Journal
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM
Volume 35, Issue 1, Pages 1-5Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/jcbfm.2014.180
Keywords
ischemic stroke; protein aggregation; small ubiquitin-related modifier; ubiquitin
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Funding
- National Institute of Health [R37-NS34179]
- American Heart Association [10SDG2600298]
- NHMRC Australia CJ Martin Fellowship
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Protein modifications cooperatively act to protect the proteome from cellular stress. Focal cerebral ischemia increases protein ubiquitination, resulting in formation of ubiquitin-rich aggregates. A concurrent elevation in small ubiquitin-related modifier (SUMO)-conjugated proteins has also been reported, but a potential connection to ubiquitin remains unexplored. Here we show that SUMO2/3 conjugates are present in postischemic ubiquitin-rich aggregates, physically associated with ubiquitin. The coaggregation of SUMO2/3 and ubiquitin is induced rapidly after ischemia, depends on reperfusion, and is also observed in the absence of ischemic damage. The association between SUMO and ubiquitin suggests overlapping functional roles after ischemia/reperfusion.
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