ライフサイエンスコーパス: proteasome inhibitor

1 egulation of Mfn2, which can be blocked by a proteasome inhibitor.

2 rectly interfering with the efficacy of this proteasome inhibitor.

3 d their interaction was enhanced by MG132, a proteasome inhibitor.

4 an investigational, orally bioavailable 20S proteasome inhibitor.

5 molecules resulting from treatment with this proteasome inhibitor.

6 Carfilzomib is a neuropathy-sparing proteasome inhibitor.

7 Here, we show that Ecm29 acts as a proteasome inhibitor.

8 wild-type (wt) virus after treatment with a proteasome inhibitor.

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

10 ingosine kinase inhibitor, and bortezomib, a proteasome inhibitor.

11 dentify patients most likely to benefit from proteasome inhibitors.

12 HopM1, HopAO1, HopA1, and HopG1 as putative proteasome inhibitors.

13 are combined with immunomodulatory agents or proteasome inhibitors.

14 CSK9 gene transcription can be eradicated by proteasome inhibitors.

15 way for the rational design of high-affinity proteasome inhibitors.

16 hatidylinositol 3-kinase inhibitors, but not proteasome inhibitors.

17 form were more efficient and compromised by proteasome inhibitors.

18 onarily conserved mechanism of resistance to proteasome inhibitors.

19 additives and/or alternatives to competitive proteasome inhibitors.

20 decrease of cyclin A that can be reversed by proteasome inhibitors.

21 l investigation of this class as noncovalent proteasome inhibitors.

22 cellular systems that could be prevented by proteasome inhibitors.

23 y if water-soluble porphyrins can be used as proteasome inhibitors.

24 mice that were treated in vivo with JAK2 or proteasome inhibitors.

25 were designed, synthesized, and evaluated as proteasome inhibitors.

26 roducing DeltaV-kappaLCs highly sensitive to proteasome inhibitors.

27 and novel mechanism of FOXM1 suppression by proteasome inhibitors.

28 proteasome activity after pulse exposure to proteasome inhibitors.

29 and is not blocked by high concentrations of proteasome inhibitors.

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

31 pies (range, 1-3 prior therapies), including proteasome inhibitors (91%), alkylating agents (91%), au

32 Previous studies demonstrated that proteasome inhibitors abrogate the ability of TRIM5alpha

33 We determined that proteasome inhibitors act on rAAV through proteasome inh

34 ndria induced by calcium or treatment with a proteasome inhibitor, although only CSA inhibited calciu

35 Proteasome inhibitors, although initially developed for

36 This depletion was sensitive to a proteasome inhibitor and was largely ablated by a deleti

37 vity analyses using a series of boronic acid proteasome inhibitors and correlate cytotoxicity with in

38 Both proteasome inhibitors and heat shock activators were abl

39 of these novel therapies.We hypothesize that proteasome inhibitors and IMiDs are highly active becaus

40 ated significant activity when combined with proteasome inhibitors and immunomodulatory agents.

41 velopment of 2 new classes of active agents, proteasome inhibitors and immunomodulatory drugs (IMiDs)

42 rapy received (64% had disease refractory to proteasome inhibitors and immunomodulatory drugs and 64%

43 101 (95%) were refractory to the most recent proteasome inhibitors and immunomodulatory drugs used, a

44 h at least three lines of therapy (including proteasome inhibitors and immunomodulatory drugs), or we

45 odulatory drugs), or were refractory to both proteasome inhibitors and immunomodulatory drugs, were r

46 with multiple myeloma that is refractory to proteasome inhibitors and immunomodulatory drugs.

47 nts who had received previous treatment with proteasome inhibitors and immunomodulatory drugs.

