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Byoung Joo Gwag
Researcher at Ajou University
Publications - 113
Citations - 7770
Byoung Joo Gwag is an academic researcher from Ajou University. The author has contributed to research in topics: Apoptosis & Neuroprotection. The author has an hindex of 43, co-authored 108 publications receiving 7349 citations. Previous affiliations of Byoung Joo Gwag include Drexel University & The Catholic University of America.
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Journal ArticleDOI
The Role of Zinc in Selective Neuronal Death After Transient Global Cerebral Ischemia
TL;DR: The toxic influx of zinc may be a key mechanism underlying selective neuronal death after transient global ischemic insults and could be prevented by the intraventricular injection of a zinc chelating agent.
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Mediation of neuronal apoptosis by enhancement of outward potassium current.
Shan Ping Yu,Chen Hsiung Yeh,Stefano L. Sensi,Byoung Joo Gwag,Lorella M.T. Canzoniero,Z. Shadi Farhangrazi,Howard S. Ying,Min Tian,Laura L. Dugan,Dennis W. Choi +9 more
TL;DR: Attenuating outward K+ current with tetraethylammonium or elevated extracellular K+, but not blockers of Ca2+, Cl-, or other K+ channels, reduced apoptosis, even if associated increases in intracellular Ca2+ concentration were prevented.
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Potentiated necrosis of cultured cortical neurons by neurotrophins
TL;DR: Certain neurotrophins may have opposing effects on different types of death in the same neurons, as shown in the cases of brain-derived neurotrophic factor and neurotrophin-4/5.
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Cellular and molecular pathways of ischemic neuronal death.
TL;DR: Evidence is being accumulated that excitotoxicity, oxidative stress, and apoptosis propagate through distinctive and mutually exclusive signal transduction pathway and contribute to neuronal loss following hypoxic-ischemic brain injury.
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Blockade of glutamate receptors unmasks neuronal apoptosis after oxygen-glucose deprivation in vitro
TL;DR: It is suggested that oxygen-glucose deprivation can induce in cortical neurons both excitotoxic necrosis, and apoptosis dependent on new macromolecule synthesis.