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Therapeutic manipulation of SRSF1 mitigates genome-wide transcriptome alterations and neuronal hyperexcitability in C9ORF72-linked amyotrophic lateral sclerosis
PubMed Full text in PMC Similar studies Analyze with GEO2RSRA Run Selector
iPSC derived motor neuron cultures from C9ORF72 carriers
CRISPR-Cas9 screens in human cells and primary neurons identify modifiers of C9orf72 dipeptide repeat protein toxicity
PubMed Full text in PMC Similar studies SRA Run Selector
Distinct brain transcriptome profiles in c9orf72-associated and sporadic ALS
Profiling nucleo/cytoplasmic distribution of mRNAs identifies a role for the Golgi-to-ER trafficking in C9orf72 toxicity
PubMed Full text in PMC Similar studies Analyze with GEO2R
Single-cell RNA-seq analysis of the brainstem of mutant SOD1 mice reveals perturbed cell types and pathways of amyotrophic lateral sclerosis
C9ORF72 GGGGCC expanded repeats produce splicing dysregulation which correlates with disease severity in amyotrophic lateral sclerosis
C9ORF72 GGGGCC expanded repeats produce splicing dysregulation which correlates with disease severity in amyotrophic lateral sclerosis [HuEx-1_0-st]
C9ORF72 GGGGCC expanded repeats produce splicing dysregulation which correlates with disease severity in amyotrophic lateral sclerosis [HG-U133_Plus_2]
Conserved DNA methylation combined with differential frontal cortex and cerebellar expression distinguishes C9orf72-associated and sporadic ALS, and implicates SERPINA1 in disease.
Targeted degradation of sense and antisense C9orf72 RNA foci as therapy for amyotrophic lateral sclerosis and frontotemporal dementia
PubMed Full text in PMC Similar studies
Targeted degradation of sense and antisense C9orf72 RNA foci as therapy for amyotrophic lateral sclerosis and frontotemporal dementia (strand specific RNA-seq)
Targeted degradation of sense and antisense C9orf72 RNA foci as therapy for amyotrophic lateral sclerosis and frontotemporal dementia (Multiplex Analysis of PolyA-linked Sequences)
Identification and therapeutic rescue of autophagosome and glutamate receptor defects in C9ORF72 and sporadic ALS neurons
Differential Toxicity of Nuclear RNA Foci Versus Dipeptide Repeat Proteins in a Drosophila Model of C9ORF72 FTD/ALS
NYGC ALS Consortium data
Unexpected similarities between C9ORF72 and sporadic forms of ALS/FTD suggest a common disease mechanism
C9orf72-ALS human iPSC microglia are pro-inflammatory and toxic to co-cultured motor neurons via MMP9
Longitudinal and transversal comparison of iPSC-derived ALS_C9orf72 and healthy motor neurons at DIV21 and DIV42
KCNJ2 inhibition mitigates mechanical injury in human brain organoids [scRNA-seq]
PubMed Similar studies
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