ライフサイエンスコーパス: competitive inhibition

1 ith IC(50) of 0.06 muM and K(i) = 0.025 muM (competitive inhibition).

2 x (enzyme production) and K m (indicative of competitive inhibition).

3 its active site in a manner consistent with competitive inhibition.

4 vided insights into the biochemical basis of competitive inhibition.

5 mutant allele to create a function-specific competitive inhibition.

6 bstrate methotrexate (10 microM), indicating competitive inhibition.

7 ine of the enzyme, resulting in nonclassical competitive inhibition.

8 sents an intriguing alternative to substrate-competitive inhibition.

9 LT-IIb-B(5), albeit not as potently as self-competitive inhibition.

10 related amprenavir, while saquinavir showed competitive inhibition.

11 as performed for two cases and confirmed the competitive inhibition.

12 range of 0.8 to 11 muM, utilizing mixed-mode competitive inhibition.

13 ne (SAM), conferring SAM-dependent substrate-competitive inhibition.

14 rotein to the DNA, often operating by simple competitive inhibition.

15 coli CTPS, suggesting allosteric rather than competitive inhibition.

16 in C2 cells, indicating stereoselective and competitive inhibition.

17 , energy independent, and subject to similar competitive inhibition.

18 alysis with GMP yielded a signature plot for competitive inhibition.

19 and reveal the interactions responsible for competitive inhibition.

20 ation pathway, suggests a novel mechanism of competitive inhibition.

21 tryptophan, in the reaction did not show any competitive inhibition.

22 Importantly, we find little support for competitive inhibition accounts.

23 rhodanine scaffold, exhibited low micromolar competitive inhibition against acetyl-CoA (AcCoA) and pr

24 s demonstrate that the new compound exhibits competitive inhibition against both ATP and 2,3-dihydrox

25 permine-acetyl-coenzyme A, exhibited linear, competitive inhibition against both substrates with a tr

26 attern representative of slow, tight-binding competitive inhibition against DXP.

27 ol-4-ylazo]-4-su lfo-benzoic acid) displayed competitive inhibition against the natural cofactor, 10-

28 Lapatinib exhibited potent competitive inhibition against UGT1A1 activity with a Ki

29 ibition on several UGTs, particularly potent competitive inhibition against UGT2B17 with a Ki of 0.4

30 Consequently, competitive inhibition among chlorinated ethenes was exa

31 Competitive inhibition among substrates and the parallel

32 ultiplex qPCR assay with the luc IAC avoided competitive inhibition and accurately quantified Dhc abu

33 Substrate competition with organic carbon (competitive inhibition and catabolic repression) was not

34 signaling, and dampens NHE1 activity through competitive inhibition and depletion of PI(4,5)P(2).

35 ellular proteasome activity, consistent with competitive inhibition and formation of suicidal high mo

36 Kinetic studies revealed competitive inhibition and high selectivity toward the M

37 s in endothelial cells are disrupted by both competitive inhibition and HS degradation.

38 regulate intracellular PPI, alternatives to competitive inhibition and the use of antibodies to enab

39 his method to A-->products, without and with competitive inhibition, and commented briefly on A+B-->p

40 hematical solutions to uncompetitive and non-competitive inhibition, and demonstrate that in most cas

41 ferentiated varying amounts of MPO activity, competitive inhibition, and MPO deficiency in living ani

42 ic characterization clearly demonstrated ATP-competitive inhibition, and several additional biochemic

43 Michaelis-Menten, competitive inhibition, and site-directed mutagenesis st

44 obeys Michaelis-Menten kinetics and exhibits competitive inhibition, and the substrate scope displays

45 crophage immunostaining and MRI correlation, competitive inhibition, and various other analyses were

46 n state analogs inhibit their targets by non-competitive inhibition are discussed.

47 Monod kinetics with competitive inhibition are used to describe biodegradati

48 tive ProT(S195A) mutant were compatible with competitive inhibition as an alternate nonproductive sub

49 anism of action involves competitive and non-competitive inhibition as well as generation of unstable

50 say, a novel SPR sensor based on an indirect competitive inhibition assay (ICIA) is developed for det

51 lective detection of ssDNA based on indirect competitive inhibition assay (ICIA).

