robert S. Balaban;Fabio DiLisa.
Circulation Research (2016)
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