Pages that link to "Q27342067"
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The following pages link to FUS transgenic rats develop the phenotypes of amyotrophic lateral sclerosis and frontotemporal lobar degeneration (Q27342067):
Displaying 50 items.
- Pathogenic mutation of UBQLN2 impairs its interaction with UBXD8 and disrupts endoplasmic reticulum-associated protein degradation (Q24339534) (← links)
- From animal models to human disease: a genetic approach for personalized medicine in ALS (Q26741250) (← links)
- Mechanisms of FUS mutations in familial amyotrophic lateral sclerosis (Q26749169) (← links)
- Dysregulated axonal RNA translation in amyotrophic lateral sclerosis (Q26753110) (← links)
- Converging mechanisms in ALS and FTD: disrupted RNA and protein homeostasis (Q26863439) (← links)
- The function of RNA-binding proteins at the synapse: implications for neurodegeneration (Q26991684) (← links)
- Mitochondrial dysfunction in amyotrophic lateral sclerosis - a valid pharmacological target? (Q27013585) (← links)
- Early lethality and neuronal proteinopathy in mice expressing cytoplasm-targeted FUS that lacks the RNA recognition motif. (Q27334411) (← links)
- Structural and energetic basis of ALS-causing mutations in the atypical proline–tyrosine nuclear localization signal of the Fused in Sarcoma protein (FUS) (Q27670694) (← links)
- Pathogenesis of FUS-associated ALS and FTD: insights from rodent models (Q28067147) (← links)
- The neurogenetics of alternative splicing (Q28069349) (← links)
- Emerging mechanisms of molecular pathology in ALS (Q28081239) (← links)
- Oxr1 improves pathogenic cellular features of ALS-associated FUS and TDP-43 mutations (Q28383058) (← links)
- FUS Interacts with HSP60 to Promote Mitochondrial Damage (Q28547727) (← links)
- Aberrant localization of FUS and TDP43 is associated with misfolding of SOD1 in amyotrophic lateral sclerosis (Q28730723) (← links)
- Reduced expression of BTBD10, an Akt activator, leads to motor neuron death (Q30519553) (← links)
- Overexpression of human wild-type FUS causes progressive motor neuron degeneration in an age- and dose-dependent fashion (Q30532680) (← links)
- Recruitment into stress granules prevents irreversible aggregation of FUS protein mislocalized to the cytoplasm (Q30559680) (← links)
- Expression of ALS-linked TDP-43 mutant in astrocytes causes non-cell-autonomous motor neuron death in rats (Q30575773) (← links)
- Characterization of genetic loss-of-function of Fus in zebrafish. (Q30836650) (← links)
- CRISPR/Cas9-mediated targeted gene correction in amyotrophic lateral sclerosis patient iPSCs. (Q33628110) (← links)
- AAV2 mediated retrograde transduction of corticospinal motor neurons reveals initial and selective apical dendrite degeneration in ALS. (Q33726831) (← links)
- Mutant human FUS Is ubiquitously mislocalized and generates persistent stress granules in primary cultured transgenic zebrafish cells (Q33727167) (← links)
- RNA metabolism in neurodegenerative disease. (Q33746283) (← links)
- The ALS gene FUS regulates synaptic transmission at the Drosophila neuromuscular junction. (Q33784500) (← links)
- Multistep process of FUS aggregation in the cell cytoplasm involves RNA-dependent and RNA-independent mechanisms. (Q34155410) (← links)
- Activity-dependent FUS dysregulation disrupts synaptic homeostasis (Q34480824) (← links)
- TDP-43 potentiates alpha-synuclein toxicity to dopaminergic neurons in transgenic mice (Q34648581) (← links)
- ALS-associated FUS mutations result in compromised FUS alternative splicing and autoregulation (Q35034350) (← links)
- A fruitful endeavor: modeling ALS in the fruit fly (Q35268719) (← links)
- Model systems of motor neuron diseases as a platform for studying pathogenic mechanisms and searching for therapeutic agents (Q35540393) (← links)
- Understanding the role of TDP-43 and FUS/TLS in ALS and beyond. (Q35587208) (← links)
- Mutant TDP-43 in motor neurons promotes the onset and progression of ALS in rats (Q35640609) (← links)
- Amelioration of toxicity in neuronal models of amyotrophic lateral sclerosis by hUPF1. (Q35796020) (← links)
- Identification of pharmacological targets in amyotrophic lateral sclerosis through genomic analysis of deregulated genes and pathways. (Q36087937) (← links)
- Severe respiratory changes at end stage in a FUS-induced disease state in adult rats (Q36177447) (← links)
- Mechanisms of disease in frontotemporal lobar degeneration: gain of function versus loss of function effects (Q36241872) (← links)
- Entorhinal cortical neurons are the primary targets of FUS mislocalization and ubiquitin aggregation in FUS transgenic rats (Q36317708) (← links)
- XBP1 depletion precedes ubiquitin aggregation and Golgi fragmentation in TDP-43 transgenic rats (Q36501464) (← links)
- ALS-associated mutant FUS induces selective motor neuron degeneration through toxic gain of function (Q36548825) (← links)
- Neurodegeneration the RNA way (Q36638284) (← links)
- Pathogenic Ubqln2 gains toxic properties to induce neuron death (Q36649076) (← links)
- Reactive astrocytes secrete lcn2 to promote neuron death (Q36673303) (← links)
- Toxic gain of function from mutant FUS protein is crucial to trigger cell autonomous motor neuron loss (Q36906420) (← links)
- Fused in sarcoma (FUS) protein lacking nuclear localization signal (NLS) and major RNA binding motifs triggers proteinopathy and severe motor phenotype in transgenic mice (Q37132099) (← links)
- Genetics of amyotrophic lateral sclerosis: an update. (Q37153922) (← links)
- Amyotrophic lateral sclerosis-linked FUS/TLS alters stress granule assembly and dynamics (Q37153932) (← links)
- RNA-binding proteins in neurodegenerative disease: TDP-43 and beyond (Q37155206) (← links)
- Changes in the Expression of FUS/TLS in Spinal Cords of SOD1 G93A Transgenic Mice and Correlation with Motor-Neuron Degeneration. (Q37348694) (← links)
- Systemic HMGB1 Neutralization Prevents Postoperative Neurocognitive Dysfunction in Aged Rats (Q37359665) (← links)