52 In a competitive inhibition assay format, a multiplexed test

53 Antibodies were selected based on a competitive inhibition assay to isolate those with the h

54 Using direct or competitive inhibition assays for receptor binding or ce

55 Competitive inhibition assays showed similar binding of

56 Competitive inhibition assays using labeled 13H11 MAb an

57 ate receptors for infection, as evidenced by competitive inhibition assays with lectins, glycans, and

58 omplemented with various PsrP constructs and competitive inhibition assays with recombinant proteins,

59 using a combination of recombinant antigens, competitive inhibition assays, and a unique peptide-on-b

60 In competitive inhibition assays, we show that our lead com

61 range of solid-supported sensors to conduct competitive inhibition assays.

62 s and microtiter plate-based CBM capture and competitive-inhibition assays are described.

63 with either strong allosteric inhibition or competitive inhibition at one of the peptide agonist bin

64 6-Substituents that favor competitive inhibition at the ATP binding site of CDK2 w

65 it abolished the BayK effect (presumably by competitive inhibition at the DHPR).

66 ubiquitin oxyester substrate analog exhibits competitive inhibition at the high-affinity Site 1 (Ki =

67 hibitory response to capsaicin, suggesting a competitive inhibition at TRPV1.

68 on by divalent cations, especially Mg2+, and competitive inhibition behavior with Cl- ions are simila

69 This prominent competitive inhibition between interneuron types leads t

70 For screening, a semi-automated competitive inhibition binding assay was combined with f

71 O-azepin-onartuzumab was assessed in vivo by competitive inhibition (blocking) studies.

72 We found that the deviation from competitive inhibition by ADP was inconsistent with mode

73 Competitive inhibition by an isosteric UbcH7C86S-ubiquit

74 transport of E(2)17betaG was susceptible to competitive inhibition by both amphiphiles, such as leuk

75 The structures reveal that activation and competitive inhibition by both GluN1 and GluN2 antagonis

76 f p53 during limb regeneration, based on its competitive inhibition by DeltaNp73.

77 take is receptor-dependent, diminishing with competitive inhibition by dextran.

78 y be important for promoting neuritogenesis, competitive inhibition by ES or low affinity matrix impa

79 However, the lack of significant effect of competitive inhibition by exogenous neoglycoproteins in

80 tween slow tight-binding and fast reversible competitive inhibition by invoking global conformational

81 or, UDP-glucose and UDP-hexanol amine caused competitive inhibition by Lineweaver-Burk plots.

82 pong behavior with pNPS adding to E.PAP, and competitive inhibition by naphthol consistent with forma

83 of its structure-function relationships and competitive inhibition by O(2), it may be possible to en

84 ding to agonist-gating and subunit-dependent competitive inhibition by providing multiple structures

85 substrate cleavage by separase and suggests competitive inhibition by securin.

86 rameters of T cell signaling, sensitivity to competitive inhibition by soluble CTLA-4-Ig indicated th

87 s of root and shoot Se accumulation and less competitive inhibition by sulfate or by high-S pretreatm

88 Competitive inhibition by the inactive substrate and pro

89 ate (GAP) and a 60-fold increase in K(i) for competitive inhibition by the intermediate analogue 2-ph

90 ing portions of the ICAM-1 molecule explains competitive inhibition by these mAbs.

91 receptors (P2X(3)) may mask the detection of competitive inhibition by TNP-ATP.

92 We also show that competitive inhibition can be achieved by interfering wi

93 el included negative feedback in the form of competitive inhibition (CI).

94 Cys274, and solution studies show reversible competitive inhibition, consistent with a reversible cov

95 with a strong competitive component [i.e., a competitive inhibition constant (K(ic)) of 0.12 +/- 0.02

96 The pH dependence of the competitive inhibition constant, K(i), for CdBcII with l

97 uation is invalid for the calculation of the competitive inhibition constants (Ki values) for inhibit

98 s were confirmed experimentally by measuring competitive inhibition constants KI2 for propidium and t

99 ed and pristine sites at depth exhibited non-competitive inhibition (decreased V max), whilst uncompe

100 using affinity-purified anti-beta(2)GPI in a competitive inhibition ELISA and with whole serum in a d

101 Competitive inhibition ELISA showed that high pressure s

102 binding of peanut extracts was analysed by a competitive inhibition ELISA.

