ライフサイエンスコーパス: IDE

1 IDE activity has been historically associated with insul

2 IDE binds PtdInsPs from solution, immobilized on membran

3 IDE can also rapidly degrade hormones that are held toge

4 IDE degrades insulin and a variety of small proteins inc

5 IDE exhibits a remarkable specificity to degrade insulin

6 IDE inhibitors that are active in vivo are therefore nee

7 IDE is a ubiquitously expressed cytosolic protein, where

8 IDE is an unusual metallopeptidase in that it is alloste

9 IDE is inhibited irreversibly by compounds that covalent

10 IDE is known to bind the cytoplasmic intermediate filame

11 IDE possesses an enclosed catalytic chamber that engulfs

12 IDE rapidly cleaves ANP and CNP, thus inactivating their

13 IDE selects its substrates based on size, charge, and fl

14 IDE specifically degrades bradykinin and kallidin at the

15 entative structures derived from the Abeta40-IDE and Abeta42-IDE simulations accurately reproduced th

16 res derived from the Abeta40-IDE and Abeta42-IDE simulations accurately reproduced the locations of t

17 ide at high concentrations can also activate IDE.

18 InsPs activate IDE by up to approximately 95-fold, affecting primarily

19 Polyanions activate IDE toward some substrates, yet an endogenous polyanion

20 rt the discovery of a physiologically active IDE inhibitor identified from a DNA-templated macrocycle

21 , such as oral glucose administration, acute IDE inhibition leads to substantially improved glucose t

22 resence of a disulfide bond in amylin allows IDE to cut at an additional site in the middle of the pe

23 Thus, action of the swinging door allows IDE to recognize amyloidogenicity by substrate-induced s

24 nt from a disulfide bond in amylin can alter IDE cleavage sites.

25 ts in IDE activity in the absence of altered IDE expression, further supporting a role for IDE in AD

26 surprisingly impairs glucose tolerance in an IDE-dependent manner.

27 cted modifications play a key role, since an IDE mutant devoid of all 13 cysteines is insensitive to

28 The amino portion of IDE, as well an IDE mutant in the catalytic domain of the protein, bound

29 an IDE-IGF-II and IDE-TGF-alpha at 2.3 A and IDE-amylin at 2.9 A.

30 mined the structures of human IDE-IGF-II and IDE-TGF-alpha at 2.3 A and IDE-amylin at 2.9 A.

31 zing mutations at the interface of IDE-N and IDE-C (D426C and K899C), resulting in an increase in Vma

32 t Ser-55, the interaction between nestin and IDE is phosphorylation independent.

33 The Ub-bound IDE structure and IDE mutants reveal that the interaction of the exosite w

34 oteins, and we find that alpha-synuclein and IDE levels are inversely correlated in beta-cells of Ide

35 lthough the interaction between vimentin and IDE is enhanced by vimentin phosphorylation at Ser-55, t

36 g frame 68) coprecipitated IDE and that anti-IDE antibody coprecipitated gE.

37 n the endoplasmic reticulum; again, the anti-IDE antibody coprecipitated a 73-kDa gE product.

38 hene-coated interdigitated electrode arrays (IDE-arrays) towards ultrafast, label-free screening of h

39 lize the disrupted catalytic site resided at IDE door subdomain for their degradation by IDE.

40 Au IDEs were coated with gravure films of the Tyr-containin

41 esulted in loss of the ability of gE to bind IDE.

42 define the region of VZV gE required to bind IDE.

43 teract with IDE in vitro, but vimentin binds IDE with a higher affinity than nestin.

44 Our amylin-bound IDE structure offers insight into how the structural con

45 1.9 A crystal structure of bradykinin-bound IDE reveals the binding of bradykinin to the exosite and

46 determined a 2.6-A resolution insulin-bound IDE structure.

47 The Ub-bound IDE structure and IDE mutants reveal that the interactio

48 harge transfer through the microwire-bridged IDEs, while upon analyte binding to the immobilized apta

49 dditionally, the cleavages of ANP and BNP by IDE render them active with NPR-B and a reduction of IDE

50 Thus, Ub degradation by IDE should be regulated.

51 IDE door subdomain for their degradation by IDE.

52 w that Abeta is degraded more efficiently by IDE carrying destabilizing mutations at the interface of

53 the recognition and unfolding of insulin by IDE, we determined a 2.6-A resolution insulin-bound IDE

54 selective inactivation of MIP-1 monomers by IDE could aid in controlling the MIP-1 chemotactic gradi

55 he cleavage of bradykinin-mimetic peptide by IDE is increased 2- to 3-fold.

