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
| Autor: | Stephen J. Lockett, Prashant Sharma, Evgenij Evdokimov, Michael R. Kuehn, Margaret Lualdi |
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| Rok vydání: | 2008 |
| Předmět: |
Genetics
Gene isoform Tumor Suppressor Proteins GTPase-Activating Proteins SUMO-1 Protein Mutant SUMO protein Nuclear Proteins Cell Biology SUMO2 Fibroblasts Promyelocytic Leukemia Protein Biology medicine.disease_cause Phenotype Mice Mutant Strains Mice Family member Small Ubiquitin-Related Modifier Proteins medicine Animals Carcinogenesis Ubiquitins Cells Cultured Transcription Factors |
| Zdroj: | Journal of Cell Science. 121:4106-4113 |
| ISSN: | 1477-9137 0021-9533 |
| DOI: | 10.1242/jcs.038570 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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