103 Competitive-inhibition ELISAs indicate the antibodies bi

104 xol and Baccatin III when quantified through competitive inhibition enzyme immunoassay (CIEIA), showe

105 infection prevalence of 29% as determined by competitive inhibition enzyme-linked immunosorbent assay

106 rotease or cyanogen bromide treatment and by competitive inhibition enzyme-linked immunosorbent assay

107 ly described monoclonal antibody (MAb)-based competitive-inhibition enzyme-linked immunosorbent assay

108 at higher concentrations, fumarate caused a competitive inhibition, excluding the substrate malate f

109 r having a chain length of 13 monomer units, competitive inhibition experiments reveal that methyl io

110 Direct binding assays and competitive inhibition experiments showed that the FabG

111 Competitive inhibition experiments with other pneumococc

112 Competitive inhibition experiments with unacylated subst

113 raction with HepG2 cells in culture, whereas competitive inhibition experiments with unlabeled Abeta

114 In competitive inhibition experiments, anti-CK1, anti-uPAR,

115 In competitive inhibition experiments, beta(2)GPI prevented

116 servations, taken together with results from competitive inhibition experiments, suggest that eIF4A m

117 Based on competitive inhibition experiments, the use of amino aci

118 to macrophages that was nearly abolished in competitive inhibition experiments.

119 viscosity while indirect approaches detail: competitive inhibition experiments; fluorescence and abs

120 ditionally, SV40 seroreactivity confirmed by competitive-inhibition experiments (i.e., blocked by add

121 arate in single-substrate assays, but strong competitive inhibition favored utilization of caffeate a

122 thrapyrazolone compound, SP600125, exhibited competitive inhibition for ATP and noncompetitive inhibi

123 e mixed inhibition of CYP1A2 and CYP2D1, and competitive inhibition for CYP2B1, CYP2C11 and CYP2E1 wi

124 The competitive inhibition for PSAO and the partially compet

125 titive inhibition for PSAO and the partially competitive inhibition for rhDAO are consistent with O(2

126 nd Y21H/E) and tested substrate activity and competitive inhibition for several compound series.

127 The iSPR assay was based on a competitive inhibition format with secondary antibodies

128 ction of 17beta-Estradiol (E2) following the competitive inhibition format.

129 ut also on three-dimensional RNA structures, competitive inhibition from other RBPs, and input from c

130 ease in electrochemical signal response in a competitive inhibition immunoassay format for diuron det

131 These peptides exhibit mutual competitive inhibition in binding to beta-tubulin, while

132 These results argue against models of competitive inhibition in neostriatum, including those i

133 The Dhc* IAC exhibited competitive inhibition in qPCR with the Dhc 16S rRNA gen

134 lso used one of the compounds to demonstrate competitive inhibition in regard to external [K(+)] vers

135 by metabolic-intermediate complex formation, competitive inhibition, irreversible type II coordinatio

136 s study suggest that at higher feeding rates competitive inhibition is important and mRNA provides a

137 pure noncompetitive and mixed-type/partially competitive inhibition is observed.

138 nism based on Michaelis-Menten kinetics with competitive inhibition is proposed for both the Zr-catal

139 This competitive inhibition is rescued by addition of ACF, su

140 ion in neostriatum, including those in which competitive inhibition is transiently effective during d

141 Although pppCH2dU shows apparent competitive inhibition, it acts by a surprising alloster

142 PP(i) exhibits competitive inhibition, K(i) = 0.320 mm, under varied PR

143 ples of neuronal selection also suggest that competitive inhibition may occur in early valuation stag

144 We show how this competitive inhibition may operate through protein acety

145 s dual-binding feature of helicase enables a competitive inhibition mechanism by which Mhrt sequester

146 Due to this homology and the competitive inhibition mechanism of Rep78, we propose th

147 e SSB stimulation of ExoI activity through a competitive inhibition mechanism, indicating that the pe

148 itch, supporting inhibitor specificity and a competitive inhibition mechanism.

149 (A) domain of the LDL receptor, suggesting a competitive inhibition mechanism.

150 xed-type (combination of competitive and non-competitive) inhibition mechanism, FBG reduced the V(max

151 s with Ki values between 1.5 and 1.8 muM and competitive inhibition mechanisms.

152 The non-competitive inhibition mode of CS was determined by Line

153 ockets of the active site, consistent with a competitive inhibition mode.

