Abstract
Sumoylation is an important post-translational modification, which is also involved in the pathogenesis of many neurodegenerative diseases. We previously reported that DJ-1 decreases Bcl-2 associated X protein expression through repressing p53 transcriptional activity. Here we show that DJ-1(K130R), the non-sumoylatable mutant form of DJ-1, shifts from nucleus to cytoplasm, fails to repress p53 transcriptional activity and loses its protective function against ultraviolet induced cell death. Our findings suggest that sumoylation is critical for DJ-1 to repress p53 transcriptional activity.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Active Transport, Cell Nucleus
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Animals
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Apoptosis
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Cell Line
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Cell Nucleus / metabolism
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Humans
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Intracellular Signaling Peptides and Proteins / genetics
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Intracellular Signaling Peptides and Proteins / metabolism*
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Mice
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Mutation
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Oncogene Proteins / genetics
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Oncogene Proteins / metabolism*
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Promoter Regions, Genetic
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Protein Deglycase DJ-1
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Protein Processing, Post-Translational
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Small Ubiquitin-Related Modifier Proteins / metabolism*
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Transcription, Genetic
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Tumor Suppressor Protein p53 / antagonists & inhibitors*
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bcl-2-Associated X Protein / genetics
Substances
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Intracellular Signaling Peptides and Proteins
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Oncogene Proteins
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Small Ubiquitin-Related Modifier Proteins
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Tumor Suppressor Protein p53
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bcl-2-Associated X Protein
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PARK7 protein, human
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Protein Deglycase DJ-1