{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Xiao H"],"funding":["China Scholarship Council"],"pagination":["e02525-20"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7845644"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["12(1)"],"pubmed_abstract":["The HIV-1 Rev protein is a nuclear export factor for unspliced and incompletely spliced HIV-1 RNAs. Without Rev, these intron-retaining RNAs are trapped in the nucleus. A genome-wide screen identified nine proteins of the spliceosome, which all enhanced expression from the HIV-1 unspliced RNA after CRISPR/Cas knockdown. Depletion of DHX38, WDR70, and four proteins of the Prp19-associated complex (ISY1, BUD31, XAB2, and CRNKL1) resulted in a more than 20-fold enhancement of unspliced HIV-1 RNA levels in the cytoplasm. Targeting of CRNKL1, DHX38, and BUD31 affected nuclear export efficiencies of the HIV-1 unspliced RNA to a much larger extent than splicing. Transcriptomic analyses further revealed that CRNKL1 also suppresses cytoplasmic levels of a subset of cellular mRNAs, including some wi"],"journal":["mBio"],"pubmed_title":["CRNKL1 Is a Highly Selective Regulator of Intron-Retaining HIV-1 and Cellular mRNAs."],"pmcid":["PMC7845644"],"funding_grant_id":["201204910157"],"pubmed_authors":["Silva ABOV","Landthaler M","Grewe B","Full F","Uberla K","Jungnickl D","Wyler E","Kirchner P","Milek M","Ekici A","Thomas M","Ensser A","Xiao H"],"additional_accession":[]},"is_claimable":false,"name":"CRNKL1 Is a Highly Selective Regulator of Intron-Retaining HIV-1 and Cellular mRNAs.","description":"The HIV-1 Rev protein is a nuclear export factor for unspliced and incompletely spliced HIV-1 RNAs. Without Rev, these intron-retaining RNAs are trapped in the nucleus. A genome-wide screen identified nine proteins of the spliceosome, which all enhanced expression from the HIV-1 unspliced RNA after CRISPR/Cas knockdown. Depletion of DHX38, WDR70, and four proteins of the Prp19-associated complex (ISY1, BUD31, XAB2, and CRNKL1) resulted in a more than 20-fold enhancement of unspliced HIV-1 RNA levels in the cytoplasm. Targeting of CRNKL1, DHX38, and BUD31 affected nuclear export efficiencies of the HIV-1 unspliced RNA to a much larger extent than splicing. Transcriptomic analyses further revealed that CRNKL1 also suppresses cytoplasmic levels of a subset of cellular mRNAs, including some wi","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Jan","modification":"2026-06-06T03:28:33.871Z","creation":"2025-04-27T01:36:44.184Z"},"accession":"S-EPMC7845644","cross_references":{"pubmed":["33468685"],"doi":["10.1128/mBio.02525-20"]}}