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Francesco Resta

Researcher at University of Florence

Publications -  23
Citations -  410

Francesco Resta is an academic researcher from University of Florence. The author has contributed to research in topics: Optogenetics & AMPA receptor. The author has an hindex of 11, co-authored 23 publications receiving 291 citations. Previous affiliations of Francesco Resta include European Laboratory for Non-Linear Spectroscopy.

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Kynurenic acid and zaprinast induce analgesia by modulating HCN channels through GPR35 activation.

TL;DR: GPR35 agonists, by reducing adenylate cyclase activity and inhibiting Ih in DRG neurons may represent a promising new group of analgesic drugs, and are tested in an in vivo model of PGE2-induced thermal hyperalgesia.
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Selective HCN1 block as a strategy to control oxaliplatin-induced neuropathy.

TL;DR: This study strengthens the evidence for a disease‐specific role ofHCN1 in CIPN, and proposes HCN1‐selective inhibitors as new‐generation pain medications with the desired efficacy and safety profile.
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Identification of the Nicotinamide Salvage Pathway as a New Toxification Route for Antimetabolites

TL;DR: The identification of Vacor as a substrate metabolized by the consecutive action of NAMPT and NMNAT2 into the NAD analog Vacor adenine dinucleotide (VAD) causes unprecedented rapid NAD depletion, glycolytic block, energy failure, and necrotic death of NM NAT2-proficient cancer cells.
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PARP-1 activation causes neuronal death in the hippocampal CA1 region by increasing the expression of Ca2 +-permeable AMPA receptors

TL;DR: The results show that activation of the nuclear enzyme PARP-1 may change the expression of membrane proteins and Ca(2+) permeability of AMPA channels, thus affecting the function and survival of CA1 pyramidal cells.
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Selective Blockade of HCN1/HCN2 Channels as a Potential Pharmacological Strategy Against Pain.

TL;DR: Selective blockade of HCN1/HCN2 channels, over HCN4 isoform, was able to modulate electrophysiological properties of DRG neurons similarly to that reported for classical Ih blockers, ivabradine, resulting in a pain-relieving activity.