FMRP stalls ribosomal translocation on mRNAs linked to synaptic function and autism
Jennifer C. Darnell,Sarah J. Van Driesche,Chaolin Zhang,Ka Ying Sharon Hung,Aldo Mele,Claire E. Fraser,Elizabeth F. Stone,Cynthia Chen,John J. Fak,Sung Wook Chi,Donny D. Licatalosi,Joel D. Richter,Robert B. Darnell,Robert B. Darnell +13 more
TLDR
A brain polyribosome-programmed translation system is developed, revealing that FMRP reversibly stalls ribosomes specifically on its target mRNAs and suggests multiple targets for clinical intervention in FXS and ASD.About:
This article is published in Cell.The article was published on 2011-07-22 and is currently open access. It has received 1861 citations till now. The article focuses on the topics: FMR1 & RNA-binding protein.read more
Citations
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Reversal of ultrasonic vocalization deficits in a mouse model of Fragile X Syndrome with minocycline treatment or genetic reduction of MMP-9.
TL;DR: Results suggest that minocycline may reverse USV call rate deficits in Fmr1 KO mice through attenuation of MMP-9 levels, which is thought to be effective in reducing FXS symptoms by lowering matrix-metalloproteinase-9 (MMP- 9) levels.
Journal ArticleDOI
Dynamic landscape of the local translation at activated synapses.
Tamara M. Khlebodarova,Vladislav V. Kogai,E A Trifonova,Vitaly A. Likhoshvai,Vitaly A. Likhoshvai +4 more
TL;DR: The results suggest that autistic disorders associated with mTOR pathway hyperactivation may be due to impaired proteome stability associated with the formation of complex dynamic regimes of PSD protein synthesis in response to stimulation of mGluR receptors on the postsynaptic membrane of excitatory synapses on pyramidal hippocampal cells.
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The mTOR Signaling Pathway Activity and Vitamin D Availability Control the Expression of Most Autism Predisposition Genes.
TL;DR: It is hypothesized that genetic and/or environment mTOR hyperactivation, including provocation by vitamin D deficiency, might be a common mechanism controlling the expressivity of most autism predisposition genes and even core symptoms of autism.
Journal ArticleDOI
Polysomes identified by live imaging of nascent peptides are stalled in hippocampal and cortical neurites.
TL;DR: The SunTag technique corroborates in situ evidence of stalled polysomes and will allow for the live examination of these translational structures as a mechanism for mRNA transport and regulated protein synthesis.
Journal ArticleDOI
Seizure-Induced Regulations of Amyloid-β, STEP61, and STEP61 Substrates Involved in Hippocampal Synaptic Plasticity.
TL;DR: It is proposed that upregulation of STEP61 and downregulation of GluN2B and ERK 1/2 phosphorylation mediate compensatory weakening of synaptic strength in response to acute enhancement of hippocampal network activity, whereas delayed decrease in ERK1/2 expression and increase in APP and Aβ expression may contribute to the maintenance of this synaptic weakening.
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