{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Kawada J"],"funding":["Intramural NIH HHS","NCI NIH HHS"],"pagination":["17102-17109"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC2719348"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["284(25)"],"pubmed_abstract":["Tubacin is a small molecule inhibitor of histone deacetylase 6 and blocks aggresome activity. We found that Epstein-Barr virus (EBV)-positive Burkitt lymphoma (BL) cells were generally killed by lower doses of tubacin than EBV-transformed lymphoblastoid cells (LCLs) or EBV-negative BL cells. Tubacin induced apoptosis of LCLs, which was inhibited by pretreatment with a pancaspase inhibitor but not by butylated hydroxyanisole, which inhibits reactive oxygen species. In contrast, tubacin killed EBV-positive BL cells in a caspase-3-independent pathway that involved reactive oxygen species and was blocked by butylated hydroxyanisole. Previously, we showed that bortezomib, a proteasome inhibitor, induces apoptosis of EBV LCLs and that LCLs are killed by lower doses of bortezomib than EBV-positiv"],"journal":["The Journal of biological chemistry"],"pubmed_title":["Tubacin kills Epstein-Barr virus (EBV)-Burkitt lymphoma cells by inducing reactive oxygen species and EBV lymphoblastoid cells by inducing apoptosis."],"pmcid":["PMC2719348"],"funding_grant_id":["P01CA078048","K08CA128972"],"pubmed_authors":["Bradner JE","Cohen JI","Zou P","Mazitschek R","Kawada J"],"additional_accession":[]},"is_claimable":false,"name":"Tubacin kills Epstein-Barr virus (EBV)-Burkitt lymphoma cells by inducing reactive oxygen species and EBV lymphoblastoid cells by inducing apoptosis.","description":"Tubacin is a small molecule inhibitor of histone deacetylase 6 and blocks aggresome activity. We found that Epstein-Barr virus (EBV)-positive Burkitt lymphoma (BL) cells were generally killed by lower doses of tubacin than EBV-transformed lymphoblastoid cells (LCLs) or EBV-negative BL cells. Tubacin induced apoptosis of LCLs, which was inhibited by pretreatment with a pancaspase inhibitor but not by butylated hydroxyanisole, which inhibits reactive oxygen species. In contrast, tubacin killed EBV-positive BL cells in a caspase-3-independent pathway that involved reactive oxygen species and was blocked by butylated hydroxyanisole. Previously, we showed that bortezomib, a proteasome inhibitor, induces apoptosis of EBV LCLs and that LCLs are killed by lower doses of bortezomib than EBV-positiv","dates":{"release":"2009-01-01T00:00:00Z","publication":"2009 Jun","modification":"2025-04-05T15:59:39.978Z","creation":"2019-03-27T00:23:55Z"},"accession":"S-EPMC2719348","cross_references":{"pubmed":["19386607"],"doi":["10.1074/jbc.M809090200","10.1074/jbc.m809090200"]}}