ライフサイエンスコーパス: EGCG

1 EGCG antagonized the ConA-induced CSF-2 and CSF-3 gene e

2 EGCG could attenuate Pg LPS-enhanced production of MMP-1

3 EGCG dose dependently attenuated clinical symptoms and p

4 EGCG inhibits the ability of preformed oligomers to perm

5 EGCG is a flavonoid present in green tea extract belongi

6 EGCG is a new, interesting anti-HCV molecule that could

7 EGCG normalized the palmitate-induced impairment of auto

8 EGCG protons were mapped to the protein surface by trian

9 EGCG reduced the amyloid-specific fluorescent thioflavin

10 EGCG specifically inhibited the second aggregation phase

11 EGCG was found to be more efficient than EC as inhibitor

12 EGCG was shown in transmission electron microscopy (TEM)

13 EGCG's poor stability and intestinal permeability, howev

14 EGCG+RES supplementation did not affect the fasting plas

15 EGCG+RES supplementation significantly increased oxidati

16 EGCG, a small molecule that was previously shown to dire

17 EGCG, as a chain breaker, produced fewer procyanidin oli

18 EGCG, GA and caffeine were resolved with Rf values 0.54,

19 EGCG, gallic acid, and curcumin were identified as a mul

20 After 24h, EGCG (5-100 muM) was observed to exhibit pro-oxidant act

21 ric flavan-3-ol esterified with gallic acid (EGCG) had a five to ten times higher affinity to caseins

22 sed MMP-1 production in HGFs, whereas adding EGCG significantly attenuated this enhanced production o

23 After EGCG, there was a shift to a higher and more stable CHOx

24 ng exercise, postprandial EE was lower after EGCG than after placebo, indicating an increased working

25 Although EGCG treatment of hepatocytes alone had little effect on

26 regulation of EC functions implying that an EGCG dependent activation of these phosphatases leads to

27 hereas beta-R (1), THyF (3), TMPyP4 (6), and EGCG (4) inhibit both enzymes.

28 ded greater peroxide scavenging activity and EGCG stability.

29 ions of caffeine, catechin, EC, EGC, ECG and EGCG were found to be in the ranges 0.086-2.23, 0.113-2.

30 reventive potential of green tea extract and EGCG after tannase-mediated hydrolysis.

31 n of specific OGmiRs and TSmiRs by 4-HPR and EGCG inhibited growth of malignant neuroblastomas.

32 Combination of 4-HPR and EGCG most significantly decreased expression of OGmiRs (

33 occurring in both Abeta(1-40) oligomers and EGCG during remodeling offer a foundation for understand

34 's disease, especially for Down syndrome and EGCG which inhibits Dyrk1A may have potential effect on

35 ggests that diet-derived polyphenols such as EGCG may exert chemopreventive action through pharmacolo

36 o the positive inotropic effects observed at EGCG concentrations >1 muM.

37 ish structure-activity relationships between EGCG and Hsp90.

38 nstrated the utility of the bioflavonoid (-)-EGCG, a natural product as a chiral solvating agent for

39 on might be due to the inhibition of IL-6 by EGCG.

40 , and Na(+)-K(+)-ATPase were not affected by EGCG </= 1 muM.

41 oxidation was not significantly affected by EGCG+RES (P-EGCG+RES = 0.46 and 0.38, respectively) but

42 of this aggregation of HMGB1 facilitated by EGCG.

43 we conclude that the conformation induced by EGCG is more aggregation-prone with higher binding free

44 quires MT1-MMP signaling and is inhibited by EGCG.

45 antly affect the efficiency of inhibition by EGCG inhibitors and should therefore be considered durin

46 jority of the amyloid remodeling observed by EGCG treatment, although how EGCG oxidation drives remod

47 roplets by palmitate was markedly reduced by EGCG.

48 Existing fibrils are remodeled by EGCG into non-amyloid aggregates.

49 ajor driving force for amyloid remodeling by EGCG treatment.

