<HashMap><database>ENA</database><scores/><additional><omics_type>Genomics</omics_type><center_name>Charles University, Department of Parasitology, Biocev</center_name><center_name>Charles University</center_name><full_dataset_link>https://www.ebi.ac.uk/ena/browser/view/PRJEB72626</full_dataset_link><long_description>Benzoxaboroles (BoBs) feature a boron-heterocyclic core and are an important recent innovation in the development of drugs against a range of pathogens and other pathologies. A broad spectrum of pharmacology is associated with chemically diverse BoB derivatives and includes multiple modes-of-action and targets. However, a consensus MoA for BoBs targeting evolutionarily diverse protozoan pathogens has emerged with the identification of CPSF3/CPSF73 in the CPSF complex in both apicomplexan and kinetoplastida parasites. We have detected a functional connection between protein sumoylation and the BoB boron-heterocyclic scaffold using comprehensive genetic screens in Trypanosoma brucei. Strikingly, as part of this sumoylation response, members of the CPSF complex are specifically and rapidly destabilised in a SUMO and proteosome-dependent manner. Here we deposit RNAseq data quantifying the effects of the benzoxaborole AN3057 exposure on the transcriptome landscape in T. brucei. Specifically, T. brucei bloodstream-form cells in logarithmic growth phase were treated with 400 nm AN3057 (3 × EC50 determined after 24h) for 20 min (T20) and 60 min (T60), respectively. Nontreated control cells were prepared in parallel. All samples were in 2 biological replicates.</long_description><repository>ENA</repository></additional><is_claimable>false</is_claimable><name>AN3057 exposure</name><description>Trypanosoma brucei transcriptome changes upon exposure to the aminomethyl-benzoxaborole AN3057</description><dates><last_updated>2024-02-12</last_updated><first_public>2024-02-12</first_public></dates><accession>PRJEB72626</accession><cross_references/></HashMap>