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1 iquitinated protein(s) to be degraded by the proteosome.
2 nd degradation of both proteins via the 26 S proteosome.
3 nomeric C and B subunits are degraded by the proteosome.
4 ys limited stability, and is degraded by the proteosome.
5 ssential for its targeted degradation by the proteosome.
6 no other evidence for the involvement of the proteosome.
7 its susceptibility to proteolysis by the 26S proteosome.
8 cuolar proteolysis and is independent of the proteosome.
9 ination controls its degradation via the 26S proteosome.
10 1 and at the post-translational level by the proteosome.
11 get of ubiquitin-mediated degradation by the proteosome.
12 erruptus for degradation by Cullin-3 and the proteosome.
13 es ABHD5 by retarding its degradation by the proteosome.
14 y cysteine protease activity rather than the proteosome.
15 Janus kinase (JAK) 1/2 were degraded by the proteosome.
16 itive to pharmacologic inhibition of the 26S proteosome.
17 cytosolic degradation of heavy chains by the proteosomes.
18 esponses than alum-adjuvanted toxoid without proteosomes.
19 ) titers when the toxoid was formulated with proteosomes.
20 gradation, mediated in part by lysosomes and proteosomes.
21 oreover, it efficiently colocalizes with the proteosome 20s subunit, which degrades proteins into pep
22 and specifically inhibits chymotrypsin-like proteosome activity at low concentrations (< 100 nM) and
23 (FPA-137) was the most potent and inhibited proteosome activity in intact human prostate cancer PC-3
25 eir functions, oppose the yeast ribosome and proteosome, along with evidence for the inverse transcri
30 ricus, including subunits of the thermosome, proteosome and ribosome, are acetylated at the N-terminu
31 catenin is ubiquitinated and degraded by the proteosome and that beta-catenin stability is regulated
32 with the capacity to interact with both the proteosome and ubiquitin ligases, in regulating nicotine
36 tion of SNC1 by CPR1 is dependent on the 26S proteosome as a protease inhibitor MG132 stabilizes SNC1
37 protein folding (chaperones), the ubiquitin-proteosome, axon transport and NDD-specific genes in ser
38 eripheral activation of microglia by a nasal proteosome-based adjuvant (Protollin) that has been give
39 Here we show that nasal vaccination with a proteosome-based adjuvant that is well tolerated in huma
40 patibility complex (MHC) class I binding and proteosome cleavage site algorithms identified 101 influ
42 tly posttranslational, mediated by ubiquitin-proteosome degradation as lactacystin, a proteosome inhi
43 h a reduction in Akt transcription, enhanced proteosome degradation of Akt, and altered levels of DJ-
44 r N-acetyl-Leu-Leu-norleucinal, which blocks proteosome degradation of IkappaB, demonstrating that NF
45 t the failure of NMJ function, activation of proteosome degradation, and a reduction of the Akt pathw
46 sequences, motifs associated with ubiquitin/proteosome degradation, that overlap the previously iden
47 tizyme targets ODC for ubiquitin-independent proteosome degradation, thereby inhibiting polyamine syn
49 ygen (O2) availability are also targeted for proteosome-dependent degradation by the E3 ubiquitin lig
50 cadherin transcriptional repressor Snail and proteosome-dependent degradation of beta-catenin protein
52 t MCL-1 protein levels rapidly decrease in a proteosome-dependent fashion, whereas those of BCL-2 are
58 tion of PTEN was most likely mediated by the proteosome-dependent pathway, we have evidence that PTEN
64 izing Ab in lung wash, and formulations with proteosomes, emulsomes, or proteosomes plus emulsomes el
65 aining monophosphoryl lipid A (MPL), MPL-AF, proteosomes, emulsomes, or proteosomes with emulsomes el
66 and greatly accelerating its degradation by proteosomes following its ubiquitination by the E1B-55K/
68 oxin B subunit with or without holotoxin, or proteosomes from Neisseria meningitidis outer membrane p
