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First published online 25 November 2008
doi: 10.1242/jcs.038570

Journal of Cell Science 121, 4106-4113 (2008)
Published by The Company of Biologists 2008
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Research Article

Loss of SUMO1 in mice affects RanGAP1 localization and formation of PML nuclear bodies, but is not lethal as it can be compensated by SUMO2 or SUMO3

Evgenij Evdokimov1, Prashant Sharma1, Stephen J. Lockett2, Margaret Lualdi3 and Michael R. Kuehn1,*

1 Laboratory of Protein Dynamics and Signaling, National Cancer Institute, National Institutes of Health, NCI-Frederick, Frederick, MD 21702, USA
2 Optical Microscopy and Analysis Laboratory, Advanced Technology Program, SAIC-Frederick, Frederick, MD 21702, USA
3 Laboratory Animal Sciences Program, SAIC-Frederick, Frederick, MD 21702, USA

* Author for correspondence (e-mail: mkuehn{at}mail.nih.gov)

Accepted 16 September 2008

Conjugation of the small ubiquitin-like modifier (SUMO) to target proteins regulates numerous biological processes and has been implicated in tumorigenesis and metastasis. The three SUMO isoforms in vertebrates, SUMO1 and the highly similar SUMO2 and SUMO3, can be conjugated to unique as well as overlapping subsets of target proteins. Yet, it is still not clear whether roles for each family member are distinct or whether redundancy exists. Here we describe a mutant mouse line that completely lacks SUMO1, but surprisingly is viable and lacks any overt phenotype. Our study points to compensatory utilization of SUMO2 and/or SUMO3 for sumoylation of SUMO1 targets. The ability of SUMO isoforms to substitute for one another has important implications for rational targeting of the SUMO pathway.

Key words: SUMO, RanGAP1, PML


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[Abstract] [Full Text] [PDF]


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