Journal article
MOZ (MYST3, KAT6A) inhibits senescence via the INK4A-ARF pathway
BN Sheikh, B Phipson, F El-Saafin, HK Vanyai, NL Downer, MJ Bird, AJ Kueh, RE May, GK Smyth, AK Voss, T Thomas
Oncogene | Published : 2015
DOI: 10.1038/onc.2015.33
Abstract
Cellular senescence is an important mechanism that restricts tumour growth. The Ink4a-Arf locus (also known as Cdkn2a), which encodes p16INK4A and p19ARF, has a central role in inducing and maintaining senescence. Given the importance of cellular senescence in restraining tumour growth, great emphasis is being placed on the identification of novel factors that can modulate senescence. The MYST-family histone acetyltransferase MOZ (MYST3, KAT6A), first identified in recurrent translocations in acute myeloid leukaemia, has been implicated in both the promotion and inhibition of senescence. In this study, we investigate the role of MOZ in cellular senescence and show that MOZ is a potent inhibi..
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Funding Acknowledgements
We thank Carmen Gatt and Faye Dabrowski for technical support. We thank Andreas Strasser for helpful discussions and Liz Valente for the provision of the anti-p21<SUP>CIP1</SUP> antibody. This work was supported by the Australian National Health and Medical Research Council (senior research fellowships to AKV and TT; scholarship to BNS), the Australian Mitochondrial Disease Foundation (MJB), Australian Postgraduate Awards (to MJB, FE and HKV) and operational infrastructure grants from the Australian Federal Government (IRISS) and the Victorian State Government (OIS).