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Neuronal development in NEIL3-deficient mice (hippocampus)

ABSTRACT: Neuronal development in NEIL3-deficient mice (hippocampus)

PROVIDER: PRJNA675494 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14648807.fastq.gz	Fastqsanger.gz
	SRR14648808.fastq.gz	Fastqsanger.gz
	SRR14648809.fastq.gz	Fastqsanger.gz
	SRR14648810.fastq.gz	Fastqsanger.gz
	SRR14648811.fastq.gz	Fastqsanger.gz

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Neuronal development in NEIL3-deficient mice (hippocampus) [CA1]

Project description:Neuronal development in NEIL3-deficient mice (hippocampus) [CA1]

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neuronal development in NEIL3-deficient mice (hippocampus) [DG]

Project description:neuronal development in NEIL3-deficient mice (hippocampus) [DG]

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Neuronal development in NEIL3-deficient mice (hippocampus) [CA3]

Project description:Neuronal development in NEIL3-deficient mice (hippocampus) [CA3]

| PRJNA732771 | ENA

Neuronal development in NEIL3-deficient mice (hippocampus)

Project description:brain tissue from all subregions (CA1, CA3, dentate gyrus) of the hippocampal formation was isolated at postnatal day 8 and at an adult age (3-6months old animals) in wildtype and NEIL3-deficient mice (n=4 at p8 and n=3 at adult age). NEILs are DNA glycosylases potentially involved in transcription regulation and hippocampal neuronal maturation. RNA was extracted and sequenced.

2021-11-25 | GSE161074 | GEO

neuronal development in NEIL3-deficient mice (hippocampus) [DG]

Project description:brain tissue from Dentate Gyrus subregion of the hippocampal formation was isolated at postnatal day 8 and at an adult age (3-6months old animals) in wildtype and NEIL3-deficient mice (n=4 at p8 and n=3 at adult age). NEILs are DNA glycosylases potentially involved in transcription regulation and hippocampal neuronal maturation. RNA was extracted and sequenced.

2021-11-25 | GSE175360 | GEO

Neuronal development in NEIL3-deficient mice (hippocampus) [CA3]

Project description:brain tissue from CA3 subregion of the hippocampal formation was isolated at postnatal day 8 and at an adult age (3-6months old animals) in wildtype and NEIL3-deficient mice (n=4 at p8 and n=3 at adult age). NEILs are DNA glycosylases potentially involved in transcription regulation and hippocampal neuronal maturation. RNA was extracted and sequenced.

2021-11-25 | GSE175359 | GEO

Neuronal development in NEIL3-deficient mice (hippocampus) [CA1]

Project description:brain tissue from CA1 subregion of the hippocampal formation was isolated at postnatal day 8 and at an adult age (3-6months old animals) in wildtype and NEIL3-deficient mice (n=4 at p8 and n=3 at adult age). NEILs are DNA glycosylases potentially involved in transcription regulation and hippocampal neuronal maturation. RNA was extracted and sequenced.

2021-11-25 | GSE175358 | GEO

Genome-wide analysis of gene expression in brain of Neil3-deficient Alzheimer's disease mouse model

Project description:Oxidative stress generating DNA damage has been shown to be a key characteristic in Alzheimer’s disease (AD). However, how it affects the pathogenesis of AD is not yet fully understood. NEIL3 is a DNA glycosylase initiating oxidative DNA repair and with a distinct expression pattern in proliferating cells. In brain, its function has been linked to hippocampal-dependent memory and to induction of neurogenesis after stroke and in prion disease. Here, we generated a novel AD mouse model deficient for Neil3 to study the impact of impaired oxidative base lesion repair on the pathogenesis of AD. Our results demonstrate an age-dependent decrease in amyloid-β (Aβ) plaque deposition in female NEIL3-deficient AD mice. Moreover, male NEIL3-deficient AD mice show reduced neural stem cell proliferation in the adult hippocampus and impaired working memory. These effects seem to be independent of DNA repair as both sexes show increased level of oxidative base lesions in the hippocampus upon loss of NEIL3. Thus, our findings suggest a sex-dependent role of NEIL3 in the progression of AD by altering cerebral Aβ accumulation and promoting adult hippocampal neurogenesis to maintain cognitive function.

2022-11-15 | GSE197199 | GEO

Transcriptome after spatial exploration in CA1-specific brain tissue from wildtype and NEIL3-deficient mice

Project description:CA1-specific brain tissue from the hippocampal formation was isolated at baseline (homecage condition) and after a spatial exploration paradigm ("open field") in wildtype and NEIL3-deficient mice. NEIL3 is a DNA glycosylase potentially involved in transcription regulation. RNA was extracted and sequenced. Subsequently, these results were correlated to an extracellular live recording of pyramidal cell activity ("place cell recording") in the same genotypes.

2021-11-01 | GSE148408 | GEO

Genome-wide analysis of gene expression in postnatal hippocampus of Neil1 and Neil2-deficient mice after hypoxia ischemia (HI)

Project description:NEIL 1-3 DNA glycosylases initiate the base excision repair pathway by removing oxidized bases from the DNA. NEIL1 and NEIL3 have been shown to protect the brain from ischemic stroke-induced injury in adult and perinatal mice, respectively. To assess the role of NEIL1 and NEIL2 in newborn mice, we used the Levine model of hypoxic-ischemic encephalopathy (HIE), modified for use in perinatal mice. We found that NEIL1 deficiency increased sensitivity to cerebral ischemia in newborn mice. In contrast, NEIL2 deficiency rendered the mice more resistant to hypoxia-ischemia. Importantly, no effect was seen in mice expressing base excision activity-deficient NEIL proteins and the global levels of the oxidative DNA lesion 5-hydroxycytosine, which is a substrate for the NEIL enzymes, did not differ significantly between the genotypes. Transcriptome analysis of NEIL1- and NEIL2-deficient hippocampus revealed changes in Neil2-deficient hippocampus that favour cell survival and limit brain injury after HI. Our data suggest a role of NEIL2 in regulating the early transcriptional stress response, critical for neuronal cell death, after brain injury. This function seems to be independent of the base excision activity of the proteins. The protective effect of NEIL2 deficiency makes NEIL2 a potential therapeutic target in treatment of perinatal HIE.

2023-12-31 | GSE236133 | GEO

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