ライフサイエンスコーパス: dead end

1 y breaking or reversed as the cell reaches a dead end.

2 ene products and is considered a replicative dead end.

3 subsequent core fusion within 20 s) and half dead-end.

4 isexuality in vertebrates is an evolutionary dead-end.

5 sign principle for future power grids: avoid dead ends.

6 flux and preventing the formation of pathway dead ends.

7 ominant selfing constitutes an "evolutionary dead end."

8 ation of nanos1 after fertilization requires Dead-end 1 (Dnd1), a vertebrate-specific germline RNA-bi

9 Here we report that Dead-End 1 (Dnd1), an RNA-binding protein required for p

10 length lipid chains, as well as a synthetic dead-end acceptor analogue, we have also shown that MurG

11 t converted to product by DEBS module 2 form dead-end acyl-enzyme intermediates.

12 ion of the oxyanion intermediate to form the dead-end adduct is more thermodynamically favored than m

13 rolysis may arise through the formation of a dead-end ADP:GroEL:ATP:GroES complex.

14 Initial velocity, product inhibition, and dead-end analog inhibition studies with the AcH4-21 and

15 The dead-end analog inhibitor H3-20 K14A was competitive ver

16 uct CoA behaves in a manner identical to the dead-end analogue desulfo-CoA, suggesting an E:alpha-ket

17 2-Amino-6-heptenoic acid was chosen as a dead-end analogue of L-AASA and is competitive vs AASA,

18 alpha-Ketoglutarate (alpha-Kg) serves as the dead-end analogue of L-glutamate and is competitive vs L

19 Dead-end analogues of alpha-ketoglutarate were used to o

20 ate (OAA), pyruvate, and glutarate behave as dead-end analogues of lysine, which suggests that the ly

21 glyoxylic acid, and L-ornithine were used as dead-end analogues of saccharopine and showed competitiv

22 d oxalylglycine serve as lysine and alpha-Kg dead-end analogues, respectively, and are uncompetitive

23 rticularly in cancer, have been fraught with dead ends and context-specific functions.

24 that tree-like connection schemes--so-called dead ends and dead trees--strongly diminish stability.

25 ithout allowing interconversions between the dead-end and open complexes.

26 The use of dead-end and product inhibition and solvent-isotope effe

27 Two-substrate, dead-end and product inhibition data, using analogues of

28 The use of dead-end and product inhibition, the solvent isotope eff

29 In contrast, a 'dead-end' antibody sublineage unable to neutralize these

30 Addition of a trans diene leads to a dead-end as the trans intermediates have insurmountable

31 ese instances, the diploid males are genetic dead ends because they are inviable or sterile.

32 Hybridization is not a mere reproductive dead end but has been suggested to play a central role i

33 tes that the inverse is also true: repairing dead ends by addition of a few transmission lines substa

34 ed the model's applicability for an infused, dead-end cavity or a non-infused joint during cyclical m

35 a means to control the colloid transport in dead-end channels by introducing a solute gradient.

36 he transport of colloidal particles into the dead-end channels can be either enhanced or completely p

37 Transport of colloids in dead-end channels is involved in widespread applications

38 circular Ty1 DNA, which is comparable to the dead-end circular products that arise during retroviral

39 l was not an alternative substrate but was a dead end competitive inhibitor versus tryptamine and an

40 ic analysis, product inhibition studies, and dead-end competitive inhibition studies is most consiste

41 N-Benzylglycine, a dead-end competitive inhibitor with respect to N-methyl-

42 dNTP binding affinity as measured using the dead end complex formation.

43 rate inhibition by formation of an E.ADP.APS dead end complex.

44 es at PcopA in the absence of nucleotides: a dead-end complex and an open complex, constituting a bra

45 a(max) approximately 350 nm is assigned as a dead-end complex between the enzyme-persulfide and a sec

46 ors versus nitroethane due to formation of a dead-end complex between the oxidized enzyme and the pro

47 Dead-end complex formation by noncomplementary dNTP's or

48 ing, incorporation into primer/template, and dead-end complex formation in the presence of the next d

49 By contrast, dead-end complex formation on primer terminated with did

50 gth of the primer/template duplex region for dead-end complex formation was between 20 and 32 base pa

51 on the template, analogues of dTTP supported dead-end complex formation with increased apparent Kd (d

52 a mismatched primer terminus did not support dead-end complex formation, and primer terminated with 3

53 This latter structure likely simulates a dead-end complex in the reaction mixture.

54 With the fast substrate D-arginine a dead-end complex of the reduced enzyme and the substrate

55 both E.NADPH and E.NADP(+), only the latter dead-end complex shows significant inhibition of the ste

56 o the oxidized form of the enzyme produced a dead-end complex that could be titrated by following a 1

57 values if unphosphorylated SK and RR form a dead-end complex that prevents SK autophosphorylation.