50 GB1, are repositioned and packed together by EGCG.

51 The multiple-ring compounds, EGCG, resveratrol, and curcumin, redirect Abeta(17-36) f

52 ddition of PD98059, LY294002, NAC, curcumin, EGCG, and SB203580 markedly inhibited TGM-2 expression i

53 gulated by PD98059, LY294002, NAC, curcumin, EGCG, and SB203580.

54 e chemopreventive properties of diet-derived EGCG alter MT1-MMP-mediated intracellular signaling.

55 Here, we dissect EGCG's mechanism of action.

56 (at 10 mug ml(-1) of the catechins EC, EGC, EGCG and ECG) were 2.6x10(3)+/-1.2x10(3), 1.7x10(-3)+/-4

57 iours of (+)-catechin, (-)-epicatechin, EGC, EGCG and BHT.

58 a dynamic region of the protein that enables EGCG to control opening and closure of the enzyme's acti

59 Female C57BL/6 mice were fed EGCG (0%, 0.15%, 0.3%, and 0.6% in diet) for 30 days and

60 Finally, EGCG+RES had no effect on insulin-stimulated glucose dis

61 s of Abeta(17-36) aggregation is as follows: EGCG > resveratrol > curcumin > vanillin, consistent wit

62 ify its biofilm and strengthens the case for EGCG as a candidate in multidrug treatment of persistent

63 r receptors, it was shown that, at least for EGCG, tea polyphenols can enter the cells and directly i

64 anocomplexes provided greater protection for EGCG than each protective component alone.

65 protein kinase kinase beta was required for EGCG-induced LC3-II formation, as evidenced by the fact

66 with multiple independent binding sites for EGCG with a Kd approximately 10-fold lower than that for

67 Numerous molecular targets for EGCG have been proposed, but the mechanisms of its antic

68 ivity in PCa cell lines compared to the free EGCG.

69 ompact peptide conformations than those from EGCG-untreated Abeta species; and (ii) ternary EGCG-meta

70 Furthermore, EGCG+RES supplementation attenuated the increase in plas

71 (NAC), curcumin, epigallocatechin-3 gallate (EGCG), and p38 inhibitor SB203580 were added to find the

72 red by sugars to epigallocatechin-3-gallate (EGCG) against deterioration.

73 in (EGC) and (-)-epigallocatechin-3-gallate (EGCG) and butylated hydroxytoluene (BHT) correlate with

74 allate (ECG) and epigallocatechin 3-gallate (EGCG) and caffeine in 29 commercial green tea samples av

75 egation, such as epigallocatechin-3-gallate (EGCG) and dopamine (DA).

76 chins such as (-)epigallocatechin-3-gallate (EGCG) are known to improve energy metabolism at rest and

77 we identify (-)-epigallocatechin-3-gallate (EGCG) as a new inhibitor of hepatitis C virus (HCV) entr

78 d polyphenol (-)-epigallocatechin-3-gallate (EGCG) has been extensively studied for its antioxidant a

79 (4-HPR) and (-)-epigallocatechin-3-gallate (EGCG) in altering expression of oncogenic microRNAs (OGm

80 nicals including epigallocatechin-3-gallate (EGCG) in green tea polyphenols (GTPs) and sulforaphane (

81 e the polyphenol epigallocatechin-3-gallate (EGCG) is emerging as an experimental secondary treatment

82 een tea catechin epigallocatechin-3-gallate (EGCG) is generally considered to be the biologically mos

83 Epigallocatechin-3-gallate (EGCG) is the major polyphenol in green tea.

84 Epigallocatechin-3-gallate (EGCG) is the most biologically potent polyphenol of gree

85 en tea component epigallocatechin-3-gallate (EGCG) may be beneficial in autoimmune diseases; however,

86 f the polyphenol epigallocatechin 3-gallate (EGCG) on hCT fibrillation was also investigated by NMR a

87 l, curcumin, and epigallocatechin-3-gallate (EGCG) on the aggregation of Abeta(17-36) peptides.