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

49 dation of cyclin B and Cdc25C is reversed by proteasome inhibitors and is enhanced following DNA dama

50 ral, we recommend against the use of boosted proteasome inhibitors and nonnucleotide reverse transcri

51 3 was structurally distinct from other known proteasome inhibitors and selectively killed cancer cell

52 gimen that combines standard chemotherapy, a proteasome inhibitor, and high-dose melphalan and autolo

53 ls that had been treated with lactacystin, a proteasome inhibitor, and thapsigargin, an inducer of en

54 CXCR4, BCL2, and CD27/CD70 signaling, novel proteasome inhibitors, and chimeric antigen receptor-mod

55 cisions, indications for B-cell receptor and proteasome inhibitors, and future clinical trial initiat

56 pare the active-site specificity of clinical proteasome inhibitors, and to demonstrate that many hema

57 with poor outcome in myeloma patients, where proteasome inhibitors are a mainstay of treatment.

58 To establish whether proteasome inhibitors are active on B cells, being plasm

59 Proteasome inhibitors are key parts of our armamentarium

60 Proteasome inhibitors are known to impair parasite proli

61 recombinant adeno-associated viruses (AAV), proteasome inhibitors are known to prevent degradation o

62 Proteasome inhibitors are of great interest clinically,

63 )), and ixazomib (Ninlaro(R)), confirms that proteasome inhibitors are therapeutically useful against

64 Several new small-molecule proteasome inhibitors are under various stages of active

65 eins has received little attention, although proteasome inhibitors are widely used in research and ca

66 Proteasome inhibitors are widely used in the treatment o

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

68 tion of a noncovalent and rapidly reversible proteasome inhibitor as potential anticancer agents agai

69 clinical proof of concept for the use of 19S proteasome inhibitors as a novel therapeutic strategy fo

70 ibility of the development of noncompetitive proteasome inhibitors as additives and/or alternatives t

71 We identified proteasome inhibitors as the first type of drugs that ta

72 h bortezomib (BTZ) is one of the most potent proteasome inhibitors available, still possesses limitat

73 lso brings new insights into the efficacy of proteasome inhibitor-based therapy in this pathology.

74 aRD offers a neuropathy-sparing approach for proteasome inhibitor-based therapy in WM.

75 Proteasome inhibitors benefit patients with multiple mye

76 lls with acquired resistance to the founding proteasome inhibitor bortezomib (BTZ).

77 both TRAIL versions in combination with the proteasome inhibitor bortezomib (BZB) in hepatoma cells

78 ore the use of the selective and therapeutic proteasome inhibitor bortezomib (currently used for trea

79 The proteasome inhibitor bortezomib (Velcade) is a promising

80 xpression by miRNA-221 overexpression or the proteasome inhibitor bortezomib also reduced 3BP2 and MI

81 The proteasome inhibitor bortezomib and immunomodulatory dru

82 treatment of beta-thalassemic mice with the proteasome inhibitor bortezomib did not enhance the accu

83 In addition, we show evidence that FOXM1/proteasome inhibitor bortezomib in combination with the

84 Combining MLN4924 with the proteasome inhibitor bortezomib induces synergistic apop

85 Proteasome inhibitor bortezomib is a novel therapeutic a

86 The proteasome inhibitor bortezomib is effective in hematolo

87 his study, we investigated the effect of the proteasome inhibitor bortezomib on anaplastic thyroid ca

88 ere more profound than those mediated by the proteasome inhibitor bortezomib or a commonly used antii

89 was further enhanced by combination with the proteasome inhibitor bortezomib or a second mitochondria

90 t, are resistant to apoptosis induced by the proteasome inhibitor bortezomib or the alkylating agent

91 These findings provide evidence that the proteasome inhibitor bortezomib partially reduces lamini

92 Strikingly, inclusion of the proteasome inhibitor bortezomib reduces thrombotic risk,

93 ollidine mice and of Mdr2(-/-) mice with the proteasome inhibitor bortezomib restored PC2 expression

94 The proteasome inhibitor bortezomib reversed the defective G

95 The proteasome inhibitor bortezomib was initially approved f

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

97 model we study myeloma cells exposed to the proteasome inhibitor bortezomib, a first-line therapy.

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

99 the Food and Drug Administration include the proteasome inhibitor bortezomib, immunomodulator lenalid

100 ivated when HNSCC cells are treated with the proteasome inhibitor bortezomib, proposed as an alternat

101 s, one of which is the clinically successful proteasome inhibitor bortezomib, used for treatment of m

102 th the clinically approved chymotrypsin-like proteasome inhibitor bortezomib, VR23 produced a synergi

103 nism distinct from that of the classical 20S proteasome inhibitor bortezomib.

