<HashMap><database>ENA</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/DRR538/DRR538926/DRR538926_subreads.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/DRR538/DRR538924/DRR538924_subreads.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/DRR538/DRR538922/DRR538922_subreads.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/DRR538/DRR538916/DRR538916_subreads.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/DRR538/DRR538920/DRR538920_subreads.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/DRR538/DRR538918/DRR538918_subreads.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/DRR538/DRR538919/DRR538919_subreads.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/DRR538/DRR538917/DRR538917_subreads.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/DRR538/DRR538925/DRR538925_subreads.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/DRR538/DRR538923/DRR538923_subreads.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/DRR538/DRR538915/DRR538915_subreads.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/DRR538/DRR538921/DRR538921_subreads.fastq.gz</Fastqsanger.gz></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Genomics</omics_type><strain>Human Embryonic Kidney cells 293</strain><center_name>Brain research Institute, Niigata University</center_name><full_dataset_link>https://www.ebi.ac.uk/ena/browser/view/PRJDB17735</full_dataset_link><scientific_name>Homo sapiens</scientific_name><long_description>We used 293 cells stably expressing one copy of wild-type TREX1 or 3' frameshift mutant TREX1 (RVCL TREX1) in a doxycycline (Dox)-inducible manner using the Flp-in expression system. Double-strand breaks (DSB) were induced by CRISPR/Cas9 in each cell line expressing exogenous TREX1, and the deletion status at the cut site after DSB repair was analyzed by long-read sequencing. Sequence analysis was performed by acquiring HiFi reads using the PacBio Revio/Sequel IIe. The target gene was human ACTB, which was amplified using a primer flanking the cut site. Sequencing analysis was performed on an amplicon of approximately 3800 bp. The sample groups consisted of four groups: Dox-untreated wild-type TREX1-expressing cells and RVCL-expressing cells as controls, and each cell line sample that was Dox-treated and expressed exogenous TREX1. Three biological replicates were obtained for each group and the total sequence data consisted of 12 samples.</long_description><tag>xref:EuropePMC:PMC11144269</tag><repository>ENA</repository></additional><is_claimable>false</is_claimable><name>Homo sapiens strain:Human Embryonic Kidney cells 293</name><description>Analysis of the effects of human wild-type TREX1 and 3' frameshift mutant TREX1 (RVCL TREX1) expression on CRISPR/Cas9-induced DSB repair.</description><dates><last_updated>2025-09-24</last_updated><first_public>2024-03-30</first_public></dates><accession>PRJDB17735</accession><cross_references><taxon>9606</taxon></cross_references></HashMap>