Abstract:
:The tumour suppressor ARF (alternative reading frame), which is mutated or silenced in various tumours, has a crucial role in tumour surveillance to suppress unwarranted cell growth and proliferation. ARF has also been linked to the DNA-damage-induced response of p53 because of its ability to inhibit murine double minute 2 (MDM2). Here, however, we provide genetic evidence for a role of ARF in nucleotide excision repair (NER) that is independent of p53. Cells lacking ARF are deficient in NER. Expression of ARF restores the repair activity, which coincides with increased expression of the damaged-DNA recognition protein xeroderma pigmentosum, complementation group C (XPC). We provide evidence that, by disrupting the interaction between E2F transcription factor 4 (E2F4) and DRTF polypeptide 1 (DP1), ARF reduces the interaction of the E2F4-p130 repressor complex with the promoter of XPC to ensure high-level expression of XPC. Together, our results point to an important 'care-taker'-type tumour-suppression function for ARF in NER through the increased expression of XPC.
journal_name
EMBO Repjournal_title
EMBO reportsauthors
Dominguez-Brauer C,Chen YJ,Brauer PM,Pimkina J,Raychaudhuri Pdoi
10.1038/embor.2009.139subject
Has Abstractpub_date
2009-09-01 00:00:00pages
1036-42issue
9eissn
1469-221Xissn
1469-3178pii
embor2009139journal_volume
10pub_type
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