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Maria Ankarcrona

Researcher at Karolinska Institutet

Publications -  74
Citations -  9206

Maria Ankarcrona is an academic researcher from Karolinska Institutet. The author has contributed to research in topics: Mitochondrion & Presenilin. The author has an hindex of 33, co-authored 70 publications receiving 8625 citations.

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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

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.
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The amyloid β-peptide is imported into mitochondria via the TOM import machinery and localized to mitochondrial cristae

TL;DR: This work presents a unique import mechanism for Aβ in mitochondria and demonstrates both in vitro and in vivo that Aβ is located to the mitochondrial cristae, and shows that extracellulary applied Aβ can be internalized by human neuroblastoma cells and can colocalize with mitochondrial markers.
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p53 expression in nitric oxide-induced apoptosis

TL;DR: Nitric oxide generation in response to a cytokine induced NO‐synthase or by NO donors stimulates the expression of the tumor suppressor gene, p53, in RAW 264.7 macrophages or pancreatic RINm5F cells prior to apoptosis.

Different Prooxidant Levels Stimulate Growth, Trigger Apoptosis, or Produce Necrosis of Insulin-secreting RINm5F Cells

TL;DR: A disturbance of polyamine biosynthesis occurred prior to cell growth or apoptosis elicited by oxidative stress, and effects as opposite as cell proliferation and deletion can be induced, in the same system, by varying the exposure to a prooxidant.