{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["31(2)"],"submitter":["La Marca JE"],"pubmed_abstract":["Whole-genome screens using CRISPR technologies are powerful tools to identify novel tumour suppressors as well as factors that impact responses of malignant cells to anti-cancer agents. Applying this methodology to lymphoma cells, we conducted a genome-wide screen to identify novel inhibitors of tumour expansion that are induced by the tumour suppressor TRP53. We discovered that the absence of Arrestin domain containing 3 (ARRDC3) increases the survival and long-term competitiveness of MYC-driven lymphoma cells when treated with anti-cancer agents that activate TRP53. Deleting Arrdc3 in mice caused perinatal lethality due to various developmental abnormalities, including cardiac defects. Notably, the absence of ARRDC3 markedly accelerated MYC-driven lymphoma development. Thus, ARRDC3 is a "],"journal":["Cell death and differentiation"],"pagination":["150-158"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10850147"],"repository":["biostudies-literature"],"pubmed_title":["Genome-wide CRISPR screening identifies a role for ARRDC3 in TRP53-mediated responses."],"pmcid":["PMC10850147"],"pubmed_authors":["Milla L","Wilcox S","Kelly GL","Tai L","Diepstraten ST","Yang B","Aubrey BJ","Strasser A","Herold MJ","La Marca JE","Heinzel S","Vremec D","Kueh A","Whelan L","Konig C","Kaloni D","Voss AK","Chang C","Wang Z"],"additional_accession":[]},"is_claimable":false,"name":"Genome-wide CRISPR screening identifies a role for ARRDC3 in TRP53-mediated responses.","description":"Whole-genome screens using CRISPR technologies are powerful tools to identify novel tumour suppressors as well as factors that impact responses of malignant cells to anti-cancer agents. Applying this methodology to lymphoma cells, we conducted a genome-wide screen to identify novel inhibitors of tumour expansion that are induced by the tumour suppressor TRP53. We discovered that the absence of Arrestin domain containing 3 (ARRDC3) increases the survival and long-term competitiveness of MYC-driven lymphoma cells when treated with anti-cancer agents that activate TRP53. Deleting Arrdc3 in mice caused perinatal lethality due to various developmental abnormalities, including cardiac defects. Notably, the absence of ARRDC3 markedly accelerated MYC-driven lymphoma development. Thus, ARRDC3 is a ","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Feb","modification":"2025-04-04T10:42:01.813Z","creation":"2025-04-04T10:42:01.813Z"},"accession":"S-EPMC10850147","cross_references":{"pubmed":["38097622"],"doi":["10.1038/s41418-023-01249-3"]}}