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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.
- Source :
-
Journal of cell science [J Cell Sci] 2008 Dec 15; Vol. 121 (Pt 24), pp. 4106-13. Date of Electronic Publication: 2008 Nov 25. - Publication Year :
- 2008
-
Abstract
- 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.
- Subjects :
- Animals
Cells, Cultured
Fibroblasts ultrastructure
Mice
Mice, Mutant Strains
Promyelocytic Leukemia Protein
SUMO-1 Protein genetics
Small Ubiquitin-Related Modifier Proteins genetics
Ubiquitins genetics
Fibroblasts metabolism
GTPase-Activating Proteins metabolism
Nuclear Proteins metabolism
SUMO-1 Protein metabolism
Small Ubiquitin-Related Modifier Proteins metabolism
Transcription Factors metabolism
Tumor Suppressor Proteins metabolism
Ubiquitins metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 0021-9533
- Volume :
- 121
- Issue :
- Pt 24
- Database :
- MEDLINE
- Journal :
- Journal of cell science
- Publication Type :
- Academic Journal
- Accession number :
- 19033381
- Full Text :
- https://doi.org/10.1242/jcs.038570