88 nd influence (-)-epigallocatechin-3-gallate (EGCG) oxidation (400muM) in Tween- or sodium dodecyl sul

89 In contrast, epigallocatechin-3-gallate (EGCG) signals ECs via the 67 kDa laminin-receptor (67LR)

90 n green tea, (-)-epigallocatechin-3-gallate (EGCG)'s potential benefits to human health have been wid

91 o treatment with Epigallocatechin-3-gallate (EGCG), a Dyrk1a inhibitor, modulated trisomic NCC defici

92 have shown that epigallocatechin-3-gallate (EGCG), a major constituent of green tea extract, exhibit

93 (-)-Epigallocatechin-3-gallate (EGCG), a major polyphenol component of green tea, has re

94 ly attributed to epigallocatechin-3-gallate (EGCG), a polyphenolic compound from the group of catechi

95 polyphenol, (-)-epigallocatechin-3-gallate (EGCG), and matrix pH (2-7) on the net anti-/pro-oxidant

96 n tea catechin, epigallo-catechin 3-gallate (EGCG), and the major dietary protein and allergen, ovalb

97 ea catechin, (-)-epigallocatechin-3-gallate (EGCG), but effects were observed only at micromolar conc

98 s, FK506 and (-)-epigallocatechin-3-gallate (EGCG), known to inhibit alphaSYN fibril formation, was i

99 tive ingredient, epigallocatechin-3-gallate (EGCG), protects cells from subsequent OGD/R-induced cell

100 Epigallocatechin-3-gallate (EGCG), the principal polyphenol isolated from green tea,

101 Epigallocatechin-3-gallate (EGCG), the principal polyphenol present in green tea, ha

102 polyphenol, (-)-epigallocatechin-3-gallate (EGCG).

103 picatechin, or (-)-epigallocatechin gallate (EGCG) added as chain breakers.

104 phenolic compounds epigallocatechin gallate (EGCG) and silibinin bind to specific conformers within a

105 ed property of (-)-epigallocatechin gallate (EGCG) as a chiral solvating agent for enantiodiscriminat

106 (-)-Epigallocatechin gallate (EGCG) effectively reduces the cytotoxicity of the Alzhei

107 The flavonoid epigallocatechin gallate (EGCG) has previously been shown to redirect the aggregat

108 n tea catechin and epigallocatechin gallate (EGCG) in soy lecithin liposomes was examined at four con

109 picatechin (EC) or epigallocatechin gallate (EGCG) inhibited formation of highly reactive intermediar

110 Epigallocatechin gallate (EGCG) is a major polyphenol in green tea that has benefi

111 commonly used (-)-epigallocatechin gallate (EGCG) is a much less efficient amyloid inhibitor at a ph

112 Epigallocatechin gallate (EGCG) is a powerful antioxidant and commonly used nutrac

113 Epigallocatechin gallate (EGCG) is often described as the most potently chemopreve

114 ementation high in epigallocatechin gallate (EGCG) on blood lipids in healthy postmenopausal women.

115 amyloid inhibitor epigallocatechin gallate (EGCG) on the aggregation pathway.

116 a shoot (GL) while epigallocatechin gallate (EGCG) recorded higher levels in GL.

117 echins, especially epigallocatechin gallate (EGCG) were found in green teas.

118 in this study that epigallocatechin gallate (EGCG), a green tea-derived catechin, acts as a potent su

119 Epigallocatechin gallate (EGCG), a major form of tea catechins, possesses immunomo

120 ine, curcumin, (-)-epigallocatechin gallate (EGCG), gallic acid, propyl gallate, resveratrol, and alp

121 chin (EGC) and (-)-epigallocatechin gallate (EGCG), respectively.

122 chin (EGC) and (-)-epigallocatechin gallate (EGCG), respectively.

