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dc.contributor.authorJoo, Yuyoung
dc.contributor.authorBenavides, David R
dc.date.accessioned2021-04-20T18:39:10Z
dc.date.available2021-04-20T18:39:10Z
dc.date.issued2021-03-10
dc.identifier.urihttp://hdl.handle.net/10713/15431
dc.description.abstractAutism spectrum disorder (ASD) is a heritable neurodevelopmental condition associated with impairments in social interaction, communication and repetitive behaviors. While the underlying disease mechanisms remain to be fully elucidated, dysfunction of neuronal plasticity and local translation control have emerged as key points of interest. Translation of mRNAs for critical synaptic proteins are negatively regulated by Fragile X mental retardation protein (FMRP), which is lost in the most common single-gene disorder associated with ASD. Numerous studies have shown that mRNA transport, RNA metabolism, and translation of synaptic proteins are important for neuronal health, synaptic plasticity, and learning and memory. Accordingly, dysfunction of these mechanisms may contribute to the abnormal brain function observed in individuals with autism spectrum disorder (ASD). In this review, we summarize recent studies about local translation and mRNA processing of synaptic proteins and discuss how perturbations of these processes may be related to the pathophysiology of ASD.en_US
dc.description.urihttps://doi.org/10.3390/ijms22062811en_US
dc.language.isoenen_US
dc.publisherMDPI AGen_US
dc.relation.ispartofInternational Journal of Molecular Sciencesen_US
dc.subjectRNA binding proteinen_US
dc.subjectRNA processingen_US
dc.subjectautismen_US
dc.subjectlocal translationen_US
dc.subjectneuronal plasticityen_US
dc.subjectsynaptic proteinen_US
dc.titleLocal Protein Translation and RNA Processing of Synaptic Proteins in Autism Spectrum Disorderen_US
dc.typeArticleen_US
dc.identifier.doi10.3390/ijms22062811
dc.identifier.pmid33802132
dc.source.volume22
dc.source.issue6
dc.source.countryUnited States
dc.source.countrySwitzerland


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