Roberta Felici

ORCID: 0000-0002-3457-717X
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About
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Research Areas
  • PARP inhibition in cancer therapy
  • Mitochondrial Function and Pathology
  • Sirtuins and Resveratrol in Medicine
  • Cancer, Hypoxia, and Metabolism
  • DNA Repair Mechanisms
  • ATP Synthase and ATPases Research
  • Neuroblastoma Research and Treatments
  • Amyotrophic Lateral Sclerosis Research
  • Cardiac electrophysiology and arrhythmias
  • Ion Channels and Receptors
  • Calcium signaling and nucleotide metabolism
  • Histone Deacetylase Inhibitors Research
  • Thermal Regulation in Medicine
  • Advanced Glycation End Products research
  • Lung Cancer Research Studies
  • CRISPR and Genetic Engineering
  • Neuroscience of respiration and sleep
  • Inflammasome and immune disorders
  • RNA modifications and cancer
  • Adrenal and Paraganglionic Tumors
  • Neurogenetic and Muscular Disorders Research
  • Coenzyme Q10 studies and effects
  • Neuroendocrine regulation and behavior
  • Metabolism and Genetic Disorders
  • Thermoregulation and physiological responses

University of Florence
2012-2018

Queen Mary University of London
2013

During the last several years, evidence that various enzymes hydrolyze NAD into bioactive products prompted scientists to revisit or design strategies able increase intracellular availability of dinucleotide. However, plasma membrane permeability and mitochondrial origin dinucleotide still wait be clearly defined. Here, we report contents increased upon exposure cell lines primary cultures exogenous (eNAD). precursors could not reproduce effects eNAD, they were found in incubating medium...

10.1124/mol.111.073916 article EN Molecular Pharmacology 2011-09-14

Poly(ADP-ribose) polymerase-1 (PARP-1) is a NAD-consuming enzyme with an emerging key role in epigenetic regulation of gene transcription. Although PARP-1 expression characteristically restricted to the nucleus, few studies report mitochondrial localization and its ability regulate organelle functioning. Here, we show that, despite exclusive nuclear PARP-1, homeostasis compromised cell lines exposed pharmacological inhibitors or small interfering RNA. suppression reduces integrity DNA...

10.1124/mol.110.070110 article EN Molecular Pharmacology 2011-03-11

Among the enzymes involved in NAD homeostasis, nicotinamide mononucleotide adenylyltransferases (NMNAT1-3) are central to intracellular formation. Although NMNAT3 is postulated be a mitochondrial enzyme contributing NAD-dependent organelle functioning, information on endogenous proteins lacking. We report that human cells single gene nmnat3 localized chromosome 3 codes for two mRNA splice variants NMNATv1 and FKSG76, whereas previously reported NMNAT3v2 transcript not present. However,...

10.1371/journal.pone.0076938 article EN cc-by PLoS ONE 2013-10-14

Although treatment of stroke patients with mild hypothermia is a promising therapeutic approach, chemicals inducing prompt and safe reduction body temperature are an unmet need. We measured the effects transient receptor potential vanilloid-1 (TRPV1) agonist rinvanil on thermoregulation ischemic brain injury in mice. Intraperitoneal or intracerebroventricular injection induces that prevented by antagonist capsazepine. Both intraischemic postischemic treatments provide permanent...

10.1038/jcbfm.2012.36 article EN Journal of Cerebral Blood Flow & Metabolism 2012-03-21

Therapeutic hypothermia is of relevance to treatment increased body temperature and brain injury, but drugs inducing selective, rapid, safe cooling in humans are not available. Here, we show that injections adenosine 5′-monophosphate (AMP), an endogenous nucleotide, promptly triggers mice by directly activating A1 receptors (A1R) within the preoptic area (POA) hypothalamus. Inhibition constitutive degradation extracellular AMP targeting ecto 5′-nucleotidase, also suffices prompt rodents....

10.1038/jcbfm.2012.157 article EN Journal of Cerebral Blood Flow & Metabolism 2012-10-24

Mitochondrial disorders are devastating genetic diseases for which efficacious therapies still an unmet need. Recent studies report that increased availability of intracellular NAD obtained by inhibition the NAD-consuming enzyme poly(ADP-ribose) polymerase (PARP)-1 or supplementation with NAD-precursor nicotinamide riboside (NR) ameliorates energetic derangement and symptoms in mouse models mitochondrial disorders. Whether these pharmacological approaches also improve bioenergetics human...

10.1124/mol.114.097204 article EN Molecular Pharmacology 2015-03-18

Purpose.: We evaluated the potential protective effects of Coenzyme Q10 (CoQ10) on human corneal cells and rabbit eyes after ultraviolet B (UVB) exposure a model wound healing in epithelium removal. Methods.: Human (HCE) were exposed to source UVB radiation (312 nM) presence different CoQ10 concentrations or vehicle. The mitochondrial function cell survival by means 3-(4,5-dimethylthiazole-2-yl)2,5-diphenyl-tetrazolium (MTT) reduction lactic dehydrogenase (LDH) release. Furthermore,...

10.1167/iovs.14-15306 article EN Investigative Ophthalmology & Visual Science 2014-10-10

NAD biosynthesis is emerging as a key regulator of immune cell functions. Accordingly, inhibitors the NAD‐synthesizing enzyme nicotinamide phosphoribosyltransferase (NAMPT) have anti‐inflammatory effects, counteract hematological malignancies and are being tested in clinical trials. Still, their effect on different types still waits to be fully investigated. Here we show that NAMPT inhibitor FK866 induces depletion various mouse organs but selectively causes dramatic atrophy spleen red pulp....

10.1038/icb.2013.85 article EN Immunology and Cell Biology 2013-11-26

Among the enzymes involved in NAD homeostasis, nicotinamide mononucleotide adenylyltransferases (NMNAT1-3) are central to intracellular formation.Although NMNAT3 is postulated be a mitochondrial enzyme contributing NADdependent organelle functioning, information on endogenous proteins lacking.We report that human cells single gene nmnat3 localized chromosome 3 codes for two mRNA splice variants NMNATv1 and FKSG76, whereas previously reported NMNAT3v2 transcript not present.However, NMNAT3v1...

10.1371/annotation/f5e6107f-a911-4c15-a881-7cb7e4946ff6 article EN cc-by PLoS ONE 2013-12-11
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