His primary areas of study are Cell biology, Thrombin, Apoptosis, Programmed cell death and Internal medicine. His Cell biology research is multidisciplinary, relying on both Downregulation and upregulation, Neurodegeneration and Biochemistry. His Thrombin study combines topics in areas such as Proteases, Serpin, Protease, Receptor and Molecular biology.
His Apoptosis research is multidisciplinary, incorporating elements of Spinal cord injury and Immunology. His Internal medicine research includes elements of Endocrinology and Cardiology. His Endocrinology research is multidisciplinary, incorporating perspectives in Amyotrophic lateral sclerosis and Severity of illness.
His primary areas of investigation include Biochemistry, Cell biology, Internal medicine, Thrombin and Skeletal muscle. His study in Cell biology is interdisciplinary in nature, drawing from both Cell culture, Apoptosis, Programmed cell death, Neurodegeneration and Tissue transglutaminase. His research investigates the connection with Programmed cell death and areas like Spinal cord which intersect with concerns in Downregulation and upregulation.
His biological study spans a wide range of topics, including Gastroenterology and Endocrinology. The various areas that Barry W. Festoff examines in his Thrombin study include Proteases, Molecular biology, Serpin and Receptor. The Skeletal muscle study combines topics in areas such as Myocyte, Neuromuscular junction and Denervation.
Barry W. Festoff mostly deals with Cell biology, Thrombin, Neuroscience, Receptor and Neurodegeneration. Barry W. Festoff interconnects Thrombin receptor, Biochemistry, Tissue transglutaminase, Messenger RNA and Gene isoform in the investigation of issues within Cell biology. His work deals with themes such as Apoptosis, Signal transduction, Neuroprotection and p38 mitogen-activated protein kinases, which intersect with Thrombin.
His studies in Neuroprotection integrate themes in fields like Caspase and Spinal cord injury, Spinal cord. In his research on the topic of Neurodegeneration, Motor neuron is strongly related with Central nervous system. His research in Immunology intersects with topics in Gastroenterology, Internal medicine and Blood–brain barrier.
Barry W. Festoff spends much of his time researching Receptor, Cell biology, Neurodegeneration, Neuroscience and Thrombin. The concepts of his Receptor study are interwoven with issues in Hippocampal formation and Pathogenesis. His Cell biology study integrates concerns from other disciplines, such as Tissue transglutaminase and Gene isoform.
His studies deal with areas such as Gene family and Alternative splicing, Biochemistry, Gene, Messenger RNA as well as Neurodegeneration. His research on Thrombin often connects related topics like Microglia. The study of Internal medicine and Endocrinology are components of his Tumor necrosis factor alpha research.
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.
Xeroderma pigmentosum. An inherited diseases with sun sensitivity, multiple cutaneous neoplasms, and abnormal DNA repair.
Jay H. Robbins;Kenneth H. Kraemer;Marvin A. Lutzner;Barry W. Festoff.
Annals of Internal Medicine (1974)
Effect of recombinant human insulin-like growth factor-I on progression of ALS A placebo-controlled study
Eugene C. Lai;K. J. Felice;B. W. Festoff;M. J. Gawel.
Neurology (1997)
Apoptosis in Cellular Compartments of Rat Spinal Cord After Severe Contusion Injury
Chi Yong;Paul M. Arnold;Paul M. Arnold;Mikhail N. Zoubine;Mikhail N. Zoubine;Bruce A. Citron;Bruce A. Citron.
Journal of Neurotrauma (1998)
Minocycline neuroprotects, reduces microgliosis, and inhibits caspase protease expression early after spinal cord injury.
Barry W. Festoff;Syed Ameenuddin;Paul M. Arnold;Paul M. Arnold;Andrea Wong.
Journal of Neurochemistry (2006)
Participation of protease‐activated receptor‐1 in thrombin‐induced microglial activation
Zhiming Suo;Min Wu;Syed Ameenuddin;Heidi E. Anderson.
Journal of Neurochemistry (2002)
PROTEOLYTIC ACTION OF THROMBIN IS REQUIRED FOR ELECTRICAL ACTIVITY-DEPENDENT SYNAPSE REDUCTION
Yuan Liu;R. D. Fields;B. W. Festoff;P. G. Nelson.
Proceedings of the National Academy of Sciences of the United States of America (1994)
Microglial activation, increased TNF and SERT expression in the prefrontal cortex define stress-altered behaviour in mice susceptible to anhedonia
Yvonne Couch;Daniel C. Anthony;Oleg Dolgov;Alexander Revischin.
Brain Behavior and Immunity (2013)
Thrombin perturbs neurite outgrowth and induces apoptotic cell death in enriched chick spinal motoneuron cultures through caspase activation.
Victoria L. Turgeon;Elizabeth D. Lloyd;Siwei Wang;Barry W. Festoff.
The Journal of Neuroscience (1998)
Protein crosslinking, tissue transglutaminase, alternative splicing and neurodegeneration.
Bruce A Citron;Zhiming Suo;Zhiming Suo;Karen SantaCruz;Peter J.A Davies.
Neurochemistry International (2002)
Biochemical studies of synapses in vitro. 3. Ionic activation of protein synthesis.
Stanley H. Appel;Lucila Autilio;Barry W. Festoff;Antonio V. Escueta.
Journal of Biological Chemistry (1969)
If you think any of the details on this page are incorrect, let us know.
We appreciate your kind effort to assist us to improve this page, it would be helpful providing us with as much detail as possible in the text box below:
Houston Methodist
Texas A&M University
National Institutes of Health
Maastricht University
University of Oxford
Boston University
University of Rouen
University of Kansas
University of Kansas
Université Paris Cité
University of Navarra
Aalto University
Max Planck Institute for Dynamics and Self-Organization
École Polytechnique
Chinese Academy of Sciences
University of Glasgow
University of Copenhagen
University of Manchester
University of Bern
Baylor College of Medicine
German Cancer Research Center
Catholic University of Portugal
MIT
University of Pittsburgh
Harvard University
University of Groningen