123 Epigallocatechin gallate (EGCG), the major polyphenol in green tea and the main bi

124 n-3-ol substrates, epigallocatechin gallate (EGCG), was employed.

125 f SULT1A1 bound to epigallocatechin gallate (EGCG).

126 green tea flavonol epigallocatechin-gallate (EGCG), from gestation to adulthood suppressed 3R-tau exp

127 hypothesized that epigallocatechin-gallate (EGCG), the main catechin present in green tea, forms com

128 (-)-Epigallocatechin-3-O-gallate (EGCG), a major ingredient of green tea, has been shown,

129 green tea, (-)-epigallocatechin-3-O-gallate (EGCG), has been shown to have cancer-preventive and ther

130 wed by complexation of poly(ethylene glycol)-EGCG to form the shell.

131 d pro-oxidant effects observed at the higher EGCG concentrations (100-500 muM) tested.

132 ing observed by EGCG treatment, although how EGCG oxidation drives remodeling remains unclear.

133 ng, and electron microscopy to elucidate how EGCG remodels Abeta oligomers.

134 However, EGCG does not affect oligomer size distribution or secon

135 However, EGCG is hydrophilic with poor cellular absorption and th

136 These studies indicated that (i) EGCG was bound to Abeta monomers and dimers, generating

137 ase, the larger number of rotatable bonds in EGCG might be accountable for this difference.

138 Results showed significant reduction in EGCG content after one, three and six months: 24.00%, 28

139 the effect of homotaurine, scyllo-inositol, EGCG, the benzofuran derivative KMS88009, ZAbeta3W, the

140 the ability of Fap to form fibrils; instead, EGCG stabilizes protein oligomers.

141 ed and validated for determination of % loss EGCG.

142 plement containing 1315 mg catechins (843 mg EGCG) on biomarkers of breast cancer risk.

143 cognized actions of nanomolar and micromolar EGCG should be considered when the therapeutic and toxic

144 Moreover, EGCG inhibited expression of transcription factors T-box

145 Moreover, EGCG is not able to disaggregate existing amyloid fibril

146 Moreover, EGCG+RES reduced fasting (P-time x treatment = 0.03) and

147 ons were detected in samples with 25-500 muM EGCG at 24h.

148 Thus, nanomolar EGCG increases contractility in intact myocytes by coord

149 age-clamp experiments demonstrate that 10 nM EGCG significantly inhibits the Na(+)-Ca(2+) exchanger.

150 ect molecular explanation for the ability of EGCG to disrupt P. aeruginosa QS and modify its biofilm

151 These findings indicate that the ability of EGCG to inhibit myeloperoxidase activity is one of the m

152 The ability of EGCG to mediate its inhibitory activity is counter-regul

153 nomer-protofibril contacts in the absence of EGCG, undergo a direct-to-tethered contact shift.

154 lipid accumulation, suggesting the action of EGCG is through autophagosomal degradation.

155 ts into the molecular mechanism of action of EGCG provide boundary conditions for exploring amyloid r

156 -7) on the net anti-/pro-oxidant activity of EGCG in flaxseed oil-in-water (o/w) emulsions were syste

157 The antiviral activity of EGCG on HCV entry was confirmed with pseudoparticles exp

158 However, the addition of EGCG significantly attenuated the IL-6 expression and NF

159 Further, administration of EGCG to dextran sodium sulfate-induced colitic mice sign

160 HCV, suggesting the potential application of EGCG as a new anti-HCV agent for HCV therapy.

161 The behavior of EGCG encapsulated in NPs in modulating apoptosis and cel

162 Binding of EGCG to 2S albumins affects protein conformation, by cau

163 The binding of EGCG to casein micelles was quantified using HPLC.

164 atechin; however, the low bioavailability of EGCG is a limiting factor for its biological effect.

165 absorption and increased bioavailability of EGCG.

166 Biotransformation of EGCG decreased its toxicity without affecting its antipr

167 was in the range described for complexes of EGCG and other dietary proteins.

