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1 es and deconjugates Nedd8/Rub1 from cullins (deneddylation).
2 ddylation) and deactivated by NEDD8 removal (deneddylation).
3 ed with substrate are normally refractory to deneddylation.
4 losome regulates CDT2 stability through CUL4 deneddylation.
5 process and ubiquitin chain elongation after deneddylation.
6 alpha stabilization independent of Cullin 2 deneddylation.
7 nt flowers without an obvious defect in CUL1 deneddylation.
8 indicating that CSN2 is essential in cullin deneddylation.
10 IM2 exhibit reduced nuclear accumulation and deneddylation activity of the CSN toward the cullin 1 an
11 While there was no obvious influence on CSN deneddylation activity, the increase in CSN subunits and
13 ed conformational changes are retained after deneddylation, allowing both initiation of the ubiquitin
14 ith an F-box-Skp1 complex markedly inhibited deneddylation, although the magnitude varied considerabl
17 mpaired CSN holocomplex formation and cullin deneddylation and resulted in decreases in F-box protein
20 This inhibition is independent of cullin deneddylation but mediated by the CSN-associated deubiqu
22 Upon consumption of substrate and subsequent deneddylation, CSN can remain stably bound to the CRL an
23 and demonstrate that the cullin neddylation-deneddylation cycle is not only required to activate CRL
24 Together, these mechanisms enable a dynamic deneddylation-disassembly cycle that promotes rapid remo
26 quitin ligases, where neddylation as well as deneddylation, facilitated by the protease activity of t
27 It promotes cleavage of the Nedd8 conjugate (deneddylation) from the cullin component of SCF ubiquiti
28 sought to determine the role of CSN-mediated deneddylation in UPS function and postnatal cardiac deve
29 complexes known to regulate neddylation and deneddylation, including the COP9 signalosome, Nub1, and
30 provide evidence that cullin neddylation and deneddylation is highly dynamic, that its equilibrium ca
31 whereas selectively promoting CSN5-mediated deNEDDylation may be beneficial in all stages of atheros
32 ects of csn mutants and monitored the cullin deneddylation/neddylation ratio during embryonic and ear
34 -1) deneddylation, we found a dose-dependent deneddylation of Cul-1 by Ado receptor stimulation predo
35 unit of the COP9 signalosome responsible for deneddylation of Cul-1, partially reversed HPC-mediated
38 r (TLR) and reactive oxygen species-mediated deneddylation of Cul3, which is essential for Cul3/Keap1
40 s ubiquitin-dependent protein degradation by deneddylation of cullin-based ubiquitin ligases and, the
42 ied by subunit 5 (CSN5/Jab1), resides in the deneddylation of the CRLs that is the hydrolysis of the
43 ochemical activity intrinsic to the complex, deneddylation of the Cullin subunits from Cullin-RING ub
46 Csn8/CSN plays an essential role in cullin deneddylation, UPS-mediated degradation of a subset of p
48 bition of NF-kappaB through cullin-1 (Cul-1) deneddylation, we found a dose-dependent deneddylation o
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