58 tide phosphate (E.NADP(+)) to form a ternary dead-end complex that prevents turnover in the steady st

59 pressor form reinforces the dominance of the dead-end complex to repress transcription, and the holo-

60 cts that the self-enhancing formation of the dead-end complex transforms the network into a largely i

61 concluded that Ca(2+)-ATPase is locked in a dead-end complex upon binding TG with an affinity of <1

62 Dead-end complex was formed between HIV-1 RT, dideoxynuc

63 mer terminated with 3'-azidothymidine formed dead-end complex with 25-fold elevated apparent Kd.

64 The free reduced enzyme forms a dead-end complex with nitroethane, with a K(ai) value of

65 In contrast, the dead-end complex with terreic acid is open, is free of U

66 The crystal structure of the MurA dead-end complex with terreic acid revealed that the qui

67 mB, holo(haem)CcmE binds to CcmC in a stable dead-end complex, indicating high affinity binding of ha

68 hat sorbinil binds to E.NADP(+) to produce a dead-end complex, the so-called sorbinil trap, which pre

69 hosphorylated SK EnvZ and the RR OmpR form a dead-end complex.

70 versus P-DME, consistent with formation of a dead-end complex.

71 with formation of an enzyme-NADP(+)-AcAc-CoA dead-end complex.

72 CoA, suggesting an E:alpha-ketoglutarate:CoA dead-end complex.

73 binding to the IMP site and forming a tight, dead-end complex.

74 a result of formation of the E.PAP.naphthol dead-end complex; formation of the complex is corroborat

75 gma factor for sigma(F) forms a long-lived, "dead-end" complex with its anti-anti-sigma factor and AD

76 cycloaddition requires dissociation of the (dead-end) complex.

77 both E-MgADP-FAK-tide and E-MgATP-P-FAK-tide dead-end complexes form.

78 yme and that both the E.PAP.E2S and E.PAP.E2 dead-end complexes form.

79 ects of ppGpp to drive formation of inactive dead-end complexes formed by RNA polymerase at the ArgX

80 utL-E32K mutation is due to the formation of dead-end complexes in which the MutL-E32K protein is una

81 s between topoisomerase I and DNA can become dead-end complexes that lead to cell death.

82 M, Ala), suggesting that this compound forms dead-end complexes with multiple enzyme states.

83 -competent orientation or form high-affinity dead-end complexes, both RT/NNRTI/DNA complexes being un

84 ly suggest a Random Bi Bi mechanism with two dead-end complexes.

85 g that self-fertilization is an evolutionary dead end conflates two distinct claims: the transition f

86 Imaging experiments in vivo reveal that Dead end-containing vesicles are associated with recycli

87 s such as DNA polymerase beta (Polbeta) form dead-end, covalent intermediates in vitro during attempt

88 s from the complexity of intra-, inter-, and dead-end cross-linked peptide mixtures.

89 et of unique interpeptide, intrapeptide, and dead-end cross-linked products that provides protein str

90 as well as the array of inter-, intra-, or "dead-end"-cross-linked peptides that may be generated fr

91 lt: the chemically reasonable formation of a dead-end cysteine-cofactor adduct when NAD+ was in the "

92 2 represents a long road traveled, with many dead-ends, disappointments, and delays.

93 Zebrafish dead end (dnd) mRNA is specifically expressed in primord

94 This phenomenon termed dead-end docking has not been investigated until now.

95 ction for this acceptor complex in mediating dead-end docking.

96 onovalent oxyanion dissociation constants of dead end E.MgATP.oxyanion complexes were all increased.

97 nal oxyanion.) Chlorate and perchlorate form dead-end E.MgATP.oxyanion complexes.

98 brium random mechanism with the formation of dead-end EAP and EBQ complexes.

99 es a rapid equilibrium random mechanism with dead-end EAP and EBQ complexes.

100 es a rapid equilibrium random mechanism with dead-end EAP and EBQ complexes.

101 a new protein design algorithm based on the dead-end elimination (DEE) algorithm, which we call iMin

102 A popular method is to combine the dead-end elimination (DEE) and A* tree search algorithms

103 Dead-End Elimination (DEE) is a powerful algorithm capab

104 The dead-end elimination (DEE) theorems are powerful tools f

105 We further derive a dead-end elimination (DEE)-based criterion for pruning c

106 heorem for the identification of the GMEC is Dead-End Elimination (DEE).

107 (GA); self-consistent mean field (SCMF); and dead-end elimination (DEE).

