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GA-CFP data for the manuscript "Correction of dysregulated lipid metabolism normalizes gene expression in oligodendrocytes and prolongs lifespan in female poly-GA C9orf72 mouse model"

ABSTRACT: GA-CFP data for the manuscript "Correction of dysregulated lipid metabolism normalizes gene expression in oligodendrocytes and prolongs lifespan in female poly-GA C9orf72 mouse model"

PROVIDER: PRJNA1224267 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32360473_1.fastq.gz	Fastqsanger.gz
	SRR32360473_2.fastq.gz	Fastqsanger.gz
	SRR32360474_1.fastq.gz	Fastqsanger.gz
	SRR32360474_2.fastq.gz	Fastqsanger.gz
	SRR32360475_1.fastq.gz	Fastqsanger.gz

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GA-CFP data for the manuscript "Correction of dysregulated lipid metabolism normalizes gene expression in oligodendrocytes and prolongs lifespan in female poly-GA C9orf72 mouse model"

Project description:These sequences support the following paper abstract: Clinical and genetic research links altered cholesterol metabolism with ALS development and progression, yet pinpointing specific pathomechanisms remain challenging. We investigated how cholesterol dysmetabolism interacts with protein aggregation, demyelination, and neuronal loss in ALS. Bulk RNAseq transcriptomics showed decreased cholesterol biosynthesis and increased cholesterol export in ALS mouse models (GA-Nes, GA-CFP, rNLS8) and patient samples (spinal cord), suggesting an adaptive response to cholesterol overload. Consequently, we assessed the efficacy of the cholesterol-binding drug 2-hydroxypropyl-β-cyclodextrin (CD) in a fast-progressing C9orf72 ALS mouse model with extensive poly-GA expression and myelination deficits. CD treatment normalized cholesteryl ester levels, lowered neurofilament light chain levels, and prolonged lifespan in female but not male GA-Nes mice, without impacting poly-GA aggregates. Single nucleus transcriptomics indicated that CD primarily affected oligodendrocytes, significantly restored myelin gene expression, increased density of myelinated axons, inhibited the disease-associated oligodendrocyte response, and downregulated the lipid-associated genes Plin4 and ApoD. These results suggest that reducing excess free cholesterol in the CNS could be a viable ALS treatment strategy.

2025-03-08 | GSE289729 | GEO

Transcriptome analysis on OVA-GA(10) immunized GA-CFP mice

Project description:The goal of the study is to perform unbiased transcriptome analysis on spinal cord samples of immunized GA-CFP mice to configure the effect of OVA-GA(10) vaccination in a C9orf72 mouse model.

2019-10-04 | GSE138413 | GEO

GA-Camk2a mouse RNAseq data for the manuscript by Rezaei et al: Correction of dysregulated lipid metabolism normalizes gene expression in oligodendrocytes and prolongs lifespan in female poly-GA C9orf72 mouse model

Project description:These sequences support the following paper abstract: "Clinical and genetic research links altered cholesterol metabolism with ALS development and progression, yet pinpointing specific pathomechanisms remain challenging. We investigated how cholesterol dysmetabolism interacts with protein aggregation, demyelination, and neuronal loss in ALS. Bulk RNAseq transcriptomics showed decreased cholesterol biosynthesis and increased cholesterol export in ALS mouse models (GA-Nes, GA-CFP, rNLS8) and patient samples (spinal cord), suggesting an adaptive response to cholesterol overload. Consequently, we assessed the efficacy of the cholesterol-binding drug 2-hydroxypropyl-β-cyclodextrin (CD) in a fast-progressing C9orf72 ALS mouse model with extensive poly-GA expression and myelination deficits. CD treatment normalized cholesteryl ester levels, lowered neurofilament light chain levels, and prolonged lifespan in female but not male GA-Nes mice, without impacting poly-GA aggregates. Single nucleus transcriptomics indicated that CD primarily affected oligodendrocytes, significantly restored myelin gene expression, increased density of myelinated axons, inhibited the disease-associated oligodendrocyte response, and downregulated the lipid-associated genes Plin4 and ApoD. These results suggest that reducing excess free cholesterol in the CNS could be a viable ALS treatment strategy."

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Transcriptome analysis on OVA-GA(10) immunized GA-CFP mice

Project description:Transcriptome analysis on OVA-GA(10) immunized GA-CFP mice

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Correction of dysregulated lipid metabolism normalizes gene expression in oligodendrocytes and prolongs lifespan in female poly-GA C9orf72 mouse model

2025-03-10 | GSE262778 | GEO

Project description:GA-Camk2a mouse RNAseq data for the manuscript by Rezaei et al: Correction of dysregulated lipid metabolism normalizes gene expression in oligodendrocytes and prolongs lifespan in female poly-GA C9orf72 mouse model

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iPSC data for the paper "Correction of dysregulated lipid metabolism normalizes gene expression in oligodendrocytes and prolongs lifespan in female poly-GA C9orf72 mouse model"

2025-03-08 | GSE285209 | GEO

Correction of dysregulated lipid metabolism normalizes gene expression in oligodendrocytes and prolongs lifespan in female poly-GA C9orf72 mouse model

Project description:Correction of dysregulated lipid metabolism normalizes gene expression in oligodendrocytes and prolongs lifespan in female poly-GA C9orf72 mouse model

| PRJNA1093372 | ENA

iPSC data for the paper "Correction of dysregulated lipid metabolism normalizes gene expression in oligodendrocytes and prolongs lifespan in female poly-GA C9orf72 mouse model"

Project description:iPSC data for the paper "Correction of dysregulated lipid metabolism normalizes gene expression in oligodendrocytes and prolongs lifespan in female poly-GA C9orf72 mouse model"

| PRJNA1201847 | ENA

Effect of cFP on gene expression in Vibiro cholerae

Project description:Vibrio cholerae is a Gram negative, motile, facultative anaerobic bacterium, and the causative agent of cholera, a severe diarrhoeal disease, which untreated can rapidly lead to dehydration, hypotensive shock, and death. Cholera is a significant human disease that is estimated to affect 3-5 million people each year. The mechanism by which V. cholerae regulates virulence gene expression in vivo is unknown, but a number of studies have suggested that low molecular weight signally molecules may be important in modulating gene expression. cFP is a low molecular weight cyclic dipeptide produced by multiple Vibrio species. Evidence previously generated in our laboratory showed that cFP inhibited the production of the virulence factors cholera toxin (CT) and the toxin coregulated pilus (TCP) in O1 El Tor V. cholerae strain N16961 during growth under virulence gene inducing conditions. cFP inhibition of CT and TCP production correlated with reduced transcription of several regulators that belong to the ToxR regulon. To identify additional cFP-responsive genes we performed microarray experiments with the O1 El Tor V. cholerae strain N16961. In these experiments N16961 was grown under virulence gene inducing conditions in the presence and absence of cFP before RNA was extracted and hybridized to microarrays. The results showed that cFP positively affected the expression of the LysR-family regulatory protein LeuO. This finding suggests the possibility that LeuO may be mediating cFP-dependent regulation of gene expression in response to environmental cFP. V. cholerae N16961 was grown under AKI growth condition in the presence or absence of 1 mM cFP for 2.5 or 3 hours when total RNA was extracted, differentially labelled and hybridized to microarrays. Four independent experiments were performed.

2013-08-13 | E-GEOD-38272 | biostudies-arrayexpress

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