ライフサイエンスコーパス: proteasome

1 three active catalytic subunits of the plant proteasome.

2 n and, hence, inefficient degradation by the proteasome.

3 ikely because of impaired degradation in the proteasome.

4 of substrates that might otherwise enter the proteasome.

5 uring the escort of aberrant peptides to the proteasome.

6 ubsequently causing their degradation by the proteasome.

7 degradation is regulated by Pib1 and the 26S proteasome.

8 nkage, which is normally not targeted to the proteasome.

9 uminated new intricacies and dynamics of the proteasome.

10 ed from the ER membrane, and degraded by the proteasome.

11 ide generation, proteins are degraded by the proteasome.

12 menin was ubiquitinated and degraded by the proteasome.

13 with the CP in the ATP-hydrolysis-competent proteasome.

14 e cytosol where they are degraded by the 26S proteasome.

15 se compounds target the beta5 subunit of the proteasome.

16 itin-independent FOS degradation via the 20S proteasome.

17 by ubiquitin, which then directs them to the proteasome.

18 e ALY epitope compared with the constitutive proteasome.

19 which contains the proteolytic sites of the proteasome.

20 has been proposed as the "ancestral" form of proteasomes.

21 scopy structures of both human and yeast 26S proteasomes.

22 RA190-induced accumulation of substrates at proteasomes.

23 ralogs of each catalytic subunit into active proteasomes.

24 that differ in shape from both HslV and 20S proteasomes.

25 acted from the membrane, and degraded by the proteasome-a pathway termed endoplasmic reticulum-associ

26 However, only recruitment into the proteasome activates Uch37.

27 tin-like beta-grasp domain that precedes the proteasome-activating carboxyl terminus.

28 Infection with wild-type PtoDC3000 causes proteasome activities that range from strongly induced b

29 NPCs, HD-iPSC-derived neurons showed reduced proteasome activity and diminished FOXO4 expression comp

30 HD iPSCs exhibited elevated proteasome activity and higher levels of FOXO1 and FOXO4

31 derstand the pathogenesis of HD, we analyzed proteasome activity and the expression of FOXO transcrip

32 tion therapies that enhance PP2A and inhibit proteasome activity as novel therapeutic strategies for

33 selective proteolysis, and the regulation of proteasome activity by interacting proteins and subunit

34 cell characteristics, whereas enhancement of proteasome activity conferred attributes of memory lymph

35 lex control over the proteasome, suppressing proteasome activity even when inactive in deubiquitinati

36 Inhibition of GA production and proteasome activity feminized male flowers.

37 proteomic analyses revealed that modulating proteasome activity in CD8+ T cells affected cellular me

38 Pharmacologic reduction of proteasome activity in CD8+ T cells early during differe

39 However, NAC did not affect the loss of proteasome activity in response to MG132, demonstrating

40 ken together, these results demonstrate that proteasome activity is an important regulator of CD8+ T

41 devastating neurodegenerative disorder, how proteasome activity is regulated in HD affected stem cel

42 Impaired proteasome activity may also enhance accumulation of oth

43 te and raise the possibility that increasing proteasome activity may be a useful therapeutic strategy

44 This mechanism enables proteasome activity to adapt to the supply of substrates

45 reciable increase in K6a gene expression and proteasome activity, a higher level of cytosolic K6a res

46 These data suggest that FOXOs modulate proteasome activity, and thus represents a potentially v

47 AKT activity increased both FOXO4 level and proteasome activity, indicating a potential role of AKT

48 o exhibited low and high rates of endogenous proteasome activity, respectively.

49 of FOXO4 but not FOXO1 expression decreased proteasome activity.

50 , G93A-SOD1 mice showed elevation of OMI and proteasome activity.

51 ons of GA and inhibitors of GA synthesis and proteasome activity.

52 efficient bortezomib-mediated inhibition of proteasome activity.

53 proteins and pathways that are sensitive to proteasome activity.

54 pendent localization of SUMO, ubiquitin, and proteasomes along chromosome axes was mediated largely b

55 t the non-proteolytic 19S subunit of the 26S proteasome also regulates the spreading of inactive chro

56 7 is unique in being a component of both the proteasome and a second multisubunit assembly, the INO80

57 a signaling pathway as well as the ubiquitin-proteasome and autophagy-lysosome pathways, resulting in

58 ch has been linked to inhibition of both the proteasome and autophagy.

