Sumoylation: Implications for Neurodegenerative Diseases.

Autor: Anderson DB; Ipsen Bioinnovation Ltd, Units 4-10 The Quadrant, Barton Lane, Abingdon, OX14 3YS, UK., Zanella CA; Department of Pharmacology, Federal University of Santa Catarina, Campus Universitario - Trindade, Florianopolis, CEP, 88040-900, Brazil., Henley JM; MRC Centre for Synaptic Plasticity, School of Biochemistry, University of Bristol, University Walk, Bristol, BS8 1TD, UK., Cimarosti H; Department of Pharmacology, Federal University of Santa Catarina, Campus Universitario - Trindade, Florianopolis, CEP, 88040-900, Brazil. helena.cimarosti@ufsc.br.
Jazyk: angličtina
Zdroj: Advances in experimental medicine and biology [Adv Exp Med Biol] 2017; Vol. 963, pp. 261-281.
DOI: 10.1007/978-3-319-50044-7_16
Abstrakt: The covalent posttranslational modifications of proteins are critical events in signaling cascades that enable cells to efficiently, rapidly and reversibly respond to extracellular stimuli. This is especially important in the CNS where the processes affecting synaptic communication between neurons are highly complex and very tightly regulated. Sumoylation regulates the function and fate of a diverse array of proteins and participates in the complex cell signaling pathways required for cell survival. One of the most complex signaling pathways is synaptic transmission.Correct synaptic function is critical to the working of the brain and its alteration through synaptic plasticity mediates learning, mental disorders and stroke. The investigation of neuronal sumoylation is a new and exciting field and the functional and pathophysiological implications are far-reaching. Sumoylation has already been implicated in a diverse array of neurological disorders. Here we provide an overview of current literature highlighting recent insights into the role of sumoylation in neurodegeneration. In addition we present a brief assessment of drug discovery in the analogous ubiquitin system and extrapolate on the potential for development of novel therapies that might target SUMO-associated mechanisms of neurodegenerative disease.
Databáze: MEDLINE