E
Emanuela Bonfoco
Researcher at Karolinska Institutet
Publications - 14
Citations - 4702
Emanuela Bonfoco is an academic researcher from Karolinska Institutet. The author has contributed to research in topics: Apoptosis & Programmed cell death. The author has an hindex of 11, co-authored 14 publications receiving 4644 citations. Previous affiliations of Emanuela Bonfoco include Boston Children's Hospital.
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Apoptosis and necrosis: two distinct events induced, respectively, by mild and intense insults with N-methyl-D-aspartate or nitric oxide/superoxide in cortical cell cultures
TL;DR: It is reported that exposure of cortical neurons to relatively short durations or low concentrations of NMDA, S-nitrosocysteine, or 3-morpholinosydnonimine, which generate low levels of peroxynitrite, induces a delayed form of neurotoxicity predominated by apoptotic features.
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Glutamate-induced neuronal death: A succession of necrosis or apoptosis depending on mitochondrial function
Maria Ankarcrona,Jeannette M. Dypbukt,Emanuela Bonfoco,Boris Zhivotovsky,Sten Orrenius,Stuart A. Lipton,Pierluigi Nicotera,Pierluigi Nicotera +7 more
TL;DR: It is shown that glutamate can induce either early necrosis or delayed apoptosis in cultures of cerebellar granule cells, suggesting that mitochondrial function is a critical factor that determines the mode of neuronal death in excitotoxicity.
Journal Article
Neuronal necrosis and apoptosis: two distinct events induced by exposure to glutamate or oxidative stress.
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Colchicine induces apoptosis in cerebellar granule cells.
TL;DR: The idea that colchicine-induced cytoskeletal alterations directly initiate the genetic and structural modifications that result in rat cerebellar granule cells apoptosis is supported.
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Cytoskeletal breakdown and apoptosis elicited by NO donors in cerebellar granule cells require NMDA receptor activation.
Emanuela Bonfoco,Marcel Leist,Boris Zhivotovsky,Sten Orrenius,Stuart A. Lipton,Pierluigi Nicotera,Pierluigi Nicotera +6 more
TL;DR: It is suggested that Ca2+ influx through NMDA‐R‐gated ion channels is a critical event in CGC apoptosis induced by NO donors, which depends on NMDA receptor (NMda‐R) activation leading to intracellular Ca2- overload.