ライフサイエンスコーパス: competitive inhibition

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

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

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

4 sents an intriguing alternative to substrate-competitive inhibition.

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

6 related amprenavir, while saquinavir showed competitive inhibition.

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

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

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

10 coli CTPS, suggesting allosteric rather than competitive inhibition.

11 in C2 cells, indicating stereoselective and competitive inhibition.

12 and reveal the interactions responsible for competitive inhibition.

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

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

15 s in a dose-dependent manner consistent with competitive inhibition.

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

17 vided insights into the biochemical basis of competitive inhibition.

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

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

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

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

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

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

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

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

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

27 Consequently, competitive inhibition among chlorinated ethenes was exa

28 Competitive inhibition among substrates and the parallel

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

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

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

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

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

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

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

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

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

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

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

40 netic parameters, the stereoselectivity, the competitive inhibition, and the pH dependence of the res

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

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

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

44 Monod kinetics with competitive inhibition are used to describe biodegradati

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

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

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

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

49 In a competitive inhibition assay format, a multiplexed test

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

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

52 Competitive inhibition assays showed similar binding of

53 Competitive inhibition assays using labeled 13H11 MAb an

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

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

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

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

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

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

60 6-Substituents that favor competitive inhibition at the ATP binding site of CDK2 w

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

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

63 d be defined by kinetic equations describing competitive inhibition at the lipid-water interface.

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

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

66 This prominent competitive inhibition between interneuron types leads t

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

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

69 Competitive inhibition by an isosteric UbcH7C86S-ubiquit

70 imity to its cellular receptor(s), effective competitive inhibition by antibodies may be difficult to

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

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

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

74 e demonstrated Michaelis-Menten kinetics and competitive inhibition by E4021.

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

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

77 nalysis of the types of inhibition indicated competitive inhibition by GlcNAc-P-P-dolichol toward the

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

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

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

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

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

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

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

85 Competitive inhibition by the inactive substrate and pro

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

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

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

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

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

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

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

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

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

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

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

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

98 Competitive inhibition ELISA showed that high pressure s

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

100 Competitive-inhibition ELISAs indicate the antibodies bi

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

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

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

104 A competitive-inhibition enzyme-linked immunosorbent assay

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

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

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

108 Competitive inhibition experiments with other pneumococc

109 Competitive inhibition experiments with unacylated subst

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

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

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

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

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

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

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

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

118 properties that are inconsistent with simple competitive inhibition for both SLO-1 and 15-HLO.

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

120 The competitive inhibition for PSAO and the partially compet

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

147 A simple competitive inhibition model best approximated the data

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

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

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

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

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

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

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

155 zed in vitro and demonstrated high affinity, competitive inhibition of (125)I-eotaxin and (125)I-MCP-

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

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

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

159 Reversible, competitive inhibition of alkaline phosphatase by sodium

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

161 Competitive inhibition of APP processing by BRI2 may pro

162 Competitive inhibition of APP processing by BRI3 may pro

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

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

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

166 (2)CH(CH(2)C(6)H(5))CO(2)H induce micromolar competitive inhibition of catalysis for the enzyme carbo

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

185 Competitive inhibition of HCV binding to the LDLR by low

186 Competitive inhibition of HK2-mitochondrial binding in p

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

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

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

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

191 Importantly, competitive inhibition of lysis of an otherwise suscepti

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

193 Importantly, competitive inhibition of mannose receptor and targeted

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

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

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

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

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

199 the dose-response relationship expected for competitive inhibition of myosin light chain kinase by t

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

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

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

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

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

205 Competitive inhibition of Pdpn functions with a soluble

206 This is evident as classical competitive inhibition of peptidyl substrate cleavage bu

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

208 Competitive inhibition of PMCA activity was used to meas

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

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

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

212 We now use competitive inhibition of receptor bioluminescence reson

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

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

215 The competitive inhibition of Tat-induced transactivation by

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

217 Using this improved assay, we demonstrated competitive inhibition of the binding of the fluorescent

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

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

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

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

222 (1/2) > 2.5 h for complex dissociation), Gln-competitive inhibition of the Glu-tRNA(Gln)/ATP-independ

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

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

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

226 induced developmental defects is mediated by competitive inhibition of the NMDAR by homocysteine.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

241 ic analysis in the presence of ADP yielded a competitive inhibition pattern when ATP was the varied s

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

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

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

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

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

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

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

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

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

251 Competitive inhibition studies indicate that the reactio

252 Competitive inhibition studies suggested ideal competiti

253 In vivo competitive inhibition studies were performed to evaluat

254 Competitive inhibition studies with a panel of compounds

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

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

257 using recombinant vimentin and by performing competitive inhibition studies.

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

259 This competitive inhibition suggests that all three modulator

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

261 by a modified Michaelis-Menten equation for competitive inhibition; the Hill coefficients were 4 for

262 al significance is not clear, receptor-based competitive inhibition therapy, in which soluble recepto

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

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

265 chol toward the substrate UDP-GlcNAc and non-competitive inhibition toward dolichol phosphate.

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

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

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

269 dead-end inhibitor, also demonstrated simple competitive inhibition versus AcCoA.

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

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

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

273 ion studies with PP(i) and DGPC demonstrated competitive inhibition versus their cognate substrates A

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

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

276 Competitive inhibition was observed for this enzyme-inhi

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

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

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

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

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

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

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

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

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

286 tions of GlcNAc, Scatchard plot analysis and competitive inhibition with cold GlcNAc.

287 Competitive inhibition with different glycosaminoglycans

288 properties and to determine the mechanism of competitive inhibition with fatty acids, the crystal str

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

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

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

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

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

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

295 nin1A (5-HT1A) receptors was investigated by competitive inhibition with ritanserin and pindolol, res

296 Competitive inhibition with soluble elastin completely a

297 Competitive inhibition with substrate shows an apparent

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

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

300 of the peptide, Scatchard plot analysis, and competitive inhibition with the unlabeled peptide.