56 egrading mechanisms of the Abeta peptides by IDE.

57 nt inadvertent proteolysis of cellular Ub by IDE.

58 stin potently inhibits the cleavage of Ub by IDE.

59 ive degradation of NPs and their variants by IDE.

60 his report, we demonstrate that in HEK cells IDE has little impact on insulin clearance.

61 uggest that the gE interaction with cellular IDE, gE targeting to TGN sites of virion envelopment, an

62 (scFv) were immobilized onto graphene-coated IDE-array sensor platform for electrical detection of h-

63 es onto our high-sensitivity graphene-coated IDE-arrays with identical sensor characteristics and ass

64 Thus, the evolutionarily conserved IDE may play a key role in modulating and reshaping the

65 ZV gE (open reading frame 68) coprecipitated IDE and that anti-IDE antibody coprecipitated gE.

66 own that the catalytic activity of cytosolic IDE to degrade insulin is reduced in affected versus una

67 increases IDE oligomerization, and decreases IDE thermostability.

68 Conversely, decreasing IDE expression reduces BNP-mediated signaling.

69 We detected IDE-Met(1) in brain and showed that its expression is re

70 ing largely from domain 4 of the four-domain IDE.

71 ither loss or gain of function of Drosophila IDE (dIDE) can restrict growth in a cell-autonomous mann

72 ity fabricated in interdigitated electrodes (IDE) fashion was realized and characterized, subsequentl

73 of inkjet-printed interdigitated electrodes (IDEs) thus drastically enhancing the sensitivity of chem

74 Gold (Au) interdigitated electrodes (IDEs) with sub-100 microm features were directly inkjet-

75 ement, in between interdigitated electrodes (IDEs).

76 63-bp sequence, the iron-dependent element (IDE), that is required for iron-dependent regulation of

77 ve in vivo are therefore needed to elucidate IDE's physiological roles and to determine its potential

78 Insulin degradation enzyme (IDE) is a 110-kDa zinc metalloprotease found in the cyto

79 Insulin-degrading enzyme (IDE) (insulysin) is a zinc metallopeptidase that metabol

80 S-nitrosylation of insulin-degrading enzyme (IDE) and dynamin-related protein 1 (Drp1), thus inhibiti

81 gE interacts with insulin-degrading enzyme (IDE) and facilitates VZV infection and cell-to-cell spre

82 Insulin-degrading enzyme (IDE) can degrade insulin and amyloid-beta, peptides invo

83 Mammalian insulin-degrading enzyme (IDE) cleaves insulin, among other peptidic substrates, b

84 Insulin-degrading enzyme (IDE) exists primarily as a dimer being unique among the

85 Insulin-degrading enzyme (IDE) hydrolyzes bioactive peptides, including insulin, a

86 Insulin-degrading enzyme (IDE) is a highly conserved zinc metallopeptidase that is

87 Insulin-degrading enzyme (IDE) is a protease that cleaves insulin and other bioact

88 Insulin-degrading enzyme (IDE) is a ubiquitous zinc-metalloprotease that hydrolyze

89 Insulin-degrading enzyme (IDE) is a zinc metalloprotease that degrades the amyloid

90 Insulin-degrading enzyme (IDE) is a zinc metalloprotease that hydrolyzes amyloid-b

91 Insulin-degrading enzyme (IDE) is an atypical zinc-metallopeptidase that degrades

92 Insulin-degrading enzyme (IDE) is identified as such a protease and decreased expr

93 Insulin-degrading enzyme (IDE) is involved in the clearance of many bioactive pept

94 bolism is the long insulin-degrading enzyme (IDE) isoform (IDE-Met(1)).

95 e homeostasis, and insulin-degrading enzyme (IDE) plays a key role in its clearance.

