Abstract
Our previous results showed that the polycomb protein mel-18 binds to a protein called HSF2 and inhibits HSF2 sumoylation, thereby functioning as an anti-SUMO E3 factor. This study also suggested that mel-18 regulates the sumoylation of other cellular proteins, but the identities of these other proteins were unknown. Here we show that mel-18 interacts with the RanGAP1 protein and inhibits its sumoylation, and that these activities do not require the RING domain of mel-18. The results also show that RanGAP1 sumoylation is decreased during mitosis, and that this is associated with increased interaction between RanGAP1 and mel-18 during this stage of the cell cycle. Intriguingly, this regulatory relationship is the opposite of that found for mel-18 and HSF2, in which the interaction between these two proteins decreases during mitosis, resulting in elevated HSF2 sumoylation. The results of this study strengthen the conclusion that mel-18 functions as an anti-SUMO E3 factor, and extend its targets to include regulation of the sumoylation of the important cellular protein RanGAP1.
Original language | English |
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Pages (from-to) | 252-255 |
Number of pages | 4 |
Journal | Biochemical and Biophysical Research Communications |
Volume | 375 |
Issue number | 2 |
DOIs | |
State | Published - Oct 17 2008 |
Bibliographical note
Funding Information:We thank Mike Matunis for the RanGAP1 construct, and other members of the laboratory for insightful discussions. This research was supported by NIH Grant GM64606 to K.D.S.
Keywords
- Mel-18
- Mitosis
- Polycomb
- RanGAP1
- SUMO
- SUMO-1
ASJC Scopus subject areas
- Biophysics
- Biochemistry
- Molecular Biology
- Cell Biology