168 Though higher concentration of EGCG yielded better discrimination, the use of lower con

169 , we report that nanomolar concentrations of EGCG significantly enhance contractility of intact murin

170 The cytotoxicities of EGCG and LPS were tested by cell viability tests.

171 veloped formulation for the oral delivery of EGCG and its potential for applications in food industry

172 Ester derivatives of EGCG with other fatty acids (stearic acid, SA; eicosapen

173 hese findings support further development of EGCG as a potent therapeutic for inflammatory diseases.

174 wo HMGB1 monomers are linked by the dimer of EGCG.

175 The antimicrobial effect of EGCG against the opportunistic pathogen Pseudomonas aeru

176 phagosomal degradation opposed the effect of EGCG in ectopic lipid accumulation, suggesting the actio

177 o determine whether the beneficial effect of EGCG is mediated by a mechanism involving autophagy, the

178 more, we learn that the inhibition effect of EGCG is specific to the peptide sequence, while those of

179 resent in vitro study examines the effect of EGCG on Porphyromonas gingivalis (Pg) lipopolysaccharide

180 In this study, we determined the effect of EGCG on the development of experimental autoimmune encep

181 med to investigate the longer-term effect of EGCG+RES supplementation on metabolic profile, mitochond

182 Notably, the protective effects of EGCG are abolished when AMP-activated protein kinase (AM

183 e-induced lipid accumulation, the effects of EGCG on autophagic flux and co-localization of lipid dro

184 However, the efficacy of EGCG against gut inflammation is diminished when orally

185 ployed for sample clean-up and enrichment of EGCG over caffeine.

186 t the synthesis and biological evaluation of EGCG analogues to establish structure-activity relations

187 In this study, we evaluated the impact of EGCG treatment on the expression of colony-stimulating f

188 ional chemistry to elucidate interactions of EGCG and 2S albumins.

189 Non-covalent interactions of EGCG with proteins contribute to its diverse biological

190 In order to enhance the lipophilicity of EGCG for improved bioefficiency and to take advantage of

191 for understanding the molecular mechanism of EGCG as a neurotoxicity inhibitor.

192 However, the mechanism of EGCG-induced remodeling is not fully understood.

193 emonstrate that a concentration of 50 muM of EGCG inhibits HCV infectivity by more than 90% at an ear

194 ant of HCV-infected cells in the presence of EGCG, we observed that EGCG leads to undetectable levels

195 proceeds at a slower rate in the presence of EGCG.

196 The mechanism of the interaction property of EGCG with alpha-amino acids has been understood as arisi

197 hod for evaluating the deterioration rate of EGCG using absorbance spectroscopy.

198 the distinct antiamyloidogenic reactivity of EGCG toward metal-Abeta species with a structure-based m

199 at the interaction between aromatic rings of EGCG and the aromatic side chains of the peptide may pla

200 where the -OH groups of two phenyl rings of EGCG play dominant roles.

201 r explanation for the isozyme specificity of EGCG, which is corroborated experimentally.

202 Accelerated stability of EGCG in tablet formulations was investigated.

203 was significantly inhibited by treatment of EGCG-DPA esters, and the inhibition was largely due to t

204 Use of EGCG as a chain breaker resulted in A- and B-type oligom

205 r inflammatory bowel disease with the use of EGCG treatment.

206 Twelve weeks of EGCG+RES supplementation increased mitochondrial capacit

207 is obtained by complexation of oligomerized EGCG with the anticancer protein Herceptin to form the c

208 e N-terminal residues experience an opposite EGCG-induced shift from tethered to direct contacts, exp

209 hieved from the incorporation of catechin or EGCG inside the liposome structure.

210 ) increased with the addition of catechin or EGCG.

211 s90 and display improvement in efficacy over EGCG.

212 Overall, EGCG concentration and pH both played significant roles

213 Oxidized EGCG molecules react with free amines within the amyloid

214 muscle fibers (P-time x treatment < 0.05, P-EGCG+RES < 0.05).