104 NF-kappaB signaling that is sensitive to the proteasome inhibitor bortezomib.

105 ent to overcome tumor cell resistance to the proteasome inhibitor bortezomib.

106 tivity of CCNE1-amplified tumor cells to the proteasome inhibitor bortezomib.

107 apoptose in response to UPR induction by the proteasome inhibitor bortezomib.

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

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

110 anism distinct from that of the FDA-approved proteasome inhibitor bortezomib; (ii) CuPT potently inhi

111 Strikingly, the proteasome inhibitors bortezomib and carfilzomib, which

112 ylators (bendamustine and cyclophosphamide), proteasome inhibitors (bortezomib and carfilzomib), nucl

113 Exposure of myeloma or neuronal cells to proteasome inhibitors (bortezomib, epoxomicin, and MG132

114 ne-compromised mice, that treatment with the proteasome inhibitor, bortezomib (Btz), increased surviv

115 lopment of the first clinically approved 26S proteasome inhibitor, bortezomib (BZ).

116 One proteasome inhibitor, bortezomib, has been used in trans

117 In vivo application of the proteasome inhibitor, bortezomib, partially restored exp

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

119 we examined whether the administration of a proteasome inhibitor, bortezomib, would have a protectiv

120 Here, we used clinical proteasome inhibitors, bortezomib and carfilzomib, to re

121 ators (the malleipeptins) and syrbactin-type proteasome inhibitors, both of which represent overlooke

122 Thus, the proteasome inhibitor BSc2118 is a promising new candidat

123 tion disorders, or increase effectiveness of proteasome inhibitor cancer chemotherapies.

124 The proteasome inhibitor carfilzomib (CFZ) has been used as

125 idelalisib, was highly synergistic with the proteasome inhibitor carfilzomib in lymphoma, leukemia,

126 The combination of the proteasome inhibitor carfilzomib with lenalidomide and d

127 ight review focuses on the second-generation proteasome inhibitor carfilzomib, which was recently app

128 l antibodies (ofatumumab), second-generation proteasome inhibitors (carfilzomib), mammalian target of

129 ined recombinant AAV (rAAV) effects of a new proteasome inhibitor, carfilzomib, which specifically in

130 sion methodologies, seven potent epoxyketone proteasome inhibitors (clarepoxcins A-E and landepoxcins

131 Treating Cd28(-/-) mice with a proteasome inhibitor completely rescues defective tTreg

132 AAV2 antigen presentation by over 90%, while proteasome inhibitors completely abrogated antigen prese

133 Cells treated with a proteasome inhibitor contained larger quantities of cyto

134 Importance: Proteasome inhibitors decrease or eliminate 20S CP activ

135 PI-0052, marizomib) is a naturally occurring proteasome inhibitor derived from the marine actinobacte

136 Combinations of proteasome inhibitors, dexamethasone, and alkylators ach

137 de evidence that synergies between TRAIL and proteasome inhibitors do not result from changes in the

138 l TNF-like cytokines, necroptosis induced by proteasome inhibitors does not require caspase inhibitio

139 All proteasome inhibitors dose-dependently abrogated IgM and

140 PS341 (Bortezomib) is the first proteasome inhibitor drug which has been approved in cli

141 ike TNBC lines were selectively sensitive to proteasome inhibitor drugs relative to normal epithelial

142 me dysfunction caused by pathogen attacks or proteasome inhibitor drugs.

143 Proteasome inhibitors (e.g., bortezomib, MG132) are know

144 ree patients were treated with bortezomib, a proteasome inhibitor effective in depleting plasma cells

145 -cell receptor inhibitors, second-generation proteasome inhibitors (eg, carfilzomib), and mammalian t

146 In contrast, the proteasome inhibitor epoxomicin caused a decrease in the

147 Cells pretreated in vitro with proteasome inhibitors exhibited augmented annexin V bind

148 Moreover, proteasome inhibitor experiments suggest that MKP1 is co

149 While the proteasome inhibitor field has enjoyed clinical success,

150 nction in healthy pigs, and patients using a proteasome inhibitor for cancer therapy have a higher in

151 development efforts toward subunit-specific proteasome inhibitors for applications as diverse as can

152 es are needed to determine the role of novel proteasome inhibitors for the prevention and treatment o

153 ion (group 3), anthracyclines (group 4), and proteasome inhibitors (group 5).

