Human RERE is localized to nuclear promyelocytic leukemia oncogenic domains and enhances apoptosis
Autor: | T, Waerner, P, Gardellin, K, Pfizenmaier, A, Weith, N, Kraut |
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Rok vydání: | 2001 |
Předmět: |
Cell Nucleus
Sequence Homology Amino Acid Cell Survival Kruppel-Like Transcription Factors Apoptosis Nerve Tissue Proteins Neurodegenerative Diseases Cell Compartmentation Protein Structure Tertiary DNA-Binding Proteins Alternative Splicing Neuroblastoma Proto-Oncogene Proteins c-bcl-2 Caspases Neoplasms Proto-Oncogene Proteins Sequence Homology Nucleic Acid Tumor Cells Cultured Humans Promyelocytic Leukemia Zinc Finger Protein RNA Messenger Carrier Proteins Transcription Factors bcl-2-Associated X Protein |
Zdroj: | Cell growthdifferentiation : the molecular biology journal of the American Association for Cancer Research. 12(4) |
ISSN: | 1044-9523 |
Popis: | 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. |
Databáze: | OpenAIRE |
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