154 A simple competitive inhibition model best approximated the data

155 ansient kinetic analysis using a single-step competitive inhibition model provided rate constants of

156 n of fIXa by heparin was well described by a competitive inhibition model where heparin acts as an af

157 al data show a clear deviation from a simple competitive inhibition model, but are consistent with a

158 For screening, a rapid and radiolabel-free competitive inhibition MS binding assay was developed wi

159 the NaMN binding subsite consistent with the competitive inhibition observed for the NaMN substrate (

160 Because of the non-competitive inhibition observed, docking of Trp-Val to t

161 of AKR1D1, providing an explanation for the competitive inhibition observed.

162 ncluding accumulation of oncometabolites and competitive inhibition of 2-oxoglutarate-dependent dioxy

163 Assays of competitive inhibition of [(3)H]glycylsarcosine (Gly-Sar

164 We also extend our model to describe the competitive inhibition of adhesion: the model predicts t

165 Reversible, competitive inhibition of alkaline phosphatase by sodium

166 Competitive inhibition of alpha(v)beta(3)-GNBs with alph

167 Competitive inhibition of APP processing by BRI2 may pro

168 Competitive inhibition of APP processing by BRI3 may pro

169 The digestion of a bispecific antibody with competitive inhibition of aspergillopepsin I maintained

170 This effect is likely mediated by competitive inhibition of binding of ErbB4 to PSD95.

171 ing release in the oral cavity, or including competitive inhibition of bitter sensation for example b

172 metabolic effects of resveratrol result from competitive inhibition of cAMP-degrading phosphodiestera

173 to allosteric inhibitory effects rather than competitive inhibition of CD4 binding.

174 cAMP, which paradoxically results in potent competitive inhibition of cGMP turnover by cAMP.

175 responsible for the "Kok effect," reflecting competitive inhibition of chlororespiratory electron tra

176 complex with AB1 show that the irreversible competitive inhibition of CLK1 is dependent on a Michael

177 ociation and dissociation rate constants for competitive inhibition of current through embryonic musc

178 total metabolite levels provided evidence of competitive inhibition of CYP 2E1 enzymes leading to inc

179 ide regulates mitochondrial function through competitive inhibition of cytochrome c oxidase in the el

180 oduce 2-hydroxyglutarate (2HG), resulting in competitive inhibition of DNA and protein demethylation.

181 b bound to S. pyogenes Cas9 reveal a mode of competitive inhibition of DNA binding that is distinct f

182 ffer a potential therapeutic approach to the competitive inhibition of DNA-binding transcription fact

183 data demonstrate the molecular basis for the competitive inhibition of dopamine transport by cocaine.

184 the abiogenic 7-isomer (7BH(4)), leading to competitive inhibition of epidermal phenylalanine hydrox

185 n 11 (ENOD11) expression and does so through competitive inhibition of ERF Required for Nodulation (E

186 that FHR-1 enhances complement activation by competitive inhibition of FH binding to some surfaces an

187 avity of G9a, and kinetic analysis indicates competitive inhibition of G9a by histone H3K9M.

188 We find that competitive inhibition of galectin binding results in lu

189 Upon competitive inhibition of GALR1, proliferation was up-re

190 ors, kinetic inhibition studies demonstrated competitive inhibition of gamma-secretase by the exon 9

191 molecule inhibitors, which also display non-competitive inhibition of gamma-secretase, inhibit the e

192 partyl proteases, also displayed potent, non-competitive inhibition of gamma-secretase.

193 nd L685458 unexpectedly displayed linear non-competitive inhibition of gamma-secretase.

194 Competitive inhibition of HCV binding to the LDLR by low

195 Competitive inhibition of Hg uptake by Zn speaks in favo

196 Competitive inhibition of HK2-mitochondrial binding in p

197 the generation of polyamines in addition to competitive inhibition of iNOS.

198 This simple mechanism of greater competitive inhibition of invaders that are similar to e

199 bind both H3K27M and H3K27me3 to experience competitive inhibition of its methyltransferase activity

200 hosphorylated TKD-EGFR was also resistant to competitive inhibition of ligand-binding compared with w

201 f interferes with coactivator recruitment by competitive inhibition of LXXLL motif binding.

