Akt;
cytoprotection;
hibernation;
ischaemia;
oligaemia;
small ubiquitin-related modifier (SUMO);
D O I:
10.1042/BST0341295
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
071010 [生物化学与分子生物学];
081704 [应用化学];
摘要:
Progression of acute ischaemic brain damage is complex and multifactorial. Also, evidence suggests that participating molecules and signal transduction pathways can function differently in different cellular contexts. Hibernation torpor, a model of natural tolerance to profoundly reduced blood flow and oxygen delivery to brain, along with models of induced ischaemic tolerance can guide efforts to identify cytoprotective mechanisms that are multifactorial and that target multiple mechanisms in multiple cellular contexts. Posttranslational modification of proteins by conjugation with the SUMO (small ubiquitin-related modifier) is massively increased in hibernation and may be such a mechanism.