Please use this identifier to cite or link to this item:
|Title:||BRD7 is a candidate tumour suppressor gene required for p53 function|
Del Sal, G.
|Citation:||Drost, J., Mantovani, F., Tocco, F., Elkon, R., Comel, A., Holstege, H., Kerkhoven, R., Jonkers, J., Voorhoeve, P.M., Agami, R., Del Sal, G. (2010-04). BRD7 is a candidate tumour suppressor gene required for p53 function. Nature Cell Biology 12 (4) : 380-389. ScholarBank@NUS Repository. https://doi.org/10.1038/ncb2038|
|Abstract:||Oncogene-induced senescence is a p53-dependent defence mechanism against uncontrolled proliferation. Consequently, many human tumours harbour p53 mutations and others show a dysfunctional p53 pathway, frequently by unknown mechanisms. Here we identify BRD7 (bromodomain-containing 7) as a protein whose inhibition allows full neoplastic transformation in the presence of wild-type p53. In human breast tumours harbouring wild-type, but not mutant, p53 the BRD7 gene locus was frequently deleted and low BRD7 expression was found in a subgroup of tumours. Functionally, BRD7 is required for efficient p53-mediated transcription of a subset of target genes. BRD7 interacts with p53 and p300 and is recruited to target gene promoters, affecting histone acetylation, p53 acetylation and promoter activity. Thus, BRD7 suppresses tumorigenicity by serving as a p53 cofactor required for the efficient induction of p53-dependent oncogene-induced senescence. © 2010 Macmillan Publishers Limited. All rights reserved.|
|Source Title:||Nature Cell Biology|
|Appears in Collections:||Staff Publications|
Show full item record
Files in This Item:
There are no files associated with this item.
checked on Nov 14, 2018
WEB OF SCIENCETM
checked on Nov 6, 2018
checked on Oct 19, 2018
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.