Hence, inhibition of ubiquitin-dependent degradation of topoisomerases may improve long-term therapeutic efficacy of topoisomerase-targeted drugs.
Mad2 is known to restrain the mitotic progression by preventing the activation of ubiquitin-dependent anaphase promoting proteolysis.
While the basic mechanism of ubiquitin-dependent TLS is now well accepted, several controversial issues remain.
Importantly, BubR1 acetylation was required for checkpoint function, through the inhibition of ubiquitin-dependent BubR1 degradation.
Skeletal muscle atrophy might be probably mainly due to activation of ubiquitin-dependent proteasome pathways.
Overloading or other perturbations of ubiquitin-dependent proteolysis are probably involved in inclusion myopathies, such as inclusion body myositis, the myofiber inclusions of which are strongly ubiquitin immunopositive.
Our data show that the capacity of the ubiquitin/proteasome system in progerin-expressing cells is sufficient to safeguard degradation of ubiquitin-dependent substrate.
We show that increases in the free NEDD8 to ubiquitin ratio trigger activation of NEDD8 by the ubiquitin E1 enzyme in cells (atypical NEDDylation), which probably leads to a global attenuation of ubiquitin-dependent protein degradation.
Ubiquitin-conjugating enzymes (E2) intervene the ubiquitination and turnover of specific substrates of the ubiquitin-dependent degradation pathway[24].
Moreover, PIRM syndrome is the first inherited disease of the ubiquitin-dependent pathway identified in cattle.
