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Cell Growth & Differentiation Vol. 12, 201-210, April 2001
© 2001 American Association for Cancer Research

Human RERE Is Localized to Nuclear Promyelocytic Leukemia Oncogenic Domains and Enhances Apoptosis

Thomas Waerner, Paola Gardellin, Klaus Pfizenmaier, Andreas Weith1 and Norbert Kraut

Department of Research, Boehringer Ingelheim Pharma KG, 88397 Biberach, Germany [T. W., A. W., N. K.]; Institute of Cell Biology and Immunology, University of Stuttgart, 70596 Stuttgart, Germany [K. P.]; and Institut Curie, Centre Universitaire, 91405 Orsay, France [P. G.]

RE repeats encoded (RERE) was identified recently as a protein with high homology to the atrophin-1 protein, which appears to be causal in the hereditary neurodegenerative disorder termed dentatorubral-pallidoluysian atrophy (DRPLA) caused by an abnormal glutamine expansion. We have independently identified RERE in a search for genes localized to the translocation breakpoint region at chromosome 1p36.2 in the neuroblastoma cell line NGP. Here we show that neuroblastoma tumor cell lines display reduced abundance of RERE transcripts. Furthermore, we detected RERE protein mainly in the nucleus, where it colocalizes with the promyelocytic leukemia protein in promyelocytic leukemia oncogenic domains (PODs). Overexpression of RERE recruits a fraction of the proapoptotic protein BAX to PODs. This observation correlates with RERE-induced apoptosis, which occurs in a caspase-dependent manner. These results identify RERE as a novel component of PODs and suggest an important role of RERE in the control of cell survival.




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Copyright © 2001 by the American Association of Cancer Research.