59 ontrast to the cavity characteristics of the proteasome and HslV, a classical proteasomal reaction me

60 ponent Alm1 is required to maintain both the proteasome and its anchor, Cut8, at the nuclear envelope

61 suring chymotrypsin-like activity of the 26S proteasome and messenger RNA expressions of muscle-speci

62 cluding gene expression, axonal trafficking, proteasome and mitochondrial activity, and intracellular

63 alizes tau seeds through the activity of the proteasome and the AAA ATPase p97/VCP in a similar manne

64 resents endogenous peptides processed by the proteasome and transported to the ER by the transporter

65 s revealed that PSGs are densely packed with proteasomes and contain ubiquitin but no polyubiquitin c

66 fects thus reduce ATP hydrolysis by inactive proteasomes and nonspecific proteolysis and enhance prot

67 ing nexin Snx4 in the autophagic turnover of proteasomes and several other large multisubunit complex

68 s, Usp14 and Ube3c cycle together on and off proteasomes, and the presence of ubiquitinated substrate

69 Proteasomes are essential for protein degradation in pro

70 In most organisms, proteasomes are located in both the nucleus and cytoplas

71 Proteasomes are multi-subunit proteases critical for the

72 Eukaryotic and archaeal proteasomes are paradigms for self-compartmentalizing pr

73 autophagy routes for nuclear and cytoplasmic proteasomes are unclear.

74 ogress has been made in the understanding of proteasome assembly, structure, and function.

75 n in the last step of the chaperone-mediated proteasome assembly.

76 he ubiquitin-specific protease 14 (Usp14), a proteasome-associated deubiquitinase, in direct Ag prese

77 in with an affinity similar to that of other proteasome-associated ubiquitin receptors and that RPN2,

78 a membrane, we provide evidence that nuclear proteasomes at least partially disassemble before autoph

79 We found that nitrogen starvation-induced proteasome autophagy is independent of known nucleophagy

80 aining Cav1.2 alpha1 degradation through the proteasome because a proteasome inhibitor partially rest

81 tinated proteins to cell extracts stimulated proteasome binding of both enzymes.

82 Inhibition of the proteasome (bortezomib), but not macroautophagy (3-methy

83 s with the lid in the ATP-hydrolysis-blocked proteasome, but clashes instead with the CP in the ATP-h

84 Turnover of the 26S proteasome by autophagy is an evolutionarily conserved p

85 response to pharmaceutical inhibition of the proteasome (by MG-132) or p90 ribosomal S6 kinases (by B

86 e protease at the center of this system, the proteasome, by ubiquitin tags, but ubiquitin is also use

87 The 26S proteasome can be divided into two subcomplexes: the 19S

88 three different catalytic activities of the proteasome can have different functions, but tools to mo

89 However, it is now clear that proteasomes can produce a significant portion of epitope

90 uitinated proteins without any impairment of proteasome catalytic activity.

91 We review current knowledge about proteasome-catalyzed peptide splicing (PCPS), the emergi

92 d by in vitro experiments, a decrease of the proteasome chimotrypsin activity.

93 SMD12 (aka RPN5) of the 19S regulator of 26S proteasome complex, in unrelated individuals with intell

94 au, where A152T caused neurodegeneration and proteasome compromise.

95 ha, G93A-SOD1 failed to activate OMI and the proteasome, confirming the ERalpha dependence of the res

96 The 20S proteasome core particle (20S CP) plays an integral role

97 translocates protein substrates into the Mtb proteasome core particle for degradation.

98 and hinders the interaction of Mpa with the proteasome core protease.

99 as reinhardtii, we observed that nuclear 26S proteasomes crowd around NPCs.

100 oteins particularly accumulate in HSP70- and proteasome-deficient cells, suggesting that SUMOylation

101 The molecular nature of the CaV2.1 ubiquitin-proteasome degradation pathway is currently unknown.

102 Kb expression in HEK cells is susceptible to proteasome degradation, and fusion of GFP to the C-termi

103 the C-terminus of the channel may ameliorate proteasome degradation.

104 ortezomib, suggesting that cisplatin induced proteasome dependent degradation of PID1.