96 Insulin-degrading enzyme (IDE) selectively degrades the monomer of amyloidogenic p

97 lly active form of insulin degrading enzyme (IDE) through unrestrained, all-atom MD simulations have

98 ne residues in rat insulin degrading enzyme (IDE) to serines resulted in a cysteine-free form of the

99 Insulin degrading enzyme (IDE) utilizes a large catalytic chamber to selectively b

100 Insulin-degrading enzyme (IDE) was found to rapidly cleave ANP, but the functional

101 Insulin-degrading enzyme (IDE), a 110-kDa metalloendopeptidase, hydrolyzes several

102 putative receptor insulin-degrading enzyme (IDE), replicated as extensively as rOka, producing infec

103 gion (intron 1) of insulin-degrading enzyme (IDE), was the most strongly associated SNP (p=8.91 x 10(

104 face expression of insulin degrading enzyme (IDE), which cleaves the C-terminal di-Gly of ubiquitin,

105 tes binding to the insulin-degrading enzyme (IDE), which is proposed to be a VZV receptor.

106 prilysin (NEP) and insulin-degrading enzyme (IDE).

107 exes interact with insulin degrading enzyme (IDE).

108 Insulin-degrading enzyme (IDE, insulysin) is the best characterized catabolic enzy

109 e discrete-time integro-difference equation (IDE) framework.

110 tage-structured integrodifference equations (IDEs) are deterministic models which accurately reflect

111 adostat, and/or an effector, indole ethanol (IDE).

112 Since neural cells express IDE, the gE/IDE interaction was dispensable for VZV neur

113 Ub1-72 has a markedly increased affinity for IDE ( approximately 90-fold).

114 this suggests low affinity of bradykinin for IDE.

115 amino acids 24 to 71 of gE are required for IDE binding, and the secondary structure of gE is critic

116 In this work, we propose a novel role for IDE as a heat shock protein with implications in cell gr

117 DE expression, further supporting a role for IDE in AD pathogenesis.

118 from our studies supports a minimal role for IDE in insulin metabolism in vivo and suggests IDE may b

119 One important cellular role for IDE involves the neutralization of amyloidogenic protein

120 ency (ki = 78 +/- 11 nM) and selectivity for IDE.

121 Here we report a substrate-free IDE structure in its closed conformation, revealing the

122 Furthermore, IDE exhibits a remarkable ability to preferentially degr

123 Furthermore, IDE undergoes a switch between the closed and open confo

124 ino acids in this region are required for gE/IDE binding in infected cells; this deletion reduced cel

125 Since neural cells express IDE, the gE/IDE interaction was dispensable for VZV neurotropism.

126 vitro and in vivo without disrupting the gE/IDE interaction.

127 nsor equipped with the resulting porous gold IDEs featured a sensitivity to diethyl ethylphosphonate

128 diabetes risk alleles at the CDKAL1 and HHEX-IDE loci were associated with reduced birth weight when

129 polymorphisms (SNPs) at the CDKAL1 and HHEX-IDE loci, regions that were previously implicated in the

130 type 2 diabetes loci (CDKAL1, CDKN2A/B, HHEX-IDE, IGF2BP2, and SLC30A8) in 7,986 mothers and 19,200 o

131 23-CAMK1D, CDKAL1, CDKN2A/B, EXT2, FTO, HHEX-IDE, IGF2BP2, the intragenic region on 11p12, JAZF1, KCN

132 Our data show that the same genetic HHEX-IDE variant, which is associated with type 2 diabetes fr

133 variation at 20 loci including TCF7L2, HHEX-IDE, PPARG, KCNJ11, SLC30A8, IGF2BP2, CDKAL1, CDKN2A/2B,

134 conferring G allele of rs7923837 at the HHEX-IDE locus was associated with higher pediatric BMI in bo

135 CDKAL1 and HHEX/IDE diabetes-associated alleles are associated with decr

136 CDKAL1 and HHEX/IDE diabetes-associated alleles were both associated wit

137 the recently described associations at HHEX/IDE and SLC30A8.

138 he FTO, CDKAL1, CDKN2A/CDKN2B, IGF2BP2, HHEX/IDE, and SLC30A8 gene regions.

139 KCNQ1, ADRA2A, KCNJ11, HHEX/IDE, and SLC2A2 variants affected granule docking.

140 A fourth cluster (TCF7L2, SLC30A8, HHEX/IDE, CDKAL1, CDKN2A/2B) was defined by loci influencing

141 The HHEX/IDE T2D locus is associated with decreased insulin secre

142 hat field ecologists can use the homogeneous IDE as a relatively simple modelling tool--in terms of b

143 Furthermore, our studies reveal how IDE utilizes its catalytic chamber and exosite to engulf

144 In addition, this structure shows how IDE utilizes the interaction of its exosite with the N t

145 However, IDE also degrades peptide substrates that are too short

146 However, IDE instead prefers to degrade peptides with high intrin

147 However, IDE(-/-) mice display variable phenotypes relating to fa

148 Human IDE has 13 cysteines and is inhibited by hydrogen peroxi

149 f human insulin fragments generated by human IDE.

