Pharmacogenetic inhibition of eIF4E-dependent Mmp9 mRNA translation reverses fragile X syndrome-like phenotypes. - Wikidata - wikimedia - TriplyDB

Pharmacogenetic inhibition of eIF4E-dependent Mmp9 mRNA translation reverses fragile X syndrome-like phenotypes.

Pharmacogenetic inhibition of eIF4E-dependent Mmp9 mRNA translation reverses fragile X syndrome-like phenotypes.

http://www.wikidata.org/entity/Q34959355

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Signalling to eIF4E in cancer Characterizing autism spectrum disorders by key biochemical pathways.Dysregulation and restoration of translational homeostasis in fragile X syndrome Dysregulation of Mammalian Target of Rapamycin Signaling in Mouse Models of Autism Activity dependent CAM cleavage and neurotransmission A delicate balance: role of MMP-9 in brain development and pathophysiology of neurodevelopmental disorders Matrix metalloproteinase-9 deletion rescues auditory evoked potential habituation deficit in a mouse model of Fragile X Syndrome Selective Disruption of Metabotropic Glutamate Receptor 5-Homer Interactions Mimics Phenotypes of Fragile X Syndrome in Mice.Adenosine Monophosphate-activated Protein Kinase (AMPK) Activators For the Prevention, Treatment and Potential Reversal of Pathological Pain.The Role of Proteases in Hippocampal Synaptic Plasticity: Putting Together Small Pieces of a Complex Puzzle.Multifaceted Roles of Metzincins in CNS Physiology and Pathology: From Synaptic Plasticity and Cognition to Neurodegenerative Disorders Proteolytic regulation of synaptic plasticity in the mouse primary visual cortex: analysis of matrix metalloproteinase 9 deficient mice Persistent astrocyte activation in the fragile X mouse cerebellum Targeting Translation Control with p70 S6 Kinase 1 Inhibitors to Reverse Phenotypes in Fragile X Syndrome Mice.miR-132 Regulates Dendritic Spine Structure by Direct Targeting of Matrix Metalloproteinase 9 mRNA.mTOR, a Potential Target to Treat Autism Spectrum Disorder.Protease induced plasticity: matrix metalloproteinase-1 promotes neurostructural changes through activation of protease activated receptor 1 Current Perspectives in Autism Spectrum Disorder: From Genes to Therapy.Dysfunctional mTORC1 Signaling: A Convergent Mechanism between Syndromic and Nonsyndromic Forms of Autism Spectrum Disorder?Matrix Metalloproteinase-9 as a Novel Player in Synaptic Plasticity and Schizophrenia.mTOR in health and in sickness.MMP-9 in translation: from molecule to brain physiology, pathology, and therapy.Oxytocin and Animal Models for Autism Spectrum Disorder.Genetic and Pharmacological Reversibility of Phenotypes in Mouse Models of Autism Spectrum Disorder.A normal genetic variation modulates synaptic MMP-9 protein levels and the severity of schizophrenia symptoms Unifying Views of Autism Spectrum Disorders: A Consideration of Autoregulatory Feedback Loops.Mavoglurant in fragile X syndrome: Results of two randomized, double-blind, placebo-controlled trials.Targeting AMPK for the Alleviation of Pathological Pain.Social propinquity in rodents as measured by tube cooccupancy differs between inbred and outbred genotypes.Astrocytic Contributions to Synaptic and Learning Abnormalities in a Mouse Model of Fragile X Syndrome.Genetic Reduction of Matrix Metalloproteinase-9 Promotes Formation of Perineuronal Nets Around Parvalbumin-Expressing Interneurons and Normalizes Auditory Cortex Responses in Developing Fmr1 Knock-Out Mice.Cell Type-Specific mRNA Dysregulation in Hippocampal CA1 Pyramidal Neurons of the Fragile X Syndrome Mouse Model.Overexpression of eIF4F components in meningiomas and suppression of meningioma cell growth by inhibiting translation initiation.The MNK-eIF4E Signaling Axis Contributes to Injury-Induced Nociceptive Plasticity and the Development of Chronic Pain.Metformin ameliorates core deficits in a mouse model of fragile X syndrome.Reducing eIF4E-eIF4G interactions restores the balance between protein synthesis and actin dynamics in fragile X syndrome model mice.eEF2K/eEF2 Pathway Controls the Excitation/Inhibition Balance and Susceptibility to Epileptic Seizures.Strategies to advance drug discovery in rare monogenic intellectual disability syndromes.Loss of eIF4E phosphorylation engenders depression-like behaviors via selective mRNA translation.eIF4E Phosphorylation Influences Bdnf mRNA Translation in Mouse Dorsal Root Ganglion Neurons.

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P2860

Pharmacogenetic inhibition of eIF4E-dependent Mmp9 mRNA translation reverses fragile X syndrome-like phenotypes.

http://www.wikidata.org/entity/Q34959355

description

2014 nî lūn-bûn

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2014 թուականի Նոյեմբերին հրատարակուած գիտական յօդուած

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2014 թվականի նոյեմբերին հրատարակված գիտական հոդված

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2014年の論文

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Pharmacogenetic inhibition of ...... le X syndrome-like phenotypes.

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Pharmacogenetic inhibition of ...... le X syndrome-like phenotypes.

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Pharmacogenetic inhibition of ...... le X syndrome-like phenotypes.

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J.CELREP.2014.10.064

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Pharmacogenetic inhibition of ...... le X syndrome-like phenotypes.

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Apostolia Fragkouli

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Archontia Kaminari

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Arkady Khoutorsky

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Athina K Tzinia

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Bruce W Konicek

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Jean-Claude Lacaille

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Jeremy R Graff

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Karim Nader

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Masha Prager-Khoutorsky

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Nikolaos Giannakas

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P2860

Mitogen-activated protein kinases activate the serine/threonine kinases Mnk1 and Mnk2

What can we learn about autism from studying fragile X syndrome?

FMRP stalls ribosomal translocation on mRNAs linked to synaptic function and autism

Synaptic circuit remodelling by matrix metalloproteinases in health and disease

FMRP targets distinct mRNA sequence elements to regulate protein expression

Translational control by MAPK signaling in long-term synaptic plasticity and memory

Global prevalence of autism and other pervasive developmental disorders

Identification of a gene (FMR-1) containing a CGG repeat coincident with a breakpoint cluster region exhibiting length variation in fragile X syndrome

Upstream and downstream of mTOR

Control of synaptic plasticity and memory via suppression of poly(A)-binding protein

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Theodore J. Price

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2014-11-26T00:00:00Z

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