105 ator, FoxO1 protein levels are decreased via proteasome-dependent degradation and via reactive oxygen

106 ction by regulating FoxO1 protein levels via proteasome-dependent degradation and, in turn, gluconeog

107 nctional analyses the p.R157X variant caused proteasome-dependent degradation of both the truncated a

108 EY MESSAGE: KEG is involved in mediating the proteasome-dependent degradation of FDH, a stress-respon

109 orphan receptor NR4A1, which plays a role in proteasome-dependent degradation of SMAD7.

110 a-induced beta-catenin, which then undergoes proteasome-dependent degradation.

111 lts in the accumulation of ACD11, confirming proteasome-dependent degradation.

112 ant role in AR intracellular trafficking and proteasome-dependent degradation.

113 quitylates GBP1, GBP2, and GBP4 to cause the proteasome-dependent destruction of existing GBP coats.

114 ranscription factor (HLTF) DNA helicase in a proteasome-dependent manner by redirecting the CRL4-DCAF

115 half-life of cytoplasmic Plk3 in a ubiquitin-proteasome-dependent manner.

116 y decreased in response to ATP addition in a proteasome-dependent manner.

117 dly reduced c-MYC (MYC) protein levels via a proteasome-dependent mechanism.

118 domain upon mitochondrial depolarization and proteasome-dependent outer membrane rupture.

119 Blockade of proteasome-dependent protein degradation with the 26S pr

120 idity in vitro and induces potent, rapid and proteasome-dependent self-degradation of VHL in differen

121 l Death11 (ACD11) in planta and promotes the proteasome-dependent turnover of ACD11 in cell-free degr

122 en mutated, alters species stoichiometry and proteasome-dependent turnover of nuclear MAF1.

123 bstrate and its turnover was Parkin-dose and proteasome-dependent.

124 e and the 19S regulatory particle in the 26S proteasome, disrupting the proteasome structure in respo

125 Our results provide insight into proteasome dynamics between proliferating and quiescent

126 proteins within cardiac myocytes related to proteasome dysfunction and impaired autophagy.

127 Although it has been speculated that proteasome dysfunction may contribute to the pathogenesi

128 ar substrate-processing state frequencies as proteasomes elsewhere in the cell, are ideally positione

129 quitin ligase complex and is targeted to the proteasome for degradation (the canonical mechanism).

130 and aggregated ubiquitinated proteins to the proteasome for degradation.

131 60S particles in order to escort them to the proteasome for degradation.

132 other substrates directly, targeting them to proteasomes for degradation.

133 rtance of PSMD12 as a scaffolding subunit in proteasome function during development and neurogenesis

134 However, recent studies indicate that proteasome function is also tightly regulated and determ

135 ation of interactions that are important for proteasome function, indicate ubiquitin affinities that

136 with O-phenanthroline (OPA) blocks cellular proteasome function, induces apoptosis in MM cells and o

137 We conclude that proteasome functions along meiotic chromosomes are evolu

138 Little is known about proteasome functions in quiescent cells.

139 The proteasome has pronounced preferences for the initiation

140 Inhibitors of the proteasome have been validated in the treatment of multi

141 y-based screening strategy revealed that the proteasomes have overlapping but distinct substrate spec

142 nd enzymes (such as ubiquitin ligases or the proteasome) have been identified as potential targets of

143 The proteasome holoenzyme is activated by its regulatory par

144 to the proteasome itself, these include the proteasome homolog HslV, which functions together with t

145 age-dependent and suppressed by blocking the proteasome, Hsp70-type molecular chaperones, the Pib1 E3

146 iquitination was prevented, or when purified proteasomes hydrolyzed the associated ubiquitin conjugat

147 Proteasome impairment has been detected in cardiomyopath

148 cardiomyopathy-causing mutations may lead to proteasome impairment, such as altered calcium handling

149 tes the degradation of NPR1 via the host 26S proteasome in a manner dependent on AvrPtoB's E3 ligase

150 e of the different catalytic subunits of the proteasome in different plant species.

151 uggesting further non-canonical roles of the proteasome in gene expression.

152 e for stress-triggered remodeling of the 26S proteasome in human cells.

153 e human ClC-Kb channel is highly degraded by proteasome in human embryonic kidney cells.

154 orders but exert toxicity from inhibition of proteasomes in other cells.

155 thermore, osteopontin reduces the release of proteasomes in the extracellular space.

156 g of green fluorescent protein (GFP)-labeled proteasomes in the yeast null-mutant collection.