154 Carfilzomib, a recently FDA-approved proteasome inhibitor, has remarkable anti-myeloma (MM) a

155 Proteasome inhibitors have become an integral part of my

156 protein degradation in mammalian cells, and proteasome inhibitors have been invaluable tools in clar

157 In particular, proteasome inhibitors have been shown to be toxic for th

158 Proteasome inhibitors have demonstrated that targeting p

159 Proteasome inhibitors have revolutionized outcomes in mu

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

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

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

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

164 Marizomib (MRZ) is a novel, irreversible proteasome inhibitor in clinical development for the tre

165 to detect a significant clinical activity of proteasome inhibitors in AML patients.

166 overy of new inhibitors, improve analysis of proteasome inhibitors in clinical trials, and simplify a

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

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

169 ting of this pathway pharmacologically using proteasome inhibitors in TRIB2-positive AML cells.

170 cdk5 inhibition can enhance the activity of proteasome inhibitors in vitro.

171 acy of carfilzomib, a novel and irreversible proteasome inhibitor, in combination with cyclophosphami

172 the past decades has yielded numerous potent proteasome inhibitors including compounds currently used

173 a cell precursors, we examined a set of four proteasome inhibitors, including bortezomib, carfilzomib

174 VSMC treatment with MG132, a proteasome inhibitor, indicated that PD184161 influenced

175 d SnRK1 levels in sr45-1 are suppressed by a proteasome inhibitor, indicating that SR45 promotes targ

176 and microscopy studies, we demonstrated that proteasome inhibitors induced cytotoxic autophagy in AML

177 recruitment of MLKL to RIPK3 is restricted, proteasome inhibitors induced RIPK3-dependent apoptosis.

178 t the combination of ROS inducers with FOXM1/proteasome inhibitors induces robust apoptosis in differ

179 Noncovalent proteasome inhibitors introduce an alternative mechanism

180 The action of proteasome inhibitors is not confined to plasma cells bu

181 Carfilzomib, a proteasome inhibitor, is approved in the United States a

182 Here we show that the second generation proteasome inhibitor ixazomib (MLN9708) not only inhibit

183 We tested the efficacy of an investigational proteasome inhibitor, ixazomib, alone and in a CNI minim

184 ated biologic effects of a second-generation proteasome inhibitor, ixazomib, in T-cell lymphoma and H

185 Treatment of cells with the specific proteasome inhibitor, lactacystin, resulted in a 3-fold

186 Knockdown of PA28gamma sensitized cells to proteasome inhibitor-mediated growth arrest.

187 the ubiquitination inhibitor PYR-41 and the proteasome inhibitor MG-132 but not by the nuclear expor

188 The proteasome inhibitor MG-132 interfered with this decreas

189 nd that treatment with the nonpharmaceutical proteasome inhibitor MG-132 reduces muscle pathology in

190 Pretreatment with the proteasome inhibitor MG-132 restored the expression of P

191 Treatment with proteasome inhibitor MG-132 was able to restore both non

192 lysosomal inhibitor chloroquine, rather than proteasome inhibitor MG-132.

193 roup I mGluR activation and was blocked by a proteasome inhibitor (MG-132).

194 eukemia 1 (Mcl-1), an effect reversed by the proteasome inhibitor, MG-132.

195 increased after treating seedlings with the proteasome inhibitor MG132 (carbobenzoxy-Leu-Leu-Leu-al)

196 s in the response to DNA damage, whereas the proteasome inhibitor MG132 had no effect.

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

198 ubiquitin-dependent pathway by the chemical proteasome inhibitor MG132 prevented HIF-1alpha degradat

199 The ubiquitin E1 inhibitor UBEI-41 or the proteasome inhibitor MG132 prevented IRF5 degradation, s

200 ble NOS inhibitor S-methylisothiourea or the proteasome inhibitor MG132 prevented LPS-induced LKB1 de

201 However, the proteasome inhibitor MG132 rescued DeltaSIV INa, suggest

202 manner, and treatment of the cells with the proteasome inhibitor MG132 restored KPNA1 levels.

