Nature Search

Correction to: Isoform-selective phosphoinositide 3-kinase inhibition ameliorates a broad range of fragile X syndrome-associated deficits in a mouse model

Christina Gross
Anwesha Banerjee
Gary J. Bassell
Amendments and Corrections14 Jun 2022
Neuropsychopharmacology

Volume: 47, P: 1733
Muscleblind-like proteins use modular domains to localize RNAs by riding kinesins and docking to membranes

RNA localization is mediated by kinesin motors and anchoring. However, mechanisms underlying specificity are unclear. Here, the authors find that MBNL protein’s zinc fingers prefer specific kinesins, and its unstructured tail mediates membrane anchoring.

Ryan P. Hildebrandt
Kathryn R. Moss
Eric T. Wang
ResearchOpen Access09 Jun 2023
Nature Communications

Volume: 14, P: 1-19
Single molecule–sensitive probes for imaging RNA in live cells

Upon binding multiple fluorophores and being complexed into tetramers, these RNA imaging probes show high sensitivity and can detect single endogenous RNA molecules at low probe concentration.

Philip J Santangelo
Aaron W Lifland
James E Crowe Jr
Research06 Apr 2009
Nature Methods

Volume: 6, P: 347-349
CRISPR-mediated gene correction links the ATP7A M1311V mutations with amyotrophic lateral sclerosis pathogenesis in one individual

Yeomin Yun, Sung-Ah Hong et al. compare the whole-genome sequence from a male with amyotrophic lateral sclerosis (ALS) to his healthy parents, identifying the M1311V variant in the X-lined ATP7A gene. They show that CRISPR-mediated gene correction in patient-derived neurons rescues neuronal activity.

Yeomin Yun
Sung-Ah Hong
Yoon Ha
ResearchOpen Access20 Jan 2020
Communications Biology

Volume: 3, P: 1-10
Therapeutic Strategies in Fragile X Syndrome: Dysregulated mGluR Signaling and Beyond

Christina Gross
Elizabeth M Berry-Kravis
Gary J Bassell
Reviews27 Jul 2011
Neuropsychopharmacology

Volume: 37, P: 178-195
Isoform-selective phosphoinositide 3-kinase inhibition ameliorates a broad range of fragile X syndrome-associated deficits in a mouse model

Christina Gross
Anwesha Banerjee
Gary J. Bassell
Research13 Jul 2018
Neuropsychopharmacology

Volume: 44, P: 324-333
Spatial regulation of β-actin translation by Src-dependent phosphorylation of ZBP1

Stefan Hüttelmaier
Daniel Zenklusen
Robert H. Singer
Research24 Nov 2005
Nature

Volume: 438, P: 512-515
Remembering Stephen T. Warren, a pillar of neurogenetics (1953–2021)

Peng Jin
Gary J. Bassell
Comments & Opinion13 Sept 2021
Nature Neuroscience

Volume: 24, P: 1340-1341
Biased modulators of NMDA receptors control channel opening and ion selectivity

A series of positive allosteric modulators of NMDA receptors that can increase agonist potency, increase channel-open probability, and slow receptor deactivation can also decrease single-channel conductance and decrease calcium permeability.

Riley E. Perszyk
Sharon A. Swanger
Stephen F. Traynelis
Research20 Jan 2020
Nature Chemical Biology

Volume: 16, P: 188-196
Efficient generation of a self-organizing neuromuscular junction model from human pluripotent stem cells

Here, Urzi et al. pioneered a 2D self-organizing neuromuscular junction (soNMJ) model from human pluripotent stem cells, with implications for neuromuscular disease modeling and drug screening approaches.

Alessia Urzi
Ines Lahmann
Mina Gouti
ResearchOpen Access19 Dec 2023
Nature Communications

Volume: 14, P: 1-15
Reducing glutamate signaling pays off in fragile X

A recent theory about the basis for fragile X syndrome is now validated in a mouse model. The findings point the way to treatment options targeting group 1 metabotropic glutamate receptors.

Gary J Bassell
Christina Gross
News & Views01 Mar 2008
Nature Medicine

Volume: 14, P: 249-250
Fragile balance: RNA editing tunes the synapse

Orchestration of gene expression enables coordination between the nucleus and synapses. A report now uncovers a function for the fragile X mental retardation protein in RNA editing necessary for synaptic development.