157 on of chaperone expression, autophagy or the proteasome, in addition to compromising mitochondrial qu

158 To learn how the presence of Usp14 on 26S proteasomes influences its different activities, we comp

159 ndocytosed NPs, which translated in enhanced proteasome inhibition and robust cytotoxic effect on MM

160 ion microscopy, gradient centrifugation, and proteasome inhibition approaches revealed that a large f

161 udy of ubiquitination changes in response to proteasome inhibition highlights the uniqueness of RRM d

162 onsible for MeCP2 T158M degradation and that proteasome inhibition increased MeCP2 T158M levels.

163 teolyzed at various rates and the effects of proteasome inhibition indicated that proteolytic degrada

164 Proteasome inhibition is an effective therapy for multip

165 We also demonstrate the impact of proteasome inhibition on ubiquitin and SUMO-modified pro

166 Truncated MRE11 was stabilized by proteasome inhibition, exhibited a decreased half-life a

167 y molecular changes in astrocytes, including proteasome inhibition, stress kinase activation, mechani

168 main ubiquitination decreases in response to proteasome inhibition, whereas the majority of sites inc

169 nd gametocytocidal antimalarial activity and proteasome inhibition.

170 ed HRD1, and this interaction increases upon proteasome inhibition.

171 bility, and preliminary efficacy of the oral proteasome inhibitor (PI) ixazomib in patients with rela

172 Proteasome inhibitor bortezomib is a novel therapeutic a

173 The combination of the proteasome inhibitor bortezomib with lenalidomide and de

174 olled studies have suggested efficacy of the proteasome inhibitor bortezomib, but no systematic trial

175 osis in MM cells and overcomes resistance to proteasome inhibitor bortezomib.

176 d FLIL33, reversed by treatment with the 20S proteasome inhibitor bortezomib.

177 While the proteasome inhibitor field has enjoyed clinical success,

178 e-dependent protein degradation with the 26S proteasome inhibitor MG132 largely restored c-Jun protei

179 n differentiated cells and stabilized by the proteasome inhibitor MG132.

180 e mutants were increased by treatment with a proteasome inhibitor or by combining pex26 with peroxiso

181 degradation through the proteasome because a proteasome inhibitor partially restores the alpha1 prote

182 Novel therapeutic strategies to overcome proteasome inhibitor resistance are needed.

183 teasome to enhance cytotoxicity and overcome proteasome inhibitor resistance in MM.

184 more 19S proteasome subunits show intrinsic proteasome inhibitor resistance.

185 enzymes upstream of 20S proteasome overcomes proteasome inhibitor resistance.

186 on, treatment of transgenic seedlings with a proteasome inhibitor results in the accumulation of ACD1

187 Bortezomib, a proteasome inhibitor used in the management of MM, can i

188 ecrease in PID1 protein was mitigated by the proteasome inhibitor, bortezomib, suggesting that cispla

189 rectly interfering with the efficacy of this proteasome inhibitor.

190 degradation was slowed in the presence of a proteasome inhibitor.

191 ed both an immune modulatory drug (IMiD) and proteasome inhibitor: (35 [73%] of 48) were refractory t

192 uction of immunomodulatory drugs (IMiDs) and proteasome inhibitors (PIs) has greatly improved the ove

193 sex, age, disease status, refractory to both proteasome inhibitors and immunomodulatory imide drugs,

194 Proteasome inhibitors benefit patients with multiple mye

195 In the current study, we examined whether proteasome inhibitors have similar bone-protective effec

196 R trial was a head-to-head comparison of two proteasome inhibitors in patients with relapsed or refra

197 ken together, we demonstrate a novel role of proteasome inhibitors in treating radiation-induced oste

198 The use of proteasome inhibitors to target cancer's dependence on a

199 nomodulatory derivatives (IMiDs), along with proteasome inhibitors, are key components of treatment r

200 rugs, including first- and second-generation proteasome inhibitors, immunomodulatory agents, and mono

201 tibodies, alkylating agents, purine analogs, proteasome inhibitors, immunomodulatory drugs, and mamma

202 f anti-myeloma treatment regimens containing proteasome inhibitors, immunomodulatory drugs, and monoc

203 Beyond conferring resistance to proteasome inhibitors, proteasome subunit suppression al

204 are combined with immunomodulatory agents or proteasome inhibitors.

