John L. Farber focuses on Biochemistry, Cell killing, Mitochondrion, Mitochondrial permeability transition pore and Molecular biology. His studies link Calcium with Biochemistry. The Cell killing study combines topics in areas such as Lipid peroxidation, Catalase and Glutathione reductase.
Inner membrane is closely connected to Biophysics in his research, which is encompassed under the umbrella topic of Mitochondrion. His Mitochondrial permeability transition pore research is multidisciplinary, incorporating elements of Cyclosporin a, Internal medicine and Muscle hypertrophy. His Molecular biology study incorporates themes from Apoptosis, Cytochrome c, Specific activity and Cell biology.
John L. Farber mainly focuses on Biochemistry, Cell killing, Internal medicine, Molecular biology and Pathology. His studies deal with areas such as Lipid peroxidation, Oxidative stress, DNA damage and Mitochondrion, Cell biology as well as Cell killing. The various areas that John L. Farber examines in his Mitochondrion study include Cyclosporin a, Biophysics and Mitochondrial permeability transition pore.
His work carried out in the field of Cell biology brings together such families of science as Apoptosis and Programmed cell death. He works mostly in the field of Internal medicine, limiting it down to topics relating to Endocrinology and, in certain cases, Esophageal disease and Necrosis. His Molecular biology study combines topics from a wide range of disciplines, such as Chromatin, Poly ADP ribose polymerase, DNA fragmentation and NAD+ kinase.
His primary areas of investigation include Internal medicine, Pathology, Cancer research, Immunology and Cancer. His Internal medicine research integrates issues from Gastroenterology, Endocrinology and Cardiology. The study incorporates disciplines such as Cell growth, Carcinogenesis, Inflammation, Esophageal cancer and Hyperplasia in addition to Cancer research.
In his research, Cell is intimately related to Apoptosis, which falls under the overarching field of Cell growth. His biological study spans a wide range of topics, including Transplantation and Kidney transplantation. His study in Muscle hypertrophy is interdisciplinary in nature, drawing from both Heart metabolism, Mitochondrion, Mitochondrial membrane transport protein and Mitochondrial permeability transition pore.
John L. Farber spends much of his time researching Cancer research, Pathology, Cancer, Immunology and Internal medicine. John L. Farber has included themes like Lung, Interstitial lung disease and mir-31 in his Pathology study. His Immunology research incorporates elements of Transplantation and Kidney transplantation.
In his study, PPIF is inextricably linked to Endocrinology, which falls within the broad field of Internal medicine. His work deals with themes such as Tumor progression, Cell, Apoptosis and Combination cancer therapy, which intersect with Carcinogenesis. His Muscle hypertrophy study integrates concerns from other disciplines, such as Heart metabolism, Mitochondrion, Mitochondrial membrane transport protein and Mitochondrial permeability transition pore.
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The Overexpression of Bax Produces Cell Death upon Induction of the Mitochondrial Permeability Transition
John G. Pastorino;Sing Tsung Chen;Marco Tafani;Jack W. Snyder.
Journal of Biological Chemistry (1998)
Mechanisms of cell injury by activated oxygen species.
John L. Farber.
Laboratory Investigation (1990)
Accelerated phospholipid degradation and associated membrane dysfunction in irreversible, ischemic liver cell injury.
K R Chien;J Abrams;A Serroni;J T Martin.
Journal of Biological Chemistry (1978)
Prevention of experimental allergic encephalomyelitis by targeting nitric oxide and peroxynitrite: implications for the treatment of multiple sclerosis.
D. Craig Hooper;Omar Bagasra;Joseph C. Marini;Anna Zborek.
Proceedings of the National Academy of Sciences of the United States of America (1997)
The course of etoposide-induced apoptosis from damage to DNA and p53 activation to mitochondrial release of cytochrome c.
Natalie O. Karpinich;Marco Tafani;Marco Tafani;Ronald J. Rothman;Matteo A. Russo.
Journal of Biological Chemistry (2002)
The Cytotoxicity of Tumor Necrosis Factor Depends on Induction of the Mitochondrial Permeability Transition
John G. Pastorino;Gabriella Simbula;Kazuhiko Yamamoto;Peter A. Glascott.
Journal of Biological Chemistry (1996)
Cyclophilin D controls mitochondrial pore–dependent Ca2+ exchange, metabolic flexibility, and propensity for heart failure in mice
John W. Elrod;Renee Wong;Shikha Mishra;Ronald J. Vagnozzi.
Journal of Clinical Investigation (2010)
Functional Consequences of the Sustained or Transient Activation by Bax of the Mitochondrial Permeability Transition Pore
John G. Pastorino;Marco Tafani;Ronald J. Rothman;Ausra Marcineviciute.
Journal of Biological Chemistry (1999)
Cyclosporin and carnitine prevent the anoxic death of cultured hepatocytes by inhibiting the mitochondrial permeability transition.
J G Pastorino;J W Snyder;A Serroni;J B Hoek.
Journal of Biological Chemistry (1993)
Regulation of Acetylcholinesterase in Neuroblastoma Cells
Arthur J. Blume;F. Gilbert;S. Wilson;John L. Farber.
Proceedings of the National Academy of Sciences of the United States of America (1970)
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