Worming forward: amyotrophic lateral sclerosis toxicity mechanisms and genetic interactions in Caenorhabditis elegans. - Wikidata - wikimedia - TriplyDB

Worming forward: amyotrophic lateral sclerosis toxicity mechanisms and genetic interactions in Caenorhabditis elegans.

Worming forward: amyotrophic lateral sclerosis toxicity mechanisms and genetic interactions in Caenorhabditis elegans.

http://www.wikidata.org/entity/Q38214677

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ALS Patient Stem Cells for Unveiling Disease Signatures of Motoneuron Susceptibility: Perspectives on the Deadly Mitochondria, ER Stress and Calcium Triad Tau mutant A152T, a risk factor for FTD/PSP, induces neuronal dysfunction and reduced lifespan independently of aggregation in a C. elegans Tauopathy model INaP selective inhibition reverts precocious inter- and motorneurons hyperexcitability in the Sod1-G93R zebrafish ALS model Modelling amyotrophic lateral sclerosis: progress and possibilities Royal jelly promotes DAF-16-mediated proteostasis to tolerate β-amyloid toxicity in C. elegans model of Alzheimer's disease.ALS/FTLD: experimental models and reality.FET proteins regulate lifespan and neuronal integrity.Rescue of ATXN3 neuronal toxicity in Caenorhabditiselegans by chemical modification of endoplasmic reticulum stress.Neurodegeneration in C. elegans models of ALS requires TIR-1/Sarm1 immune pathway activation in neurons.

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Worming forward: amyotrophic lateral sclerosis toxicity mechanisms and genetic interactions in Caenorhabditis elegans.

http://www.wikidata.org/entity/Q38214677

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FGENE.2014.00085

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Frontiers in Genetics

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Worming forward: amyotrophic l ...... ons in Caenorhabditis elegans.

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Martine Therrien

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

Identification of novel human genes evolutionarily conserved in Caenorhabditis elegans by comparative proteomics

Ataxin-2 intermediate-length polyglutamine expansions are associated with increased risk for ALS

C9ORF72, implicated in amytrophic lateral sclerosis and frontotemporal dementia, regulates endosomal trafficking

Heritable genome editing in C. elegans via a CRISPR-Cas9 system.

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

Lessons from C. elegans: signaling pathways for longevity

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

Mutations in prion-like domains in hnRNPA2B1 and hnRNPA1 cause multisystem proteinopathy and ALS

ALS-associated fused in sarcoma (FUS) mutations disrupt Transportin-mediated nuclear import

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85

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scholarly article

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10.3389/FGENE.2014.00085

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amyotrophic lateral sclerosis

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