205 low toxicity profile allowing enhancement of proteasome-inhibitory activity and specificity of BTZ by

206 e that the adapter protein Ecm29 is the main proteasome-interacting protein responsible for stress-tr

207 to capture and quantify several weakly bound proteasome-interacting proteins and examine their roles

208 The 26S proteasome is a large cellular assembly that mediates th

209 The eukaryotic 26S proteasome is a large multisubunit complex that degrades

210 The proteasome is a nuclear-cytoplasmic proteolytic complex

211 idated using in vitro inhibition assays with proteasomes isolated from Plasmodium falciparum.

212 artmentalizing proteases; in addition to the proteasome itself, these include the proteasome homolog

213 Furthermore, proteasomes lacking Usp14 are much more active in degrad

214 The proteasomes lacking Usp14 had higher basal peptidase act

215 ctivity of ataxin 3 to protect beclin 1 from proteasome-mediated degradation and thereby enables auto

216 ation does not arise because of overwhelming proteasome-mediated degradation but because of a general

217 ucleolar localization of SmgGDS and promotes proteasome-mediated degradation of SmgGDS, indicating th

218 n D-CDK4 and the cullin 3-SPOP E3 ligase via proteasome-mediated degradation.

219 in chains that typically target them for 26S proteasome-mediated degradation.

220 The extracellular proteasome-mediated inflammatory pathway may represent a

221 Inhibition of CDK4/CDK6 revealed proteasome-mediated Ki-67 degradation in G1 After cell-c

222 runcated SERPINB7 protein was degraded via a proteasome-mediated pathway.

223 functions: it is required for both efficient proteasome-mediated protein degradation and the dynamic

224 Although proteasome-mediated proteolysis is known to produce anti

225 fluorescent protein fusion may slow down the proteasome-mediated proteolysis.

226 The ubiquitin proteasome mutants tir1-1 and axr1-12, which show enhanc

227 bilizes the SMN protein, unrelated to global proteasome or autophagy inhibition, revealing a novel th

228 hat hRpn13 binds preferentially to hRpn2 and proteasomes over RA190.

229 ubiquitylating (DUB) enzymes upstream of 20S proteasome overcomes proteasome inhibitor resistance.

230 Phosphoinositide 3-kinase (PI3K) and the proteasome pathway are both involved in activating the m

231 PrP(C) was degraded via the proteasome pathway mediated by the ubiquitin-protein E3

232 Further, we found that the ubiquitin/proteasome pathway was responsible for MeCP2 T158M degra

233 Proteins of the ubiquitin-proteasome pathway were rapidly upregulated after two-th

234 ylated TFEB for degradation by the ubiquitin-proteasome pathway.

235 on via the beta-TrCP-mediated ubiquitination-proteasome pathway.

236 s degraded under dark conditions via the 26S proteasome pathway.

237 e hypothesized that cotargeting the PI3K and proteasome pathways might synergistically inhibit transl

238 The autophagy and proteasome pathways were activated in both muscles at va

239 The proteasome plays a crucial role in degradation of normal

240 I K63-linked polyubiquitination and that the proteasome plays a role in RIG-I degradation.

241 by promoting substrate dissociation from the proteasome prior to the commitment step.

242 d enzymatic and regulatory properties of 26S proteasomes purified from wild-type mouse embryonic fibr

243 urified Usp14 to the WT and Usp14-defficient proteasomes reduced both their basal peptidase activity

244 11, Usp14, and Uch37-are associated with the proteasome regulatory particle.

245 26S immunoproteasomes, but not standard 26S proteasomes, releasing the 20S catalytic immunoproteasom

246 ore autophagic turnover, whereas cytoplasmic proteasomes remain largely intact.

247 abeling procedure in which a series of mixed proteasome rings are prepared such that the percentage o

248 recent advances in our understanding of the proteasome's multistep ATP-dependent mechanism, its bioc

249 gradation is inhibited by its binding to the proteasome shuttle Rad23 through ubiquitin-binding site

250 be inferred from the covalent binding of the proteasome-specific inhibitor epoxomicin to BPH.

251 rticle in the 26S proteasome, disrupting the proteasome structure in response to oxidative stress.

252 inates multiple proteasome subunits, reduces proteasome subunit abundance and activity, stabilizes nu

253 n addition, mutant RAS coordinately elevates proteasome subunit expression and proteolytic activity t

254 ferring resistance to proteasome inhibitors, proteasome subunit suppression also serves as a sentinel

255 within PRE4 (YFR050C), encoding an essential proteasome subunit; Sc2.0 coding changes reduced Pre4 pr

256 ethionine sulfoxide reductase A, and the 20S proteasome subunits PSMB5 and alphabeta.

