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http://purl.uniprot.org/citations/20160719http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/20160719http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/20160719http://www.w3.org/2000/01/rdf-schema#comment"

Background

DBC1/KIAA1967 (deleted in breast cancer 1) is a putative tumour-suppressor gene cloned from a heterozygously deleted region in breast cancer specimens. Caspase-dependent processing of DBC1 promotes apoptosis, and depletion of endogenous DBC1 negatively regulates p53-dependent apoptosis through its specific inhibition of SIRT1. Hereditary breast and ovarian cancer susceptibility gene product BRCA1, by binding to the promoter region of SIRT1, is a positive regulator of SIRT1 expression.

Methods

A physical interaction between DBC1 and BRCA1 was investigated both in vivo and in vitro. To determine the pathophysiological significance of DBC1, its role as a transcriptional factor was studied.

Results

We found a physical interaction between the amino terminus of DBC1 and the carboxyl terminus of BRCA1, also known as the BRCT domain. Endogenous DBC1 and BRCA1 form a complex in the nucleus of intact cells, which is exported to the cytoplasm during ultraviolet-induced apoptosis. We also showed that the expression of DBC1 represses the transcriptional activation function of BRCT by a transient expression assay. The expression of DBC1 also inhibits the transactivation of the SIRT1 promoter mediated by full-length BRCA1.

Conclusion

These results revealed that DBC1 may modulate the cellular functions of BRCA1 and have important implications in the understanding of carcinogenesis in breast tissue."xsd:string
http://purl.uniprot.org/citations/20160719http://purl.org/dc/terms/identifier"doi:10.1038/sj.bjc.6605577"xsd:string
http://purl.uniprot.org/citations/20160719http://purl.org/dc/terms/identifier"doi:10.1038/sj.bjc.6605577"xsd:string
http://purl.uniprot.org/citations/20160719http://purl.uniprot.org/core/author"Kato S."xsd:string
http://purl.uniprot.org/citations/20160719http://purl.uniprot.org/core/author"Kato S."xsd:string
http://purl.uniprot.org/citations/20160719http://purl.uniprot.org/core/author"Matsumoto Y."xsd:string
http://purl.uniprot.org/citations/20160719http://purl.uniprot.org/core/author"Matsumoto Y."xsd:string
http://purl.uniprot.org/citations/20160719http://purl.uniprot.org/core/author"Nakagawa K."xsd:string
http://purl.uniprot.org/citations/20160719http://purl.uniprot.org/core/author"Nakagawa K."xsd:string
http://purl.uniprot.org/citations/20160719http://purl.uniprot.org/core/author"Nakagawa S."xsd:string
http://purl.uniprot.org/citations/20160719http://purl.uniprot.org/core/author"Nakagawa S."xsd:string
http://purl.uniprot.org/citations/20160719http://purl.uniprot.org/core/author"Oda K."xsd:string
http://purl.uniprot.org/citations/20160719http://purl.uniprot.org/core/author"Oda K."xsd:string
http://purl.uniprot.org/citations/20160719http://purl.uniprot.org/core/author"Saji S."xsd:string
http://purl.uniprot.org/citations/20160719http://purl.uniprot.org/core/author"Saji S."xsd:string
http://purl.uniprot.org/citations/20160719http://purl.uniprot.org/core/author"Tanikawa M."xsd:string
http://purl.uniprot.org/citations/20160719http://purl.uniprot.org/core/author"Tanikawa M."xsd:string
http://purl.uniprot.org/citations/20160719http://purl.uniprot.org/core/author"Yano T."xsd:string
http://purl.uniprot.org/citations/20160719http://purl.uniprot.org/core/author"Yano T."xsd:string
http://purl.uniprot.org/citations/20160719http://purl.uniprot.org/core/author"Shoji K."xsd:string
http://purl.uniprot.org/citations/20160719http://purl.uniprot.org/core/author"Shoji K."xsd:string
http://purl.uniprot.org/citations/20160719http://purl.uniprot.org/core/author"Taketani Y."xsd:string
http://purl.uniprot.org/citations/20160719http://purl.uniprot.org/core/author"Taketani Y."xsd:string
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