215 as not significantly affected by EGCG+RES (P-EGCG+RES = 0.46 and 0.38, respectively) but declined aft

216 Particularly, EGCG possesses antiviral activity and impairs cellular l

217 effect on TLR3 and RIG-I signaling pathways, EGCG significantly enhanced HCV dsRNAs-induced the expre

218 we extended our work and developed polymeric EGCG-encapsulated nanoparticles (NPs) targeted with smal

219 Furthermore, prenatal EGCG treatment normalized some craniofacial phenotypes,

220 Rather, EGCG immobilizes the C-terminal region and moderately re

221 All patients received EGCG (600 mg/d) and placebo over 12 wk (4-wk washout in

222 y lower in men but higher in women receiving EGCG compared with placebo.

223 cal or genetic activation of AMPK reproduces EGCG's protective effects.

224 The resulting EGCG encapsulating NPs led to an enhanced anti-prolifera

225 epigallocatechin-3-gallate and resveratrol (EGCG+RES) increased energy expenditure and improved the

226 affeine and catechins followed the sequence: EGCG>EGC>ECG>EC>C>caffeine.

227 CG-untreated Abeta species; and (ii) ternary EGCG-metal-Abeta complexes were produced.

228 TPP more potently preconditioning cells than EGCG.

229 Herein, we demonstrate that EGCG can potently inhibit the proinflammatory enzyme mye

230 g assays at 4 degrees C, we demonstrate that EGCG prevents attachment of the virus to the cell surfac

231 -II formation, as evidenced by the fact that EGCG-induced LC3-II formation was significantly impaired

232 We found that EGCG interacted with metal-Abeta species and formed smal

233 Given that EGCG has the ability to enhance HCV dsRNAs-induced intra

234 We tested the hypothesis that EGCG improves energy metabolism and substrate utilizatio

235 tated autophagic flux and further imply that EGCG may be a potential therapeutic reagent to prevent c

236 Recent experimental evidences indicate that EGCG can induce the aggregation of HMGB1 protein, a late

237 Our data indicate that EGCG given to patients with MS over 12 wk improves muscl

238 These results indicate that EGCG may attenuate experimental autoimmune encephalomyel

239 Spectral analysis indicated that EGCG prevents the peroxidase-catalyzed reaction by rever

240 ls in the presence of EGCG, we observed that EGCG leads to undetectable levels of infection after fou

241 cle and lipid metabolism, we postulated that EGCG may interfere with HCV infection.

242 issue of the JCI, Kumazoe et al. report that EGCG activates 67-kDa laminin receptor (67LR), elevates

243 Our simulation results reveal that EGCG firmly binds to HMGB1 near Cys106, which supports p

244 We show that EGCG amyloid remodeling activity in vitro is dependent o

245 We show that EGCG binds to the pocket that partly overlaps with the p

246 NMR and electron microscopy, which show that EGCG efficiently inhibits fibril formation of hCT by pre

247 We also show that EGCG has no effect on viral replication and virion secre

248 ose or neutralizing antibodies, we show that EGCG inhibits HCV cell-to-cell spread.

249 Here we show that EGCG inhibits the ability of Fap to form fibrils; instea

250 nd fiber formation, we are able to show that EGCG stabilizes nonfibrillar large aggregates during fib

251 We further showed that EGCG reduced production of interferon-gamma, IL-17, IL-6

252 Nanoindentation studies showed that EGCG reduced the stiffness of biofilm containing Fap fib

253 The results suggest that EGCG ester derivatives with anti-inflammatory potentials

254 Our data suggest that EGCG intervention does not depend on the individual LC s

255 Collectively, these findings suggest that EGCG regulates ectopic lipid accumulation through a faci

256 in quorum-sensing molecules, suggesting that EGCG interferes with QS through structural remodeling of

257 is genetically inactivated, suggesting that EGCG-mediated neuroprotection requires AMPK.