150 n, reduced amylin, and amyloid-beta by human IDE.

151 Specifically, cysteine 819 of human IDE is located inside the catalytic chamber pointing tow

152 address the kinetics and regulation of human IDE with short peptides.

153 We also determined the structures of human IDE-IGF-II and IDE-TGF-alpha at 2.3 A and IDE-amylin at

154 We also found that human IDE is potently inhibited by physiologically relevant co

155 attention on tumor cells and report that (i) IDE is overexpressed in vivo in tumors of the central ne

156 rs of the central nervous system (CNS); (ii) IDE-silencing inhibits neuroblastoma (SHSY5Y) cell proli

157 proliferation and triggers cell death; (iii) IDE inhibition is accompanied by a decrease of the poly-

158 The usual approach in implementing IDE models has been to ignore spatial variation in the d

159 Of greater importance, IDE antibody also inhibited the growth of uninfected cel

160 Importantly, IDE inhibition with NTE-1 did result in elevated plasma

161 ies may be the result of systemic defects in IDE activity in the absence of altered IDE expression, f

162 pression, suggesting the possible defects in IDE function in these AD families.

163 found that the association of rs11187065 in IDE was also associated with the phenotype in European A

164 Instead of proteolytic inactivation, IDE cleavage can lead to hyperactivation of BNP toward N

165 the V(max) for Abeta degradation, increases IDE oligomerization, and decreases IDE thermostability.

166 alloproteases, BDM44768 selectively inhibits IDE.

167 Their structural characteristics inside IDE are significantly different than the ones observed i

168 In this work, an interdigitated (IDE) biosensor was created to detect Brettanomyces using

169 long insulin-degrading enzyme (IDE) isoform (IDE-Met(1)).

170 cient to sustain plasma levels >50 times its IDE IC50 value, studies in rodents were conducted.

171 Knockout and genetic studies have linked IDE to Alzheimer's disease and type-2 diabetes.

172 ikely PtdIns(3)P, plays a role in localizing IDE to endosomes, where the enzyme reportedly encounters

173 X-ray scattering analyses show that it locks IDE in a closed conformation.

174 elation between PGC-1alpha or NRF-1 and long IDE isoform transcripts was found in non-demented brains

175 ween the activity of the zinc metalloprotein IDE and glucose homeostasis remains unclear.

176 gs demonstrate the feasibility of modulating IDE activity as a new therapeutic strategy to treat type

177 ings demonstrate that potent, small-molecule IDE inhibitors can be developed that, in certain instanc

178 icing of the canonical exons and exon 15b of IDE.

179 ause ATP is known to activate the ability of IDE to degrade short peptides, we investigated the inter

180 non-sequential cleavages and the ability of IDE to switch its substrate selectivity.

181 with a possible role for anion activation of IDE activity in vivo.

182 phosphates (PtdInsPs) serve as activators of IDE.

183 conformation for regulating the activity of IDE and provide new molecular details that will facilita

184 The insulin degradation activity of IDE is suppressed approximately 50% by either nestin or

185 sequestering and modulating the activity of IDE.

186 Our mutational analysis of IDE and peptide mass fingerprinting of GSNO-treated IDE

187 Our time-dependent analysis of IDE-digested insulin fragments reveals that IDE is highl

188 presented the first functional assessment of IDE in AD families showing the strongest evidence of the

189 Thus, the association of IDE with cellular regulators and product inhibition by U

190 The binding of IDE to either nestin or phosphorylated vimentin regulate

191 tch upon binding to the catalytic chamber of IDE can also contribute to the selective degradation of

192 f hydrogen bonds in the catalytic chamber of IDE.

193 insights into the conformational changes of IDE that govern the selective destruction of amyloidogen

194 nsights as to how the closed conformation of IDE may be kept in its resting, inactive conformation.

195 ing between open and closed conformations of IDE toward the open form.

