Journal
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM
Volume 38, Issue 1, Pages 5-16Publisher
SAGE PUBLICATIONS INC
DOI: 10.1177/0271678X17742260
Keywords
Brain ischemia; cell-therapy; drug repurposing; hypothermia; neuroprotection; stroke; SUMOylation
Categories
Funding
- Intramural Research Program of the NINDS/NIH
- NIH-OxCam Fellowship
- NIH R01 grants [NS081299, NS097554, NS099590]
- American Heart Association grant [16GRNT30270003]
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS099590, R01NS097554, R01NS081299] Funding Source: NIH RePORTER
- Medical Research Council [MC_PC_12009] Funding Source: researchfish
Ask authors/readers for more resources
Post-translational protein modification by small ubiquitin-like modifier (SUMO) regulates a myriad of homeostatic and stress responses. The SUMOylation pathway has been extensively studied in brain ischemia. Convincing evidence is now at hand to support the notion that a major increase in levels of SUMOylated proteins is capable of inducing tolerance to ischemic stress. Therefore, the SUMOylation pathway has emerged as a promising therapeutic target for neuroprotection in the face of brain ischemia. Despite this, it is prudent to acknowledge that there are many key questions still to be addressed in brain ischemia related to SUMOylation. Accordingly, herein, we provide a critical review of literature within the field to summarize current knowledge and in so doing highlight pertinent translational implications of the SUMOylation pathway in brain ischemia.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available