258 erved upon EGCG remodeling and suggests that EGCG interferes with secondary nucleation events known t

259 The EGCG-DPA esters effectively suppressed the expression of

260 The EGCG-DPA esters were evaluated for their anti-inflammato

261 e health beneficial omega 3 fatty acids, the EGCG molecule was esterified with docosapentaenoic acid

262 -40) oligomers the relative positions of the EGCG B and D rings change with respect to that of ring A

263 as used to verify identity and purity of the EGCG band.

264 we show that sequential self-assembly of the EGCG derivative with anticancer proteins leads to the fo

265 The three aromatic groups of the EGCG molecule are in a stereo (nonplanar) configuration,

266 hanism involving autophagy, the roles of the EGCG-stimulated autophagy in the context of ectopic lipi

267 vitro is dependent on auto-oxidation of the EGCG.

268 Upon binding to EGCG, the Abeta(1-40) oligomers become less solvent expo

269 tect the lycopene against degradation due to EGCG's anti-oxidant property.

270 tient-derived LC and their susceptibility to EGCG in vitro to probe commonalities and systematic diff

271 bination treatment with EGCG and tobramycin, EGCG had a moderate effect on the minimum bactericidal e

272 1-benzopyran-3-y l 3,4,5-trihydroxybenzoate; EGCG], with metal [Cu(II) and Zn(II)]-Abeta and metal-fr

273 identified a novel mechanism that underlies EGCG's beneficial effect in autoimmune disease.

274 Oxidized and unoxidized EGCG binds to amyloid fibrils, preventing the binding of

275 lains the seeding incompetency observed upon EGCG remodeling and suggests that EGCG interferes with s

276 se xenograft model of prostatic tumor, using EGCG-loaded NPs, with a model of targeted nanosystems, w

277 chins responsible for this preservation were EGCG and C, confirmed by LC-MS.

278 st wild-type P. aeruginosa biofilms, whereas EGCG had a more pronounced effect when Fap was overexpre

279 To determine whether EGCG affects palmitate-induced lipid accumulation, the e

280 Here, we examined whether EGCG can enhance hepatocyte-mediated intracellular innat

281 yocyanin, demonstrating a mechanism by which EGCG can affect the QS function of functional amyloid.

282 n support of the proposed mechanism by which EGCG interactions with the food allergens contribute to

283 nding of the molecular mechanism(s) by which EGCG remodels mature amyloid fibrils made up of Abeta(1-

284 nvestigation, such as the mechanism by which EGCG specifically activates 67LR.

285 the 67-kDa laminin receptor (67LR), to which EGCG binds with high affinity.

286 While EGCG engages AS in compact conformations, DA preferentia

287 tethered to direct contacts, explaining why EGCG remodeling occurs without release of Abeta(1-40) mo

288 how that thioflavin T strongly competes with EGCG for binding sites on IAPP fibers.

289 or enrichment of syrups or concentrates with EGCG and for the preparation of enriched beverages and f

290 , treatment of HCV-infected hepatocytes with EGCG and HCV dsRNAs inhibited viral replication.

291 ects on AS structure as assessed by IM, with EGCG leading to protein compaction and DA to its extensi

292 In addition, upon incubation with EGCG, the toxicity presented by metal-free Abeta and met

293 binding sites and similar binding modes with EGCG.

294 ker resulted in A- and B-type oligomers with EGCG as a terminal unit, indicating that the added flava

295 ase 5 inhibitor, vardenafil, synergizes with EGCG to induce cancer cell death.

296 y increased when the cells were treated with EGCG and palmitate compared with the cells treated with

297 In a combination treatment with EGCG and tobramycin, EGCG had a moderate effect on the m

298 Treatment with EGCG increased formation of LC3-II and autophagosomes in

299 g free energies as compared to those without EGCG.

300 In this work, EGCG-loaded nanostructured lipid carriers (NLC) function