203 f WFS1-depleted neuroblastoma cells with the proteasome inhibitor MG132 resulted in reduced accumulat

204 primary astrocytes from the toxicity of the proteasome inhibitor MG132 without eliciting any increas

205 f proteasomes, as it was not affected by the proteasome inhibitor MG132, but it was suppressed by baf

206 t half-life in vivo and is stabilized by the proteasome inhibitor MG132, indicating that it is degrad

207 MKP1 also can be stabilized by the proteasome inhibitor MG132, suggesting that MKP1 is cons

208 MOAP-1 that could be reversed utilizing the proteasome inhibitor MG132.

209 nd this co-localization was magnified by the proteasome inhibitor MG132.

210 xpression of DbpA, which were rescued by the proteasome inhibitor MG132.

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

212 )) protein levels, which is prevented by the proteasome inhibitor MG132.

213 and its down-regulation was inhibited by the proteasome inhibitor MG132.

214 s effect, however, can be neutralized by the proteasome inhibitor MG132.

215 EPHA2 receptor levels in the presence of the proteasome inhibitor MG132.

216 in the presence of SV1 was abrogated by the proteasome inhibitor MG132.

217 markedly decreased, an effect blocked by the proteasome inhibitor MG132.

218 Here we show that the proteasome inhibitors MG132 and bortezomib activate the

219 d notably are strongly hypersensitive to the proteasome inhibitors MG132 and bortezomib.

220 Treatment of AGS and HEK293T cells with proteasome inhibitors MG132 or Omuralide increases Drosh

221 The proteasome inhibitors MG132, lactacystin, and epoxomicin

222 emonstrates that treating P3HR1 cells with a proteasome inhibitor, MG132, causes the accumulation of

223 and this is attenuated by application of the proteasome inhibitor, MG132.

224 n MCL-1 degradation which was prevented by a proteasome inhibitor, MG132.

225 zh2 levels are reduced by treatment with the proteasome inhibitor, MG132.

226 demonstrated that this efficient response to proteasome inhibitors mostly relies on the presence of t

227 ubiquitin ligase, we examined the effect of proteasome inhibitors on IL-4-induced IRS-2 phosphorylat

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

229 degradation was slowed in the presence of a proteasome inhibitor or when yeast cells contained mutat

230 UROS mutants from early degradation by using proteasome inhibitors or chemical chaperones.

231 gen gas-purged lysis buffer, the addition of proteasome inhibitors or the prolyl hydroxylase inhibito

232 Moreover, proteasome inhibitors overcome resistance to quizartinib

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

234 ed in Elmo1(-/-) T cells, and treatment with proteasome inhibitors partially restored Dock2 levels in

235 L amyloidosis patients to the first-in-class proteasome inhibitor (PI) bortezomib, we purified and in

236 bortezomib 10 years ago, this first-in-class proteasome inhibitor (PI) has contributed substantially

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

238 how MAF overexpression impacts resistance to proteasome inhibitor (PI) therapy (Bzb and carfilzomib).

239 ith >/=3 prior lines of therapy (including a proteasome inhibitor [PI] and an immunomodulatory drug [

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

241 The development of proteasome inhibitors (PIs) has transformed the treatmen

242 Proteasome inhibitors (PIs) have been reported to induce

243 with both immunomodulatory drugs (IMiDs) and proteasome inhibitors (PIs), and 88%, 78%, and 68% were

244 , steroids, immunomodulatory agents (IMiDs), proteasome inhibitors (PIs), histone deacetylase inhibit

245 e strikingly different responses to MG132, a proteasome inhibitor; proliferating cells rapidly apopto

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

247 The unsuccessful clinical trials of proteasome inhibitor PS-341 (bortezomib) in solid tumors

248 iR-30b-5p and miR-30c-5p, are upregulated by proteasome inhibitor PS-341 treatment, in HepG2 and MDA-

249 ancer Cell, Liu and colleagues report that a proteasome inhibitor reactivates an MLL-AF4 controlled a

250 he ubiquitin proteasomal cascade to overcome proteasome inhibitor resistance and provides the framewo

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

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

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

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

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

256 WS in proteasome degradation, treatment with proteasome inhibitor reversed the expression changes in

257 decreased proteasome activity, and enhanced proteasome inhibitor sensitivity in vitro and in vivo.

