Perturbed proteostasis in autism spectrum disorders.
Perturbed proteostasis in autism spectrum disorders.
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DOI：
10.1111/jnc.13723
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发表时间：
2016-12
影响因子：
4.7
通讯作者：
Osterweil EK
中科院分区：
文献类型：
--
作者：
Louros SR;Osterweil EK
突触强度的动态变化依赖于泛素蛋白酶体系统（UPS）的从头蛋白质合成和蛋白质降解。这些细胞过程中的任何一个被破坏都会导致突触可塑性和记忆形成的严重损害。编码mRNA翻译调节因子和UPS成员的几个基因的突变与自闭症谱系障碍发展的风险增加有关。这些突变可能导致突触处蛋白质稳态（蛋白质稳态）的类似失衡。这篇综述将总结最近的工作调查的UPS在突触可塑性的作用，并提出功能失调的蛋白质稳态是一个共同的后果，与自闭症谱系障碍的几个基因突变。 突触强度的动态变化依赖于泛素蛋白酶体系统（UPS）的从头蛋白质合成和蛋白质降解。这些细胞过程中的任何一个被破坏都会导致突触可塑性和记忆形成的严重损害。编码mRNA翻译（即FMR 1）和蛋白质降解（即UBE 3A）调节因子的几种基因突变与自闭症谱系障碍和智力残疾（ASD/ID）的风险增加有关。这些突变类似地破坏蛋白质稳态（蛋白质稳态）。补偿的变化，重置率的蛋白质稳态可能有助于ASD/ID的神经症状。本文综述了最近的工作调查的UPS在突触可塑性的作用，在amphiamatergic突触，并提出，功能失调的蛋白质稳态是一个共同的后果，与ASD的几个基因突变。 这篇文章是一个迷你评论系列的一部分：“突触功能和功能障碍在脑疾病”。
Dynamic changes in synaptic strength rely on de novo protein synthesis and protein degradation by the ubiquitin proteasome system (UPS). Disruption of either of these cellular processes will result in significant impairments in synaptic plasticity and memory formation. Mutations in several genes encoding regulators of mRNA translation and members of the UPS have been associated with an increased risk for the development of autism spectrum disorders. It is possible that these mutations result in a similar imbalance in protein homeostasis (proteostasis) at the synapse. This review will summarize recent work investigating the role of the UPS in synaptic plasticity at glutamatergic synapses, and propose that dysfunctional proteostasis is a common consequence of several genetic mutations linked to autism spectrum disorders. Dynamic changes in synaptic strength rely on de novo protein synthesis and protein degradation by the ubiquitin proteasome system (UPS). Disruption of either of these cellular processes will result in significant impairments in synaptic plasticity and memory formation. Mutations in several genes encoding regulators of mRNA translation (i.e. FMR1) and protein degradation (i.e. UBE3A) have been associated with an increased risk for autism spectrum disorders and intellectual disability (ASD/ID). These mutations similarly disrupt protein homeostasis (proteostasis). Compensatory changes that reset the rate of proteostasis may contribute to the neurological symptoms of ASD/ID. This review summarizes recent work investigating the role of the UPS in synaptic plasticity at glutamatergic synapses, and proposes that dysfunctional proteostasis is a common consequence of several genetic mutations linked to ASD. This article is part of a mini review series: “Synaptic Function and Dysfunction in Brain Diseases”.
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影响因子：
64.8
作者：
Bingol, Baris;Schuman, Erin M.
通讯作者：
Schuman, Erin M.
DOI：
10.1111/j.1460-9568.2009.06950.x
发表时间：
2009-10
期刊：
The European journal of neuroscience
影响因子：
--
作者：
Citri A;Soler-Llavina G;Bhattacharyya S;Malenka RC
通讯作者：
Malenka RC
影响因子：
4.5
作者：
Chahrour MH;Yu TW;Lim ET;Ataman B;Coulter ME;Hill RS;Stevens CR;Schubert CR;ARRA Autism Sequencing Collaboration;Greenberg ME;Gabriel SB;Walsh CA
通讯作者：
Walsh CA
DOI：
10.1523/jneurosci.1617-11.2011
发表时间：
2011-06-15
期刊：
The Journal of neuroscience : the official journal of the Society for Neuroscience
影响因子：
--
作者：
Bateup HS;Takasaki KT;Saulnier JL;Denefrio CL;Sabatini BL
通讯作者：
Sabatini BL
影响因子：
4.8
作者：
Cooper, EM;Hudson, AW;Howley, PM
通讯作者：
Howley, PM