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Stefano Moro

Researcher at University of Padua

Publications -  363
Citations -  12565

Stefano Moro is an academic researcher from University of Padua. The author has contributed to research in topics: Adenosine receptor & Receptor. The author has an hindex of 55, co-authored 329 publications receiving 10894 citations. Previous affiliations of Stefano Moro include Polaris Industries & University of North Carolina at Chapel Hill.

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Medicinal Chemistry and the Molecular Operating Environment (MOE): Application of QSAR and Molecular Docking to Drug Discovery

TL;DR: This work provides a brief description of a series of studies implemented in the software MOE (Molecular Operating Environment) with particular attention to the medicinal chemistry aspects.
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FAM/USP9x, a Deubiquitinating Enzyme Essential for TGFβ Signaling, Controls Smad4 Monoubiquitination

TL;DR: This study defines a regulative ubiquitination step controlling Smads that is parallel to those impinging on R-Smad phosphorylation, and points to Smad4 monoubiquitinated and deubiquitination as a way for cells to set their TGFbeta responsiveness.
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The mitochondrial calcium uniporter is a multimer that can include a dominant-negative pore-forming subunit.

TL;DR: The structural complexity of MCU is unveiled and a novel regulatory mechanism, based on the inclusion of dominant‐negative subunits in a multimeric channel, that underlies the fine control of the physiologically and pathologically relevant process of mitochondrial calcium homeostasis is demonstrated.
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Bridging Molecular Docking to Molecular Dynamics in Exploring Ligand-Protein Recognition Process: An Overview.

TL;DR: An overview of the evolution of structure-based drug discovery techniques in the study of ligand-target recognition phenomenon, going from the static molecular docking toward enhanced molecular dynamics strategies is presented.
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Ciprofloxacin and levofloxacin attenuate microglia inflammatory response via TLR4/NF-kB pathway.

TL;DR: CPFX and LVFX inhibited LPS-induced secretion of pro-inflammatory cytokines and activation of NF-κB in primary microglia and might facilitate the development of new molecules directed at the TLR4–MD-2 complex, a potential key target for controlling neuroinflammation.