{"database":"ENA","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Fastqsanger.gz":["ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR192/076/SRR19256976/SRR19256976_1.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR192/075/SRR19256975/SRR19256975_1.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR192/076/SRR19256976/SRR19256976_2.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR192/075/SRR19256975/SRR19256975_2.fastq.gz"]},"type":"primary"},"statusCodeValue":200,"statusCode":"OK"}],"scores":null,"additional":{"omics_type":["Genomics"],"center_name":["Microbial Pathogenesis, Yale University"],"full_dataset_link":["https://www.ebi.ac.uk/ena/browser/view/PRJNA839152"],"scientific_name":["Homo sapiens"],"long_description":["In order to identify novel factors associated with regulation of HIV-1 transcription, we completed a genome-wide CRISPRi screen in a monogenic model of HIV-1. We identified SLTM mediated suppression of HIV-1 transcription. We hypothesized that SLTM would alter the chromatin acessibility at the site of HIV-1 integration. We conducted ATAC-seq of CRISPR ready cells encoding a single HIV-1 provirus in the SPECC1 gene transduced with a gRNA targetting SLTM and a Non-Targeting gRNA. We found that SLTM knockdown increased HIV-1 proviral acessibility across the provirus and host acessibility downstream of the site of HIV-1 integration. Overall design: We conducted ATAC-seq of a monogenic Jurkat line with HIV-1 integrated into SPECC1. This line stably expresses dCas9-KRAB and nontargetting and SLTM guide RNAs."],"repository":["ENA"],"additional_accession":[]},"is_claimable":false,"name":"ATAC-seq of SLTM knockdown in HIV infected Jurkats","description":"ATAC-seq of SLTM knockdown in HIV infected Jurkats","dates":{"last_updated":"2025-09-24","first_public":"2022-05-21"},"accession":"PRJNA839152","cross_references":{"GEO":["GSE203235"],"taxon":["9606"]}}