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Sara Salucci

Researcher at University of Urbino

Publications -  62
Citations -  910

Sara Salucci is an academic researcher from University of Urbino. The author has contributed to research in topics: Apoptosis & Skeletal muscle. The author has an hindex of 16, co-authored 54 publications receiving 729 citations.

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Cellular and subcellular localization of Na+-Ca2+ exchanger protein isoforms, NCX1, NCX2, and NCX3 in cerebral cortex and hippocampus of adult rat.

TL;DR: Perisynaptic localization of NCX1-3 in dendrites and spines indicates that all isoforms are favourably located for buffering [Ca(2+)](i) in excitatory postsynaptic sites, as well as shaping astrocytic transients evoked by ongoing synaptic activity.
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Anti-apoptotic activity of hydroxytyrosol and hydroxytyrosyl laurate

TL;DR: Investigating the effects of HyT and the corresponding ester hydroxytyrosyl laurate in U937 cells, a human monocytoid cell line, and in C2C12 myoblasts, a murine proliferating muscle cell model, after apoptotic death induction suggests these compounds as good candidate for novel therapeutic strategies.
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Mitochondrial localization of Na+/Ca2+ exchangers NCX1–3 in neurons and astrocytes of adult rat brain in situ

TL;DR: Quantitative and qualitative immunocytochemical data suggest that all NCX isoforms contribute to mitochondrial Ca2+ homeostasis in neurons and glial cells in vivo, and that NCXs may be particularly involved in handling Ca1+ in dendritic, subplasmalemmal mitochondria, thus emphasizing the role of mitochondrial NCX1-3 in shaping postsynaptic calcium transients.
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Ultraviolet B (UVB) Irradiation-Induced Apoptosis in Various Cell Lineages in Vitro

TL;DR: It is demonstrated that UVB radiation appears to be an ideal tool to study the apoptotic behavior in various cell models by using ultrastructural, molecular and cytofluorimetric techniques.
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C2C12 myoblast sensitivity to different apoptotic chemical triggers.

TL;DR: The results suggest that all conditions are able to induce apoptosis in C2C12 myoblasts, which occurs, considering trigger mechanisms of action, mostly following the mitochondrial pathway, if not excluding that due to DNA damage.