Research Article 3541 Identification of ANKRD11 as a p53 coactivator Paul M. Neilsen1,*, Kelly M. Cheney1, Chia-Wei Li2, J. Don Chen2, Jacqueline E. Cawrse1, Renée B. Schulz1, Jason A. Powell3, Raman Kumar1 and David F. Callen1 1Breast Cancer Genetics Group, Dame Roma Mitchell Cancer Research Laboratories, Discipline of Medicine, University of Adelaide and Hanson Institute, IMVS, Adelaide, SA 5000, Australia 2Department of Pharmacology, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, Piscataway, NJ 08854-5635, USA 3Cytokine Receptor Laboratory, Department of Human Immunology, Hanson Institute, IMVS, Adelaide, SA 5000, Australia *Author for correspondence (e-mail:
[email protected]) Accepted 29 July 2008 Journal of Cell Science 121, 3541-3552 Published by The Company of Biologists 2008 doi:10.1242/jcs.026351 Summary The ability of p53 to act as a transcription factor is critical for ANKRD11 enhanced the DNA-binding properties of mutant its function as a tumor suppressor. Ankyrin repeat domain 11, p53R273H to the CDKN1A promoter, suggesting that ANKRD11 ANKRD11 (also known as ANR11 or ANCO1), was found to can mediate the restoration of normal p53 function in some be a novel p53-interacting protein that enhanced the cancer-related p53 mutations. In addition, ANKRD11 itself was transcriptional activity of p53. ANKRD11 expression was shown found to be a novel p53 target gene. These findings demonstrate to be downregulated in breast cancer cell lines. Restoration of a role for ANKRD11 as a p53 coactivator and suggest the ANKRD11 expression in MCF-7 (wild-type p53) and MDA-MB- involvement of ANKRD11 in a regulatory feedback loop with 468 (p53R273H mutant) cells suppressed their proliferative and p53.