Sumoylation is critical for DJ-1 to repress p53 transcriptional activity

Fan, Jun; Ren, Haigang; Fei, Erkang; Jia, Nali; Ying, Zheng; Jiang, Peng; Wu, Mian; Wang, Guanghui

doi:10.1016/j.febslet.2008.03.003

« Previous Next »FEBS Letters
Volume 582, Issue 7 , Pages 1151-1156, 2 April 2008

Sumoylation is critical for DJ-1 to repress p53 transcriptional activity

Edited by Varda Rotter

Laboratory of Molecular Neuropathology, Hefei National Laboratory for Physical Sciences at Microscale, School of Life Sciences, University of Science and Technology of China, 443 Huangshan Road, Hefei, Anhui 230027, People’s Republic of China

Received 17 January 2008; received in revised form 29 February 2008; accepted 4 March 2008. published online 11 March 2008.

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.

Abbreviations: PD, Parkinson’s disease, SNc, substantia nigra pars compacta, Bax, Bcl-2 associated X protein, EGFP, enhanced green fluorescent protein, PBS, phosphate buffer solution, DMEM, Dulbecco’s modified Eagle’s medium, Erk1, extracellular signal-regulated kinases 1, ANOVA, analysis of variance, HRP, horseradish peroxidase, FITC, fluorescein isothiocyanate, PI, propidium iodide, UV, ultraviolet