Publications by authors named "S Tiano"

Dimension-engineered synthesis of atomically thin II-VI nanoplatelets (NPLs) remains an open challenge. While CdSe NPLs have been made with confinement ranging from 2 to 11 monolayers (ML), CdTe NPLs have been significantly more challenging to synthesize and separate. Here we provide detailed mechanistic insight into the layer-by-layer growth kinetics of the CdTe NPLs.

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Background: The Niemann Pick C1 (NPC1) protein is an intracellular cholesterol transporter located in the late endosome/lysosome (LE/Ly) that is involved in the mobilization of endocytosed cholesterol. Loss-of-function mutations in the NPC1 gene lead to the accumulation of cholesterol and sphingolipids in LE/Ly, resulting in severe fatal NPC1 disease. Cellular alterations associated with NPC1 inactivation affect both the integrity of lipid rafts and the endocytic pathway.

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SARS-CoV-2 pandemic clearly demonstrated the lack of preparation against novel and emerging viral diseases. This prompted an enormous effort to identify antivirals to curb viral spread and counteract future pandemics. Ribosome Inactivating Proteins (RIPs) and Ribotoxin-Like Proteins (RL-Ps) are toxin enzymes isolated from edible plants and mushrooms, both able to inactivate protein biosynthesis.

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Hypervalent iron intermediates have been invoked in the catalytic cycles of many metalloproteins, and thus, it is crucial to understand how the coupling between such species and their environment can impact their chemical and physical properties in such contexts. In this work, we take advantage of the solvent kinetic isotope effect (SKIE) to gain insight into the nonradiative deactivation of electronic excited states of the aqueous ferrate(VI) ion. We observe an exceptionally large SKIE of 9.

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Chaperone-mediated autophagy (CMA) contributes to regulation of energy homeostasis by timely degradation of enzymes involved in glucose and lipid metabolism. Here, we report reduced CMA activity in vascular smooth muscle cells and macrophages in murine and human arteries in response to atherosclerotic challenges. We show that in vivo genetic blockage of CMA worsens atherosclerotic pathology through both systemic and cell-autonomous changes in vascular smooth muscle cells and macrophages, the two main cell types involved in atherogenesis.

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