Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptome regulated by NEIL2 in human HAP1 cells

ABSTRACT: To elucidate the role of DNA glycosylase NEIL2 in transcriptome regulation, we performed RNA sequencing in human HAP1 cells of Neil2 knockout and wild type. The tanscription count was extracted and the differential expressed genes (DEGs) were analysed.

ORGANISM(S): Homo sapiens

PROVIDER: GSE240564 | GEO | 2023/12/13

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Methylome of 5mC and 5hmC regulated by NEIL2

Project description:To elucidate the role of DNA glycosylase NEIL2 in regulation of DNA methylome, we performed genome sequencing of epigenetic marker 5mC and 5hmC in genome-wide using enyme-based library methods of TAPS and CAPS. The 5mC and 5hmC profile in CpG contect was further extracted and analysed.

2023-12-13 | GSE240177 | GEO

Transcriptome regulated by NEIL2 in human HAP1 cells

Project description:Transcriptome regulated by NEIL2 in human HAP1 cells

| PRJNA1004242 | ENA

Gene expression changes in Neil1 / Neil2 / Neil3 triple knockout mouse teratoma

Project description:The bifunctional DNA glycosylases / AP lyases NEIL1 and NEIL2 excise oxidative base damages, but can also enhance the steady-state turnover of thymine DNA glycosylase (TDG) during oxidative DNA demethylation (Schomacher et al. 2016; doi:10.1038/nsmb.3151). The dual role of NEILs in antagonizing base damages and promoting epigenetic gene reactivation prompted us to investigate the consequences of NEIL deficiency during embryonic stem cell differentiation. To account for any possible functional redundancy in the NEIL family, all three paralogs NEIL1, NEIL2 and NEIL3 were inactivated using CRISPR/Cas9 in mouse embryonic stem cells.

2019-09-16 | GSE130080 | GEO

Gene expression changes in Neil1, Neil2 and Apex1 single knockout mouse embryonic stem cells prior and during embryoid body differentiation

Project description:The bifunctional DNA glycosylases/AP lyases NEIL1 and NEIL2 excise oxidative base damages, but can also enhance the steady-state turnover of thymine DNA glycosylase (TDG) during oxidative DNA demethylation (Schomacher et al. 2016; doi:10.1038/nsmb.3151) probably due to their AP lyase activity during base excision repair (BER). The dual role of NEILs in antagonizing base damages and promoting epigenetic gene reactivation prompted us to investigate the consequences of Neil-deficiency during embryonic stem cell differentiation. For comparison stem cells deficient for Apex1, the bona fide AP endonuclease during BER, were analysed in parallel.

2019-09-16 | GSE130081 | GEO

ATAC sequencing of HAP1 cells

Project description:We analysed the global effect of CHD3-KO and SENP1-KO HAP1 cell lines compared to control cell line, on chromatin accessibility using ATAC-seq.

2018-08-05 | GSE111047 | GEO

RNA sequencing of HAP1 WT and MED13 KO clones

Project description:Purpose: The aim of the experiment was to eludicate differentialy expressed genes (DEGs) upon treatment with alkylating agent MMS between WT and MED13 deficient HAP1 cells. Results: After bioinformatic processing, at ≥2-fold change and an FDR≤0.1, 446 DEGs were identified in MED13 KO cells when compared to WT. Upon the MMS treatment 394 DEGs were identified in MED13 KO cells, of which 229 were common with untreated MED13 KO cells. Conclusions: Common DEGs represented genes directly regulated by MED13.

2020-12-29 | GSE147366 | GEO

Gene expression changes in stage 23 Xenopus laevis embryos upon Neil2 knockdown

Project description:It was shown that neil2 is required for neural crest development in Xenopus (Schomacher et al. 2016; doi:10.1038/nsmb.3151). To gain further insights into the underlying molecular mechanism leading to neural crest defects and microcephaly in neil2 Morpholino injected Xenopus embryos, we performed RNA-seq transcriptome analysis of neil2 Morpholino versus control Morpholino injected embryos.

2019-09-16 | GSE130079 | GEO

Effect of BCDIN3D knock-out on gene expression in Chronic Myelogenous Leukemia (CML) Hap1 cells.

Project description:WT and BCDIN3D knocked-out Hap1 cells were analysed by RNA- and microRNA-Seq to uncover the effect of BCDIN3D on specific microRNAs and their messenger RNA targets.

2022-03-06 | GSE127973 | GEO

Methylome of 5mC and 5hmC regulated by NEIL2

Project description:Methylome of 5mC and 5hmC regulated by NEIL2

| PRJNA1002410 | ENA

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

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data