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1 ting MDM2/MDM4 interaction and inducing MDM2 self-ubiquitination.
2 ly regulated by GDU1 ubiquitination and LOG2 self-ubiquitination.
3 FD, indicating that the RFD is essential for self-ubiquitination.
4 e p27, such a mutation has no effect on Skp2 self-ubiquitination.
5 on as E3 ligases based on their capacity for self-ubiquitination.
6 heir unique N termini, resulting in enhanced self-ubiquitination.
7 ger domain and plays a critical role in Mdm2 self-ubiquitination.
8 induce a specific RING topology that enables self-ubiquitination.
10 activity and binding to p53, separating the self-ubiquitination activity of MDM2 from its ability to
13 stabilization of COP1 through reducing COP1 self-ubiquitination and decelerating COP1's turnover rat
14 d that AKR1C3 can bind Siah2 and inhibit its self-ubiquitination and degradation, thereby increasing
15 uitin ligase Trim21, thereby reducing Trim21 self-ubiquitination and degradation, which increased Tri
18 n Sumo-1 conjugation, Mdm2 is protected from self-ubiquitination and elicits greater ubiquitin-protei
19 In vitro sumoylation of Mdm2 abrogates its self-ubiquitination and increases its ubiquitin ligase a
21 orylation-dependent manner and promotes Fbw7 self-ubiquitination and protein degradation by disruptin
23 totype substrate Hmg2p-GFP, validating Hrd1p self-ubiquitination as a viable assay of ligase function
25 of Usa1p was required specifically for Hrd1p self-ubiquitination but not for degradation of either ER
26 chondrial membrane potential, caused by its (self-)ubiquitination, followed by degradation via the ub
27 dulates HECT domain activity, as measured by self-ubiquitination induced in the absence of this helix
31 om its binding to Ub chains on the E3 (after self-ubiquitination) or on the substrate, as a mutant la
32 o and in vivo experiments indicate that E6AP self-ubiquitination results primarily from an intramolec
33 ndent signaling triggered noncanonical TRAF3 self-ubiquitination that activated the interferon respon
34 dies revealed that 14-3-3sigma enhanced COP1 self-ubiquitination, thereby preventing COP1-mediated p5
35 tolerance to exogenous amino acids, and LOG2 self-ubiquitination was markedly stimulated by the GDU1