<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Kawada J</submitter><funding>Intramural NIH HHS</funding><funding>NCI NIH HHS</funding><pagination>17102-17109</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC2719348</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>284(25)</volume><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</pubmed_abstract><journal>The Journal of biological chemistry</journal><pubmed_title>Tubacin kills Epstein-Barr virus (EBV)-Burkitt lymphoma cells by inducing reactive oxygen species and EBV lymphoblastoid cells by inducing apoptosis.</pubmed_title><pmcid>PMC2719348</pmcid><funding_grant_id>P01CA078048</funding_grant_id><funding_grant_id>K08CA128972</funding_grant_id><pubmed_authors>Bradner JE</pubmed_authors><pubmed_authors>Cohen JI</pubmed_authors><pubmed_authors>Zou P</pubmed_authors><pubmed_authors>Mazitschek R</pubmed_authors><pubmed_authors>Kawada J</pubmed_authors></additional><is_claimable>false</is_claimable><name>Tubacin kills Epstein-Barr virus (EBV)-Burkitt lymphoma cells by inducing reactive oxygen species and EBV lymphoblastoid cells by inducing apoptosis.</name><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</description><dates><release>2009-01-01T00:00:00Z</release><publication>2009 Jun</publication><modification>2025-04-05T15:59:39.978Z</modification><creation>2019-03-27T00:23:55Z</creation></dates><accession>S-EPMC2719348</accession><cross_references><pubmed>19386607</pubmed><doi>10.1074/jbc.M809090200</doi><doi>10.1074/jbc.m809090200</doi></cross_references></HashMap>