期刊
JOURNAL OF CELL SCIENCE
卷 121, 期 24, 页码 4106-4113出版社
COMPANY BIOLOGISTS LTD
DOI: 10.1242/jcs.038570
关键词
SUMO; RanGAP1; PML
类别
资金
- Intramural NIH HHS Funding Source: Medline
- NCI NIH HHS [N01-CO-12400] Funding Source: Medline
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.
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