196 We have generated mixed dimers of IDE in which one or both subunits contain mutations that

197 tanding riddle about the basic enzymology of IDE with important implications for the etiology of DM2

198 ly anchor their N-terminus to the exosite of IDE and undergo a conformational switch upon binding to

199 ned the catalytic activity and expression of IDE in lymphoblast samples from 12 affected and unaffect

200 such a protease and decreased expression of IDE leads to elevated MIP-1 levels in microglial cells.

201 and Lys16-Glu22 of Abeta42) mutated forms of IDE and NMR structures of the full-length Abeta40 and Ab

202 Drosophila system to define the function of IDE in the regulation of growth and metabolism.

203 loop joining the N- and C-terminal halves of IDE for catalysis.

204 thus opening up an intriguing hypothesis of IDE as an anticancer target.

205 t type-2 diabetes, and the identification of IDE (insulin-degrading enzyme) as a diabetes susceptibil

206 Here, we interrogated the importance of IDE-mediated catabolism on insulin clearance in vivo.

207 sylated, leading to complete inactivation of IDE.

208 the general usefulness of the inhibition of IDE catalytic activity to treat diabetes.

209 In vitro inhibition of IDE increased mitAbeta and impaired mitochondrial respir

210 rigger the oligomerization and inhibition of IDE.

211 Recently, a peptide inhibitor of IDE has been shown to affect levels of insulin, amylin,

212 design the first catalytic site inhibitor of IDE suitable for in vivo studies (BDM44768).

213 developed the first effective inhibitors of IDE, peptide hydroxamates that, while highly potent and

214 development of activators and inhibitors of IDE.

215 destabilizing mutations at the interface of IDE-N and IDE-C (D426C and K899C), resulting in an incre

216 , we show that reducing expression levels of IDE profoundly alters the response of NPR-A and NPR-B to

217 strates; however, the molecular mechanism of IDE function, including substrate access to the chamber

218 n, demonstrating that chemical modulation of IDE can be both bidirectional and highly substrate selec

219 dInsPs can serve as endogenous modulators of IDE activity, as well as regulators of its intracellular

220 The amino portion of IDE, as well an IDE mutant in the catalytic domain of th

221 er them active with NPR-B and a reduction of IDE expression diminishes the ability of ANP and BNP to

222 Additionally, this inhibitory response of IDE is substrate-dependent, biphasic for Abeta degradati

223 mylin levels, suggesting the in vivo role of IDE action on amylin may be more significant than an eff

224 and expand our understanding of the roles of IDE in glucose and hormone regulation.

225 asis of the unusual substrate selectivity of IDE that may aid the development of pharmacological agen

226 olecular basis underlying the sensitivity of IDE to thiol-alkylating agents has not been elucidated.

227 active conformation of the catalytic site of IDE and new insights as to how the closed conformation o

228 functional evidence that the active site of IDE comprises two separate domains that are operational

229 alytical approximation to the wave-speeds of IDE solutions with periodic landscapes of alternating go

230 The oligomerization state of IDE did not correlate with its activity, with the dimer

231 The structure of IDE reveals the molecular basis for the long distance in

232 Based on the structure of IDE, Asn 575 was identified as a potential hydrogen bond

233 Hydrogen peroxide and GSNO treatment of IDE reduces the V(max) for Abeta degradation, increases

234 the development of pharmacological agents or IDE mutants with therapeutic value.

235 h was investigated and resulted in preferred IDE configuration.

236 As the major insulin-degrading protease, IDE is a candidate drug target in diabetes.

237 Recently, IDE has been proposed as the receptor for varicella-zost

238 Conversely, reduced IDE expression enhances the stimulation of NPR-A and NPR

239 e decrease in activity is not due to reduced IDE expression, suggesting the possible defects in IDE f

240 ons of these cysteines and how they regulate IDE function.

241 d to different stresses markedly up-regulate IDE in a heat shock protein (HSP)-like fashion.

242 nestin or phosphorylated vimentin regulates IDE activity differently, depending on the substrate.

243 abilize Ub (DeltaDeltaG<0.6 kcal/mol) render IDE hypersensitive to Ub with rate enhancements greater

244 We found that these mutations rendered IDE less sensitive to ATP activation, suggesting that AT

245 ds to oxidation or nitrosylation of secreted IDE, leading to the reduced activity.

246 d to convert the inkjet-printed dense silver IDEs into their highly porous gold counterparts under am

247 nsor equipped with the original dense silver IDEs, which suggested that the electrode material and/or

248 ated by inkjet-printing fine-featured silver IDEs on top of the sensing elements.