69 presentation to CD8(+) T cells is limited to proteosome-generated peptides from intracellular pathoge
70 ed with meningococcal outer membrane protein proteosomes has previously been shown to be immunogenic
71 nodeficiency virus (HIV) rgp160 complexed to proteosomes improved anti-gp160 serum IgA and IgG titers
77 ion, altered glycosylation, degradation by a proteosome-independent pathway, and partial retention in
78 with the hexavalent vaccine formulated with proteosomes indicated the presence of hexavalent protein
84 thway and thus maturation was blocked by the proteosome inhibitor benzyloxycarbonyl-isoleucyl-glutamy
87 degradation of CTR1 can be blocked with the proteosome inhibitor bortezomib, and this increases the
89 nsfectants were grown in the presence of the proteosome inhibitor clasto-lactacystin beta-lactone, su
90 ALLN (N-acetyl-Leu-Leu-norleucinal) and the proteosome inhibitor lactacystin inhibited the HRG-induc
91 Furthermore, co-treatment with H7 and the proteosome inhibitor LLnL prevented the accumulation of
93 oth proteins was seen in the presence of the proteosome inhibitor MG-132 suggesting that they are nor
94 )), but not total p65, was unaffected by the proteosome inhibitor MG-132, which blocks IkappaB protei
95 tion of reduced GhCesA1 ZnBD is inhibited by proteosome inhibitor MG132 and also by E64 and EGTA, sug
97 ied by treatment of wild-type roots with the proteosome inhibitor MG132 or the gibberellic acid (GA)
100 ssociated degradation (ERAD) pathway using a proteosome inhibitor resulted in marked neutropenia in G
101 -341 (bortezomib) is a potent and reversible proteosome inhibitor that functions to degrade intracell
102 NF-kappa B activation; however, the specific proteosome inhibitor, lactacystin, failed to do so.
104 or, N-acetyl-leucyl-leucyl-methional, or the proteosome inhibitor, Streptomyces metabolite, lactacyst
105 ct is abrogated by treatment of cells with a proteosome inhibitor, suggesting that CHK2(R145W) is tar
109 SRY protein expression was increased by proteosome inhibitors and by the androgen-liganded AR in
110 inhibition of IKK alpha or IKK beta, whereas proteosome inhibitors instead suppress NF-kappaB functio
112 o paxillin and treatment of the neurons with proteosome inhibitors prevented paxillin down-regulation
113 nsferase inhibitors, histone deacetylase and proteosome inhibitors, antiangiogenesis agents, Fms-like
114 e Cdk inhibitor roscovitine was prevented by proteosome inhibitors, indicating that Cdk1 stabilizes A
115 merase II inhibitors, kinase inhibitors, and proteosome inhibitors, induced functional activation of
116 emonstrate here that treatment with the 26 S proteosome inhibitors, MG132 and ALLN, leads to detectio
117 e with DSBs were restored in the presence of proteosome inhibitors, or when cells from the suspension
118 ely resembles cellular responses elicited by proteosome inhibitors, with rapid induction of heat shoc
119 ors administered in a suboptimal sequence or proteosome inhibitors.Oncogene advance online publicatio
121 ves degradation of cytosolic proteins by the proteosome into peptides, transport of the peptides acro
122 has structural similarity to the cytoplasmic proteosome is increased in leukemic cells from approxima
123 se inhibitor gefitinib or by exposure to the proteosome/lysosome inhibitor MG132, significantly reduc
125 events recruitment of the ubiquitylation/19S proteosome machinery that normally mediates the signal-d
128 se that acts on STAT proteins to cause their proteosome-mediated degradation and enhance their dephos
129 ed on the hypothesis that ubiquitination and proteosome-mediated degradation of Nrf2 in the cytoplasm
130 ndered the protein unstable and led to rapid proteosome-mediated degradation, a feature that was more
131 thway because the mdm2 protein marks p53 for proteosome-mediated degradation, thereby providing a neg
140 However, SopE is rapidly degraded through a proteosome-mediated pathway, while SptP exhibits much sl
