Targeted degradation of sense and antisense C9orf72 RNA foci as therapy for ALS and frontotemporal degeneration. - Wikidata - awgldk - TriplyDB

Targeted degradation of sense and antisense C9orf72 RNA foci as therapy for ALS and frontotemporal degeneration.

Targeted degradation of sense and antisense C9orf72 RNA foci as therapy for ALS and frontotemporal degeneration.

http://www.wikidata.org/entity/Q37340843

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From animal models to human disease: a genetic approach for personalized medicine in ALS The hnRNP family: insights into their role in health and disease There has been an awakening: Emerging mechanisms of C9orf72 mutations in FTD/ALS Dysregulated axonal RNA translation in amyotrophic lateral sclerosis Toward precision medicine in amyotrophic lateral sclerosis Phenotypic Heterogeneity of Monogenic Frontotemporal Dementia Modeling ALS and FTD with iPSC-derived neurons Clinical Trial Designs in Amyotrophic Lateral Sclerosis: Does One Design Fit All?Modeling diseases of noncoding unstable repeat expansions using mutant pluripotent stem cells.C9orf72's Interaction with Rab GTPases-Modulation of Membrane Traffic and Autophagy TDP-43 Proteinopathy and ALS: Insights into Disease Mechanisms and Therapeutic Targets.Emerging mechanisms of molecular pathology in ALS RNA-mediated pathogenic mechanisms in polyglutamine diseases and amyotrophic lateral sclerosis G-quadruplexes: Emerging roles in neurodegenerative diseases and the non-coding transcriptome C9orf72-related disorders: expanding the clinical and genetic spectrum of neurodegenerative diseases Drosophila as an In Vivo Model for Human Neurodegenerative Disease Glycine-alanine dipeptide repeat protein contributes to toxicity in a zebrafish model of C9orf72 associated neurodegeneration Approaches to Validate and Manipulate RNA Targets with Small Molecules in Cells Loss of C9ORF72 impairs autophagy and synergizes with polyQ Ataxin-2 to induce motor neuron dysfunction and cell death A C9ORF72/SMCR8-containing complex regulates ULK1 and plays a dual role in autophagy The ALS/FTLD associated protein C9orf72 associates with SMCR8 and WDR41 to regulate the autophagy-lysosome pathway.Loss of C9orf72 Enhances Autophagic Activity via Deregulated mTOR and TFEB Signaling The C9orf72 repeat expansion disrupts nucleocytoplasmic transport.Frontotemporal Dementia.Gene expression profiling for human iPS-derived motor neurons from sporadic ALS patients reveals a strong association between mitochondrial functions and neurodegeneration.Toxic PR Poly-Dipeptides Encoded by the C9orf72 Repeat Expansion Target LC Domain Polymers.Bioinformatics Data Mining Approach Suggests Coexpression of AGTPBP1 with an ALS-linked Gene C9orf72.Neuropathology of Amyotrophic Lateral Sclerosis and Its Variants.C9ORF72 hexanucleotide repeat exerts toxicity in a stable, inducible motor neuronal cell model, which is rescued by partial depletion of Pten.Exploring the effect of sequence length and composition on allele-selective inhibition of human huntingtin expression by single-stranded silencing RNAs Evaluation of Antisense Oligonucleotides Targeting ATXN3 in SCA3 Mouse Models C9orf72 nucleotide repeat structures initiate molecular cascades of disease.RNA metabolism in neurodegenerative disease.Modelling amyotrophic lateral sclerosis: progress and possibilities Sequestration of multiple RNA recognition motif-containing proteins by C9orf72 repeat expansions The role of long non-coding RNAs in neurodevelopment, brain function and neurological disease Molecular network analysis suggests a logical hypothesis for the pathological role of c9orf72 in amyotrophic lateral sclerosis/frontotemporal dementia.C9orf72 hypermethylation protects against repeat expansion-associated pathology in ALS/FTD.C9orf72 amyotrophic lateral sclerosis and frontotemporal dementia: gain or loss of function?RNA-protein interactions in unstable microsatellite diseases.

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Targeted degradation of sense and antisense C9orf72 RNA foci as therapy for ALS and frontotemporal degeneration.

http://www.wikidata.org/entity/Q37340843

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bilimsel makale

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scientific article published on 29 October 2013

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vedecký článok

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vetenskaplig artikel

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videnskabelig artikel

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vědecký článek

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name

Targeted degradation of sense ...... d frontotemporal degeneration.

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Targeted degradation of sense ...... d frontotemporal degeneration.

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Targeted degradation of sense ...... d frontotemporal degeneration.

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Targeted degradation of sense ...... d frontotemporal degeneration.

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Targeted degradation of sense ...... d frontotemporal degeneration.

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Targeted degradation of sense ...... d frontotemporal degeneration.

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PNAS.1318835110

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Proceedings of the National Academy of Sciences of the United States of America

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Targeted degradation of sense ...... d frontotemporal degeneration.

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Andrew T Watt

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C Frank Bennett

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Don W Cleveland

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Donald P Pizzo

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Frank Rigo

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Gene W Yeo

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Hai-Ri Li

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Janet Cady

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Jie Jiang

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Jinsong Qiu

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P2860

Discovery of Novel DENN Proteins: Implications for the Evolution of Eukaryotic Intracellular Membrane Structures and Human Disease

Unconventional translation of C9ORF72 GGGGCC expansion generates insoluble polypeptides specific to c9FTD/ALS

Muscleblind-like 2-mediated alternative splicing in the developing brain and dysregulation in myotonic dystrophy

A natural antisense transcript at the Huntington's disease repeat locus regulates HTT expression

The product of C9orf72, a gene strongly implicated in neurodegeneration, is structurally related to DENN Rab-GEFs

Expanded GGGGCC hexanucleotide repeat in noncoding region of C9ORF72 causes chromosome 9p-linked FTD and ALS

A hexanucleotide repeat expansion in C9ORF72 is the cause of chromosome 9p21-linked ALS-FTD

Converging mechanisms in ALS and FTD: disrupted RNA and protein homeostasis

Origins and Mechanisms of miRNAs and siRNAs

Ubiquitinated TDP-43 in frontotemporal lobar degeneration and amyotrophic lateral sclerosis

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10.1073/PNAS.1318835110

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47

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110

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Clotilde Lagier-Tourenne

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2013-10-29T00:00:00Z

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258148062

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24170860

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amyotrophic lateral sclerosis

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