Gary J Bassell
News & Views23 Nov 2011
Nature Neuroscience

Volume: 14, P: 1492-1494
A native function for RAN translation and CGG repeats in regulating fragile X protein synthesis

Rodriguez et al. define a native role for RAN translation and CGG repeats in regulating mGluR-dependent fragile X protein (FMRP) synthesis. RAN-blocking antisense oligonucleotides increase FMRP and improve survival of neurons from patients with repeat expansions.

Caitlin M. Rodriguez
Shannon E. Wright
Peter K. Todd
Research17 Feb 2020
Nature Neuroscience

Volume: 23, P: 386-397
A human forebrain organoid model of fragile X syndrome exhibits altered neurogenesis and highlights new treatment strategies

Using a human forebrain organoid model of fragile X syndrome, Kang et al. reveal a critical role of FMRP in human brain development and identify a large number of human-specific mRNAs that could be regulated by FMRP.

Yunhee Kang
Ying Zhou
Zhexing Wen
Research19 Aug 2021
Nature Neuroscience

Volume: 24, P: 1377-1391
An essential role for β-actin mRNA localization and translation in Ca²⁺-dependent growth cone guidance

Jiaqi Yao
Yukio Sasaki
James Q Zheng
Research17 Sept 2006
Nature Neuroscience

Volume: 9, P: 1265-1273
Dysregulation and restoration of translational homeostasis in fragile X syndrome

Fragile X syndrome (FXS) results from the loss of the RNA-binding protein fragile X mental retardation protein (FMRP). Here, Klann and colleagues discuss the ways in which FMRP loss disrupts mRNA translation in the brain and the outcomes of genetic and pharmacological attempts to reset translational homeostasis in FXS model mice.

Joel D. Richter
Gary J. Bassell
Eric Klann
Reviews09 Sept 2015
Nature Reviews Neuroscience

Volume: 16, P: 595-605
Genetic and acute CPEB1 depletion ameliorate fragile X pathophysiology

Fragile X syndrome (FXS) is a neurodevelopmental disorder caused by loss of the translational repressor protein FMRP. Now, Joel D. Richter and his colleagues report that knocking down the expression of the translational activator protein CPEB can restore normal levels of translation and rescue behavioral deficits in a mouse model of FXS.

Tsuyoshi Udagawa
Natalie G Farny
Joel D Richter
Research20 Oct 2013
Nature Medicine

Volume: 19, P: 1473-1477
Mutations in the profilin 1 gene cause familial amyotrophic lateral sclerosis

Mutations in the profilin 1 (PFN1) gene, which is crucial for the conversion of monomeric to filamentous actin, can cause familial amyotrophic lateral sclerosis, suggesting that alterations in cytoskeletal pathways contribute to disease pathogenesis.

Chi-Hong Wu
Claudia Fallini
John E. Landers
Research15 Jul 2012
Nature

Volume: 488, P: 499-503
Convergent and distributed effects of the 3q29 deletion on the human neural transcriptome

Esra Sefik
Ryan H. Purcell
Jennifer G. Mulle
ResearchOpen Access15 Jun 2021
Translational Psychiatry

Volume: 11, P: 1-14
ZBP1 phosphorylation at serine 181 regulates its dendritic transport and the development of dendritic trees of hippocampal neurons

Anna S. Urbanska
Aleksandra Janusz-Kaminska
Jacek Jaworski
ResearchOpen Access12 May 2017
Scientific Reports

Volume: 7, P: 1-11
Metabolic effects of the schizophrenia-associated 3q29 deletion

Rebecca M. Pollak
Ryan H. Purcell
Jennifer G. Mulle
ResearchOpen Access17 Feb 2022
Translational Psychiatry

Volume: 12, P: 1-10
Behavioral changes and growth deficits in a CRISPR engineered mouse model of the schizophrenia-associated 3q29 deletion

Timothy P. Rutkowski
Ryan H. Purcell
Jennifer Gladys Mulle
Research11 Apr 2019
Molecular Psychiatry

Volume: 26, P: 772-783
Deep phenotyping in 3q29 deletion syndrome: recommendations for clinical care

Rossana Sanchez Russo
Michael J. Gambello
Jennifer Gladys Mulle
ResearchOpen Access09 Feb 2021
Genetics in Medicine

Volume: 23, P: 872-880

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