202 Importantly, competitive inhibition of lysis of an otherwise suscepti

203 In the absence of serum opsonins, competitive inhibition of mannose receptor (MR) activity

204 Importantly, competitive inhibition of mannose receptor and targeted

205 th respiratory processes are concurrent, any competitive inhibition of methanogenesis by sulfate-redu

206 Using a conditional transgenic toolkit for competitive inhibition of miRNA function in Drosophila,

207 moderate-intensity exercise may result from competitive inhibition of mitochondrial .VO2 by nitric o

208 sim and saturation of metabolic machinery by competitive inhibition of mixture components.

209 ial surface targets for rATG were assayed by competitive inhibition of monoclonal antibody binding.

210 the inhibition constant (IC50 value) for the competitive inhibition of morphine glucuronidation by co

211 F-kappaB-reporter gene and was suppressed by competitive inhibition of NF-kappaB binding, IL-18 respo

212 The chimeric compound showed potent competitive inhibition of nuclear HDACs, with an IC50 va

213 Instead we found a strong competitive inhibition of nucleotide hydrolysis and trap

214 was found to be effective in monitoring the competitive inhibition of PA formation in the production

215 A direct, competitive inhibition of PARP-1 by minocycline (K(i) =

216 Competitive inhibition of Pdpn functions with a soluble

217 trans counterpart 2 (K(i) = 40 +/- 2 muM) in competitive inhibition of Pin1.

218 Competitive inhibition of PMCA activity was used to meas

219 for interaction with PTP1B, resulting in the competitive inhibition of PTP1B activity.

220 contribute to pulmonary hypertension via the competitive inhibition of pulmonary NOS enzymes.

221 AS effector RIN1 appears to function through competitive inhibition of RAS-RAF binding and also throu

222 We now use competitive inhibition of receptor bioluminescence reson

223 of NKCC1 (NT-NKCC1, amino acids 1-286), and competitive inhibition of SPAK-NKCC1 binding by a peptid

224 otransfer activity at the catalytic cleft by competitive inhibition of substrate binding with a pseud

225 that upregulation of HIF-1alpha arises from competitive inhibition of the 2-OG-dependent HIF hydroxy

226 Moreover, Ang II showed selective competitive inhibition of the carboxy-terminal domain of

227 In contrast, competitive inhibition of the catalytic domain of membra

228 s confirmed by experiments showing substrate-competitive inhibition of the dehydrogenase and esterase

229 This conclusion is supported by the competitive inhibition of the enzymatic reaction by D-ar

230 (1/2) > 2.5 h for complex dissociation), Gln-competitive inhibition of the Glu-tRNA(Gln)/ATP-independ

231 tion of IL-1ra in both health and disease is competitive inhibition of the IL-1RI.

232 We also show the direct competitive inhibition of the M. abscessus beta-lactamas

233 We demonstrate the competitive inhibition of the mitochondrial human type I

234 n the absence and presence of hormone and by competitive inhibition of the N/C interaction.

235 In principle, this involves the competitive inhibition of the recognition center by prod

236 y of double-stranded DNA, resulting in a non-competitive inhibition of the second messenger cyclic GM

237 These data include (1) competitive inhibition of the tubulin binding of the Vin

238 estradiol disulfate, unexpectedly exhibited competitive inhibition of the unmodified enzyme, suggest

239 nto the brains of nude mice, suggesting that competitive inhibition of the uPA-uPAR interaction on SN

240 Or do they suppress growth, as expected if competitive inhibition of their neighbors is strong?

241 nhibition of de novo purine biosynthesis and competitive inhibition of thiopurine activation.

242 iochemical studies confirmed dose-dependent, competitive inhibition of this enzyme in vitro, which wa

243 enic VEGF isoforms (via SRPK1 inhibition) or competitive inhibition of VEGF signaling by rhVEGF165b h

244 t of NleE (NleE(34-52)) in HeLa cells showed competitive inhibition of wild type NleE in the suppress

245 ion and confer a semi-dominant phenotype via competitive inhibition of wild-type SsChlI.

246 ve monovalent ligand and thus quantifies the competitive inhibition offered by a monovalent ligand.

247 Compound 2 exhibited a partial competitive inhibition pattern against ATP.

248 proliferator, WY 14,643 exhibits a pure non-competitive inhibition pattern in the aldehyde reduction

249 RK2 tightly (K(d) = 1 microM) and displays a competitive inhibition pattern toward MgATP2- and a mixe

250 Such irreversibility may explain the non-competitive inhibition pattern with respect to ATP shown

251 analysis shows that oxazolidinones display a competitive inhibition pattern with respect to both the

252 Double-reciprocal plots showed a competitive inhibition pattern with respect to pyruvate

253 s S-adenosylhomocysteine and sinefungin gave competitive inhibition patterns against AdoMet and nonco

254 Similar to an enzymatic competitive inhibition process, in the presence of a cog

255 s through the transporter, and principles of competitive inhibition remain unclear.

