Please use this identifier to cite or link to this item: https://doi.org/10.1074/jbc.M503016200
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dc.titleIdentification of TopBP1 as a c-Abl-interacting protein and a repressor for c-Abl expression
dc.contributor.authorZeng, L.
dc.contributor.authorHu, Y.
dc.contributor.authorLi, B.
dc.date.accessioned2016-12-13T05:36:34Z
dc.date.available2016-12-13T05:36:34Z
dc.date.issued2005-08-12
dc.identifier.citationZeng, L., Hu, Y., Li, B. (2005-08-12). Identification of TopBP1 as a c-Abl-interacting protein and a repressor for c-Abl expression. Journal of Biological Chemistry 280 (32) : 29374-29380. ScholarBank@NUS Repository. https://doi.org/10.1074/jbc.M503016200
dc.identifier.issn00219258
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/132790
dc.description.abstractExpression of BCR-ABL is the leading cause of chronic myelogenous leukemia. In chronic myelogenous leukemia cells, c-Abl expression is silenced by promoter methylation. In addition, the level of c-Abl needs to be tightly and constantly regulated due to its cytotoxicity and its rapid degradation after activation. Yet the regulation of c-Abl expression remains unclear. In an effort to gain better understanding of c-Abl function, we performed a glutathione S-transferase-Abl pull-down screen and identified TopBP1, a topoisomerase IIβ-binding protein that contains Brca1 C-terminal motifs and has been implicated in DNA damage response. Their physical interaction was verified by in vitro and in vivo assays with TopBP1 found as a substrate of Abl proteins. TopBP1 could repress the expression of c-Abl at both mRNA and protein levels. Reporter assays indicate that TopBP1 directly repressed the promoter activity of c-Abl. Furthermore, TopBP1 repressed expression of c-Abl through a novel mechanism that involved histone deacetylation and DNA methylation. This transcriptional repression was inhibited by c-Abl in a kinase-dependent manner. The dual antagonistic interplay between c-Abl and TopBP1 may also provide a mechanism for fine-tuning of c-Abl levels. © 2005 by The American Society for Biochemistry and Molecular Biology, Inc.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1074/jbc.M503016200
dc.sourceScopus
dc.typeArticle
dc.contributor.departmentMEDICINE
dc.description.doi10.1074/jbc.M503016200
dc.description.sourcetitleJournal of Biological Chemistry
dc.description.volume280
dc.description.issue32
dc.description.page29374-29380
dc.description.codenJBCHA
dc.identifier.isiut000231021300069
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