Author: Lyudmila Kovalchuke; Eugene V. Mosharov; Oren A. Levy; Lloyd A. Greene
Title: Stress-induced phospho-ubiquitin formation causes parkin degradation Document date: 2018_12_5
ID: ceepyyxj_2
Snippet: Though much work has examined the functions of parkin, and, more recently, the mechanisms of its activation by phospho-ubiquitin (phospho-Ub) and phosphorylation [27] , substantially less is known about how levels of both total and activated parkin are regulated in cells. An important insight into parkin regulation comes from in vitro and in vivo observations that diverse stressors cause a decrease in parkin protein levels [14] , [15] , [28] [29].....
Document: Though much work has examined the functions of parkin, and, more recently, the mechanisms of its activation by phospho-ubiquitin (phospho-Ub) and phosphorylation [27] , substantially less is known about how levels of both total and activated parkin are regulated in cells. An important insight into parkin regulation comes from in vitro and in vivo observations that diverse stressors cause a decrease in parkin protein levels [14] , [15] , [28] [29] [30] [31] . These stressors include mitochondrial complex I inhibitors [15] , [28] [29] [30] , oxidative agents [14] , [15] , [29] , [30] , and a DNA-damaging agent [31] . Mitochondrial dysfunction and oxidative stress are well-characterized aspects of PD [32] [33] [34] [35] , suggesting that parkin loss from these stresses may occur in, and possibly contribute to, the progression of this disorder. However, the mechanism(s) involved in parkin loss from these stressors are largely unclear.
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