256 y thought to inhibit estrogen action through competitive inhibition, resulting in receptor binding to

257 Using a competitive inhibition strategy, we used phage display t

258 omerization of this receptor using a peptide competitive inhibition strategy.

259 Competitive inhibition studies indicate that the reactio

260 Competitive inhibition studies indicated that the GBT tr

261 Competitive inhibition studies suggested ideal competiti

262 In vivo competitive inhibition studies were performed to evaluat

263 ith chemical inhibitors of glycosylation and competitive inhibition studies with different lectins su

264 sialosides were assessed for each siglec in competitive inhibition studies.

265 using recombinant vimentin and by performing competitive inhibition studies.

266 recipitating enzymatic substrate by way of a competitive inhibition study using beta-galactosidase at

267 solution reveals the molecular basis for the competitive inhibition, supports the proposed formation

268 MTS-12 in a dose-dependent manner through 1) competitive inhibition through direct protein-protein in

269 tems L, A and y(+)L, were examined utilising competitive inhibition to investigate the effects of Hcy

270 Computer programs are also provided for competitive inhibition, uncompetitive inhibition, and mi

271 ble, yet still potent (K(i) = 73 nM) and Gln-competitive, inhibition under full transamidation condit

272 chaelis-Menten model of enzyme kinetics, and competitive inhibition using a nonreactive guest was dem

273 -(l-cysteinyl)sulfamonyl]adenosine, exhibits competitive inhibition versus ATP and noncompetitive inh

274 re noncompetitive inhibition versus ATF2 and competitive inhibition versus ATP.

275 ow alternative keto acid substrate, exhibits competitive inhibition versus both lysine and alpha-Kg,

276 QC), the core moiety of brequinar also shows competitive inhibition versus ubiquinone.

277 genetically encodes chemical sensitivity to competitive inhibition via a bulky ATP analog.

278 ead-end analogues of saccharopine and showed competitive inhibition vs saccharopine and uncompetitive

279 Competitive inhibition was observed for this enzyme-inhi

280 The K(i) values for competitive inhibition were 1.2 and 4.0 microM for 1 and

281 acid, resorcylic acid and kojic acid showed competitive inhibition, whereas, citric acid and sodium

282 otent than the reactant (Ki 350+/-76 microM, competitive inhibition), which had previously been ident

283 rs in the presence of UVM-7-SH suggested non-competitive inhibition, which indicated that the materia

284 to be 3.57.10(-5)M and sulphanilamide showed competitive inhibition, which makes it a suitable ligand

285 Competitive inhibition with 1-adamantanecarboxylate disp

286 dependently inhibited DNMT activity, showing competitive inhibition with a K(i) of 6.89 microM.

287 thyl)pentanedioic acid (2-PMPA) demonstrated competitive inhibition with a K(i)=0.2nM.

288 The synthetic inhibitor 1 showed potent competitive inhibition with a Ki of 25.6+/-2.8 microM.

289 the trifluoroacetyl-lysine peptide displayed competitive inhibition with acetyl-lysine substrate and

290 Competitive inhibition with different glycosaminoglycans

291 phaq/11 binding is dramatically decreased by competitive inhibition with heparin, pharmacological inh

292 of Mgat5, siRNA depletion of galectin-3, or competitive inhibition with lactose stabilizes cell-cell

293 2)O(2), azide has been determined to exhibit competitive inhibition with respect to O(2) in PSAO with

294 de was found to exhibit mixed-type/partially competitive inhibition with respect to substrate O(2) in

295 scovered to exhibit either noncompetitive or competitive inhibition with respect to the amine, depend

296 endent manner, and kinetic analysis indicted competitive inhibition with respect to vinblastine bindi

297 Competitive inhibition with soluble elastin completely a

298 Competitive inhibition with substrate shows an apparent

299 l adopted ATP-like binding modes, suggesting competitive inhibition with the endogenous ligand.

300 g CHO cells, and this binding was blocked by competitive inhibition with the SR-binding ligands oxidi