Federico Sesti is an Italian-born neuroscientist and academic at the Robert Wood Johnson Medical School of Rutgers University.[1][2][3]

Federico Sesti
Born
NationalityAmerican
Alma materUniversity of Genoa
Occupation(s)Academic
Neuroscientist

Biography

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Sesti obtained his Laurea and Ph.D. in physics from the University of Genoa.[4][5] Following this, he conducted postdoctoral research at the Institut für Biologische Informationsverarbeitung, Forschungszentrum Jülich in Germany under Benjamin Kaupp and at Yale University in the USA under Steve Goldstein.[4][5] He joined the faculty of the Robert Wood Johnson Medical School in 2001.[4]

Sesti has been recognized as a Fulbright Scholar and is a member of various scientific societies.[4][6] Additionally, Sesti serves on the editorial boards of several journals and serves on panels of several international, federal, and private funding agencies.[4]

Research

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His research topics include ion channels, potassium channels, aging, oxidative stress, reactive oxygen species (ROS), Srctyrosine kinases, C. Elegans, and cell signaling.[7][4][8]

Sesti's laboratory has conducted research on the non-conducting functions of ion channels, focusing on the molecular mechanisms of neuronal aging in vertebrates and invertebrates.[4] Specifically, the lab has studied how excess oxidants affect K+ channels and the role this plays in the decline of neuronal function during aging and in neurodegenerative diseases.[4]

Selected publications

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  • Vitali et al. "Apoptotic cell death in disease--current understanding of the NCCD 2023" Cell Death & Differentiation. doi:10.1038/s41418-023-01153-w.
  • Forzisi et al. "Antagonistic roles of Ras-MAPK and Akt signaling in Integrin-K+ channel Complexes-mediated cellular apoptosis" The FASEB Journal. doi:10.1096/fj.20220 0180R
  • Wei Y. et al. "Oxidation of KCNB1 channels in the human brain and in mouse model of Alzheimer's disease". Cell Death & Differentiation. doi:10.1038/s41419-018-0886-1
  • Sesti F. Oxidation of Ion Channels in the Aging Process. ISBN 9781138196971
  • Sesti F. "Oxidation of K+ channels in aging and neurodegeneration". Aging and Disease. doi:10.14336/AD.2015.0901.
  • Cotella D. et al. "Toxic role of K+ channel oxidation in mammalian brain". The Journal of Neuroscience, doi:10.1523/JNEUROSCI.6153-11.2012.
  • Sesti F. et al. "Oxidation of K+ channels by ROS: a general mechanism of aging and neurodegeneration?". Trends in Cell Biology, doi:10.1016/j.tcb.2009.09.008
  • Cai S. and F. Sesti. "Oxidation of a potassium channel causes progressive sensory function loss during aging". Nature Neuroscience. doi:10.1038/nn.2291
  • Park K. and F. Sesti (2007). "An arrhythmia susceptibility gene in Caenorhabditis elegans" Journal of Biological Chemistry. doi:10.1074/jbc.M701625200.
  • Cai S. et al. "MPS-1 is a K+ channel β-subunit and a serine/threonine kinase". Nature Neuroscience. doi:10.1038/nn1557
  • Park K., et al. "Single-walled carbon nanotubes: A new class of ion-channel blockers". Journal of Biological Chemistry. Dec 12;278(50):50212-6 doi:10.1074/jbc.M310216200
  • Sesti F. et al. "A common polymorphism associated with cardiac arrhythmia increases sensitivity to a common antibiotic". Proceedings of the National Academy of Sciences of the United States of America, doi:10.1073/pnas.180223197
  • Abbot G.W. et al. "MiRP1 forms Ikr potassium channels with HERG and is associated with cardiac arrhythmia". Cell, doi:10.1016/s0092-8674(00)80728-x
  • Sesti F. and S.A.N. Goldstein "Single-channel characteristics of wildtype Iks channels and channels formed with two MinK mutants that cause long QT syndrome". The Journal of General Physiology, doi:10.1085/jgp.112.6.651.

References

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