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Division of Dermatology, Department of Medicine, University of British Columbia, and Vancouver Hospital and Health Sciences Center, Vancouver, British Columbia V6H 3Z6, Canada [K-J. C., P. L., G. L.], and Department of Carcinogenesis, University of Texas M. D. Anderson Cancer Center, Smithville, Texas 78957 [D. M.]
The biological functions of the tumor suppressor, ING1, have been studied extensively in the last 5 years since it was cloned. It shares many biological functions with those of p53 and has been reported to mediate growth arrest, senescence, apoptosis, anchorage-dependent growth, and chemosensitivity. Some of these functions, such as cell cycle arrest and apoptosis, have been shown to be dependent on the activity of both ING1 and p53 proteins. In this study, we report that p33ING1 (one of ING1 isoforms) is also involved in the modulation of DNA repair. We found that overexpression of p33ING1 enhances repair of UV-damaged DNA and that p53 is required for the repair process. Furthermore, binding between ING1 and GADD45 has been detected. These observations suggest that p33ING1 cooperates with p53 in nucleotide excision repair and that GADD45 may be one of its components.
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