249 ased on interdigitated electrode structures (IDEs) that have been fabricated by means of thin-film te

250 Two large prospective studies (IDE [S-ICD System IDE Clinical Investigation] and EFFORT

251 E in insulin metabolism in vivo and suggests IDE may be more important in helping regulate amylin cle

252 Reduction of cell surface IDE expression in THP-1 cells also increases the chemota

253 large prospective studies (IDE [S-ICD System IDE Clinical Investigation] and EFFORTLESS [Boston Scien

254 imentin plays the dominant role in targeting IDE to the vimentin/nestin particles in vivo, while the

255 lymorphisms (SNPs) in 12 loci (e.g., TCF7L2, IDE/KIF11/HHEX, SLC30A8, CDKAL1, PKN2, IGF2BP2, FLJ39370

256 We conclude that IDE protease binds to the 73-kDa gE precursor and that t

257 These results confirm that IDE is involved in pathways that modulate short-term glu

258 We first confirmed that IDE antibody reduced VZV spread.

259 Indeed, we demonstrate that IDE is exquisitely sensitive to Ub stability.

260 This ensures that IDE effectively splits insulin into inactive N- and C-te

261 experimental findings have established that IDE is also involved in a wide variety of physiopatholog

262 We found that IDE cleaves its substrates at multiple sites in a biased

263 From these criteria, we predict that IDE can cleave and inactivate ubiquitin (Ub).

264 ray scattering (SAXS) analysis revealed that IDE exists as a mixture of closed and open states.

265 Our structure reveals that IDE forms an enclosed catalytic chamber that completely

266 IDE-digested insulin fragments reveals that IDE is highly processive in its initial cleavage at the

267 Here, we show that IDE cleaves Ub in a biphasic manner, first, by rapidly r

268 nd obese mice with this inhibitor shows that IDE regulates the abundance and signalling of glucagon a

269 Our results suggest that IDE-Met(1) links the mitochondrial biogenesis pathway wi

270 The IDE contains two GATA-binding motifs and three octameric

271 In addition the IDE reaction rate is increased by small peptides that bi

272 ferences in average conformation between the IDE-ATP complex and unliganded IDE, but regions of the a

273 Data from the IDE and EFFORTLESS studies were pooled.

274 omosome 10q23-24 in the region harboring the IDE gene.

275 tes adopted more beta-sheet character in the IDE environment, an observation that is in line with exp

276 attempts to find potential mutations in the IDE gene in these families, we have found no coding regi

277 under ambient conditions without losing the IDE-substrate adhesion.

278 ape, charge distribution, and exosite of the IDE catalytic chamber contribute to its high affinity (

279 s complements the charge distribution of the IDE catalytic chamber for the substrate selectivity.

280 ty by substrate-induced stabilization of the IDE catalytic cleft.

281 Insertion of the IDE into the promoter region of a heterologous reporter

282 Thus, IDE can be intricately regulated by reactive oxygen or n

283 Thus, IDE retards the progression of Alzheimer's disease.

284 id not show an increased level of binding to IDE compared with that of full-length HSV gE.

285 otifs of VZV gE are important for binding to IDE or to gI.

286 n X-ray structure of the macrocycle bound to IDE reveals that it engages a binding pocket away from t

287 We have also found that total IDE mRNA levels are not significantly different in spora

288 peptide mass fingerprinting of GSNO-treated IDE using Fourier transform-ion cyclotron resonance mass

289 an amyloid beta peptide analog to wild-type IDE and to the Y609F mutant showed no difference in affi

290 nover number per active subunit as wild-type IDE.

291 Here, we captured a unique IDE conformation by using a synthetic antibody fragment

292 o newly identified ligands binding at unique IDE exosites together to construct a potent series of no

293 n between the IDE-ATP complex and unliganded IDE, but regions of the active site and C-terminal domai

294 ntracellular function relative to unmodified IDE, consistent with a possible role for anion activatio

295 tudies link the control of Ub clearance with IDE.

296 Both vimentin and nestin interact with IDE in vitro, but vimentin binds IDE with a higher affin

297 h the substrates were found to interact with IDE through several hydrogen bonding, pi-pi, CH-pi, and

298 24 to 50 of gE blocked its interaction with IDE in a concentration-dependent manner.

299 analysis of the 13 cysteine residues within IDE.

300 amber and disrupts the catalytic site within IDE door subdomain.