Fyn Tyrosine Kinase as Harmonizing Factor in Neuronal Functions and Dysfunctions.
Alzheimer’s disease
Fyn tyrosine kinase
neurodegeneration
plexins
semaphorins
synaptic plasticity
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
22 Jun 2020
22 Jun 2020
Historique:
received:
18
05
2020
revised:
19
06
2020
accepted:
20
06
2020
entrez:
26
6
2020
pubmed:
26
6
2020
medline:
20
3
2021
Statut:
epublish
Résumé
Fyn is a non-receptor or cytoplasmatic tyrosine kinase (TK) belonging to the Src family kinases (SFKs) involved in multiple transduction pathways in the central nervous system (CNS) including synaptic transmission, myelination, axon guidance, and oligodendrocyte formation. Almost one hundred years after the original description of Fyn, this protein continues to attract extreme interest because of its multiplicity of actions in the molecular signaling pathways underlying neurodevelopmental as well as neuropathologic events. This review highlights and summarizes the most relevant recent findings pertinent to the role that Fyn exerts in the brain, emphasizing aspects related to neurodevelopment and synaptic plasticity. Fyn is a common factor in healthy and diseased brains that targets different proteins and shapes different transduction signals according to the neurological conditions. We will primarily focus on Fyn-mediated signaling pathways involved in neuronal differentiation and plasticity that have been subjected to considerable attention lately, opening the fascinating scenario to target Fyn TK for the development of potential therapeutic interventions for the treatment of CNS injuries and certain neurodegenerative disorders like Alzheimer's disease.
Identifiants
pubmed: 32580508
pii: ijms21124444
doi: 10.3390/ijms21124444
pmc: PMC7352836
pii:
doi:
Substances chimiques
Proto-Oncogene Proteins c-fyn
EC 2.7.10.2
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : MIUR/PRIN2017
ID : 2017T9JNLT
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