258 1/STAT3-mediated signaling and increases the proteasome inhibitor sensitivity of myeloma cells by alt

259 d ORMDL1 degradation by cholesterol, whereas proteasome inhibitors showed no effect.

260 Accordingly, clinically used proteasome inhibitors strongly synergize ART activity ag

261 Proteasome inhibitors such as bortezomib have proved to

262 ients develop resistance to competitive-type proteasome inhibitors such as bortezomib.

263 terpretation of cell-based experiments using proteasome inhibitors such as MG132.

264 sensitivity of multiple myeloma (MM) to 20S proteasome inhibitors, such as carfilzomib.

265 lier finding [2] that high concentrations of proteasome inhibitors suppress proteasome induction and

266 ntified TJP1 as a determinant of plasma cell proteasome inhibitor susceptibility.

267 ing FLT3-ITD mutations are more sensitive to proteasome inhibitors than wild-type samples and this se

268 Ixazomib is an oral proteasome inhibitor that is currently being studied for

269 Bortezomib is a first generation proteasome inhibitor that is the frontline chemotherapy

270 n U.S. Food and Drug Administration-approved proteasome inhibitor that selectively targets and kills

271 oduction is induced by low concentrations of proteasome inhibitors that reduce proteolysis by <50%.

272 Proteasome inhibitors that selectively target combinatio

273 Nine of them were very potent proteasome inhibitors, the best of which had an IC(50) o

274 owever, because of the pleotropic effects of proteasome inhibitors, the molecular mechanisms underlyi

275 stage, previous lines of treatment, previous proteasome inhibitor therapy, and planned route of borte

276 Randomisation was stratified by previous proteasome inhibitor therapy, previous lines of treatmen

277 The alpha,beta-epoxyketone proteasome inhibitor TMC-86A was discovered as a previou

278 Ixazomib is the first investigational oral proteasome inhibitor to be studied clinically.

279 n, and it is necessary to include a specific proteasome inhibitor to determine the background for eac

280 Ixazomib is the first oral proteasome inhibitor to enter the clinic and has been st

281 This study is informative for deciding which proteasome inhibitor to use for treating this disease.

282 roxyquinoline compounds do not act as direct proteasome inhibitors to induce cell death.

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

284 describe the optimization of noncompetitive proteasome inhibitors to yield derivatives that exhibit

285 ent, increase in proteasome subunit level in proteasome inhibitor-treated cells and confirm that PcG

286 Proteasome-inhibitor treatment prevented sirtuin-induced

287 When cells were treated with proteasome inhibitor, ubiquitinated and insoluble TDP-43

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

289 bortezomib (Velcade), a clinically approved proteasome inhibitor, we observed reduced porphyrin accu

290 ctive agents including immune modulators and proteasome inhibitors, which have changed the landscape

291 Constitutive proteasome inhibitors, which have recently been introduc

292 Here we report that bortezomib, a proteasome inhibitor with anticancer and antiangiogenic

293 esults identify VR23 as a structurally novel proteasome inhibitor with desirable properties as an ant

294 mib), an orally bioavailable next-generation proteasome inhibitor with improved pharmacokinetic and p

295 results suggest that TIR-199 is a potent new proteasome inhibitor with promise for further developmen

296 Ixazomib is an investigational, oral, proteasome inhibitor with promising anti-myeloma effects

297 says and subsequent optimization, yielding a proteasome inhibitor with pyrazole scaffold.

298 t the identification of a safe and effective proteasome inhibitor with selective anticancer propertie

299 In particular, combinations of proteasome inhibitors with histone deacetylase inhibitor

300 ucted a computational search for epoxyketone proteasome inhibitors within 185 globally distributed so