143 These data expand the applicability of the proteosome mucosal vaccine delivery system to protein to
144 al development of triterpenoid dual-function proteosome/NF-kappaB inhibitors as therapeutics for huma
145 hanisms that characterize the effect of MOMP proteosomes on host cells may provide new insights for i
148 egradation of cofilin through ubiquitination-proteosome pathway and consequently inhibits cofilin act
149 lective protein degradation by the ubiquitin-proteosome pathway has recently emerged as a powerful re
150 signal, but its destruction by the ubiquitin-proteosome pathway is required to allow the cell to cont
151 to further investigate whether the ubiquitin-proteosome pathway responsible for cyclin B degradation
152 iates degradation of RON through a ubiquitin-proteosome pathway, and suggest that by targeting signal
154 oupled with the inactivity-induced atrogin-1/proteosome pathway, leads to the acute muscle loss seen
155 reticulum can be regulated by the ubiquitin-proteosome pathway, resulting in altered surface express
156 cell epitopes are generated in the ubiquitin-proteosome pathway, we also investigated the ability of
158 isplay increased activities of the ubiquitin-proteosome pathway, which degrades cyclin B, as compared
170 p160 with MPL-AF, proteosomes, emulsomes, or proteosomes plus emulsomes elicited HIV-1MN-neutralizing
171 formulations with proteosomes, emulsomes, or proteosomes plus emulsomes elicited HIV-1MN-neutralizing
175 an unstable protein that is targeted to the proteosome, probably by Scul(Cdc4)-mediated ubiquitinati
179 and suggest a possible link of the ubiquitin/proteosome proteolytic pathway and the WT1 transcription
180 e induced after intranasal immunization with proteosome-rgp160 delivered either in saline or with emu
182 estinal, and fecal IgA and IgG by intranasal proteosome-rgp160 vaccines delivered in saline or with e
183 mmune responses to intranasally administered proteosome-S. flexneri 2a LPS vaccine is similar to thos
184 t immunization of nonhuman primates with the proteosome-SEB toxoid vaccine is safe, immunogenic, and
186 cy of SEB toxoid indicates that testing such proteosome-SEB toxoid vaccines in the nonhuman primate a
187 enteral and respiratory vaccination with the proteosome-SEB toxoid, thereby supporting clinical trial
189 use of inhibitors, including lactacystin (a proteosome-specific inhibitor), suggests that Galpha(o)
191 nd LC3 co-localization without activation of proteosome, suggesting a novel Mfn2 degradation pathway
192 uld be detected only after inhibition of the proteosome, suggesting that BOS1 is a target of ubiquiti
193 nhibited by lactacystin, an inhibitor of 26S proteosome, suggesting that curcumin represses cyclin D1
194 e ubiquitin E2 UBC4, or by inhibition of the proteosome suppresses mot1-301 mutant phenotypes and inc
198 macrophages, up-regulation of the ubiquitin-proteosome system, and down-regulation of the helix-loop
199 lure of protein degredation by the ubiquitin-proteosome system, production of neurotoxic peptide olig
204 r subunits in neurons by drawing them to the proteosome, thus regulating nicotine-induced up-regulati
209 n, intranasal immunization of mice with this proteosome-toxoid vaccine elicited high levels of anti-S
211 al and systemic IgA and IgG responses by the proteosome vaccine delivered by a respiratory route are
212 ids and suggest that respiratory delivery of proteosome vaccines may be practical for enhancement of
213 g for the development of mucosally delivered proteosome vaccines to protect against SEB and other tox
215 . immunization with toxoid in saline without proteosomes was not significantly protective in either c
216 Using MOMP formed in pure protein micelles (proteosomes), we show the induction of TLR2-dependent in
219 A (MPL), MPL-AF, proteosomes, emulsomes, or proteosomes with emulsomes elicited strong gp160-specifi
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