257 ith suppressed expression of one or more 19S proteasome subunits show intrinsic proteasome inhibitor

258 UBE3A(T485A) protein ubiquitinates multiple proteasome subunits, reduces proteasome subunit abundanc

259 to cryoelectron microscopy structures of the proteasome suggests that Nas6 controls both base-lid aff

260 Usp14 exerts complex control over the proteasome, suppressing proteasome activity even when in

261 rtantly, dual inhibition of CK1alpha and the proteasome synergistically inhibited the growth of multi

262 folded protein response (UPR), the ubiquitin-proteasome system (UPS) and autophagy, appear indispensa

263 is DISC1 turnover elicited by the ubiquitin proteasome system (UPS) but that it is orchestrated by t

264 Degradation of proteins by the ubiquitin-proteasome system (UPS) is an essential biological proce

265 In eukaryotic cells, the ubiquitin-proteasome system (UPS) is responsible for the regulated

266 The ubiquitin-proteasome system (UPS) plays a critical role in removin

267 p53 and its E3 ligase MDM2 by the ubiquitin-proteasome system (UPS) promotes carcinogenesis and mali

268 We also demonstrated that the ubiquitin-proteasome system (UPS), which is known to influence syn

269 cellular survival and the rate of ubiquitin-proteasome system (UPS)-mediated proteolysis following h

270 FDH abundance is regulated by the ubiquitin proteasome system (UPS).

271 synaptic proteostasis requires the ubiquitin-proteasome system (UPS).

272 ssential role in autophagy and the ubiquitin proteasome system (UPS).

273 eratin-derived AMPs (KAMPs) by the ubiquitin-proteasome system (UPS).

274 DPPA3 is partially cleaved by the ubiquitin-proteasome system and an N-terminus fragment remains in

275 neuronal proteolytic pathways (the ubiquitin proteasome system and autophagy).

276 1 promotes hERG degradation by the ubiquitin-proteasome system at the endoplasmic reticulum to regula

277 osolic antibody recognition to the ubiquitin proteasome system brings this research into sharper focu

278 ation.Eukaryotic cells rely on the ubiquitin-proteasome system for selective degradation of proteins,

279 tients), and one patient with FTLD-ubiquitin proteasome system positive inclusions (FTLD-UPS) that st

280 polycomb-repressive complex 1.The ubiquitin-proteasome system regulates cellular reprogramming by de

281 at EXO1 is rapidly degraded by the ubiquitin-proteasome system soon after DSB induction in human cell

282 ention on E3 ligases.Targeting the ubiquitin proteasome system to modulate protein homeostasis using

283 regulation of SETD2 protein stability by the proteasome system, and the identification of SPOP, a key

284 hat its degradation depends on the ubiquitin-proteasome system.

285 ne expression through the ubiquitin-mediated proteasome system.

286 in-like modifier)-modification and ubiquitin-proteasome systems regulate the major events of meiotic

287 hes of the endosomal-lysosomal and ubiquitin-proteasome systems, in maintaining the homeostasis of th

288 the abundance and subunit complexity of the proteasome, the assembly of this 2.5MDa complex must be

289 Here, we identified a role for the proteasome, the multisubunit protease that degrades prot

290 e defective in recruiting polyubiquitin, the proteasome, the ubiquitin-binding autophagy adaptor NBR1

291 tic CDC48/p97, works in conjunction with the proteasome to degrade misfolded or damaged proteins.

292 r targeting DUB enzyme Rpn11 upstream of 20S proteasome to enhance cytotoxicity and overcome proteaso

293 urthermore, via pharmacological tethering of proteasomes to chromatin or the plasma membrane, we prov

294 These enzymes allow proteasomes to remove ubiquitin from substrates before t

295 Proteasome-ubiquitin receptor hRpn13/Adrm1 binds and act

296 and Anbu, a recently characterized ancestral proteasome variant.

297 ble for noncrossover formation, a functional proteasome was required for a coordinated transition tha

298 g that ubiquitinated PEX5 is degraded by the proteasome when the function of PEX6 or PEX26 is reduced

299 chains direct protein substrates to the 26S proteasome, where they are removed by the deubiquitinase

300 These basket-tethered and membrane-tethered proteasomes, which have similar substrate-processing sta