108 The dead-end elimination and A( *) search algorithms were us

109 The method we use is based on a variety of dead-end elimination methods and the recently discovered

110 The algorithm is based on the dead-end elimination procedure that makes it possible to

111 lizes a physically based force-field and the Dead-End Elimination theorem to compute sequences that a

112 erimental and computational approach and the Dead-End Elimination theorem to search for the optimal s

113 Dead-end elimination was used to identify global minimum

114 OLPROBITY score of 2.71 A (77th percentile), dead-end elimination with the polarizable AMOEBA force f

115 Beginning from dead-end elimination, we derive the first algorithm, to

116 this reaction is complicated by a competing dead-end equilibrium to form the thiolate complex (Fe(II

117 Because the dead-end Er.NO complex does not accumulate during the ex

118 ecies transmission episodes can be singular, dead-end events or can result in viral replication and s

119 We present an automated dead-end filling (DEF) approach, which is derived from t

120 exits from the oral cavity, (2) conventional dead-end filters that sieve particles from water exiting

121 al agent, as demonstrated by both short-term dead-end filtration and long-term cross-flow filtration

122 Long-term dead-end filtration experiments for 1 week reveal a high

123 By operation in dead-end filtration mode using the model virus MS2 (diam

124 Dead-end filtration was carried out using 10(7) and 10(8

125 , are significant drawbacks of conventional 'dead end' filtration.

126 missible, hence representing an evolutionary dead-end for the pathogen.

127 diffusive zones adjacent to flow paths or in dead-end fractures.

128 The Drosophila dead end gene is expressed in fusion cells, and encodes

129 These results indicate that the Dead end GTPase plays an important role in trafficking m

130 hanolamine lipid composition, productive and dead-end hemifusion account for 65% of all fusion events

131 ue virus infections are generally considered dead-end hosts for transmission because they do not reac

132 Our findings question the status of dead-end hosts in the WNV transmission cycle and may par

133 FV is readily zoonotic, humans may represent dead-end hosts.

134 pecies can vary from important reservoirs to dead-end hosts.

135 tem and apparently results from formation of dead-end HR DNA intermediates.

136 ly, this therapeutic "paradigm" has led to a dead end, illustrated by the failure of all randomized t

137 xpression of a constitutively active form of Dead end in S2 cells reveals that it influences the stat

138 elded both promising leads and disappointing dead ends, indicating the multifactored and complex natu

139 alvin-Benson-Bassham cycle in higher plants, dead-end inhibited complexes of Rubisco must constantly

140 g synergism was associated with formation of dead-end inhibited ternary complexes.

141 te initial velocity, product inhibition, and dead end inhibition experiments, which elucidated an ord

142 Product and dead-end inhibition analyses revealed that nicotinamide

143 Dead-end inhibition and ITC experiments revealed that AA

144 Dead-end inhibition by 2'-adenosine monophosphate (2'AMP

145 plots for product inhibition by NADH and the dead-end inhibition by 3-acetylpyridine adenine dinucleo

146 ate kinetic results of substrate titrations, dead-end inhibition by AMP and lumichrome, and product i

147 Product and dead-end inhibition data are consistent with an ordered

148 Product and dead-end inhibition data indicated that enzymatic phosph

149 Thus, initial velocity, product, and dead-end inhibition data were consistent with a di-iso p

150 Product and dead-end inhibition data with DCIP were consistent with

151 results of initial velocity and product and dead-end inhibition experiments indicate that PRMT1 util

152 At low pH (5.7) the initial velocity and dead-end inhibition patterns are consistent with a seque

153 Product and dead-end inhibition patterns indicate that binding of am

154 Product and dead-end inhibition patterns indicated a random sequenti

155 competitive substrate inhibition by ASA and dead-end inhibition patterns obtained at pH 8 are consis

156 Dead-end inhibition studies are also consistent with the

157 Two-substrate kinetic analysis and dead-end inhibition studies for 5alpha-DHP reduction and

158 he results of initial velocity, product, and dead-end inhibition studies indicate that cPRMT5 uses a

159 he results of initial velocity, product, and dead-end inhibition studies indicate that methylation by

160 al velocity studies, product inhibition, and dead-end inhibition studies indicate that MtIPMS follows

161 Initial velocity, product inhibition, and dead-end inhibition studies indicate the kinetic mechani

162 Initial velocity, product inhibition, and dead-end inhibition studies provided assignments of the

163 Initial velocity, product, and dead-end inhibition studies showed the kinetic mechanism

164 the normal reaction (alphaKG to isocitrate), dead-end inhibition studies suggest that wild-type IDH1

165 Initial velocity and dead-end inhibition studies support an ordered sequentia

166 sequential mechanism is also corroborated by dead-end inhibition studies using analogues of AASA, L-g

167 Dead-end inhibition studies were used to investigate the

168 g-pong bi-bi mechanism; however, product and dead-end inhibition studies with cytochrome c(3+) were c

169 Dead-end inhibition studies with the substrate analogues

170 of initial velocity, product inhibition, and dead-end inhibition studies, the reaction is shown to be

171 eased based on initial velocity, product and dead-end inhibition studies.

172 The mechanism is supported by product and dead-end inhibition studies.

173 rythroleukemia cells, Dnmt1, exhibits potent dead-end inhibition with a single-stranded nucleic acid

174 Initial velocity, product inhibition, dead-end inhibition, and equilibrium binding studies ind

175 The dead end inhibitor analog cyclolaudenol was competitive

176 The dead end inhibitor analog desulfo-CoA was competitive ve

177 sence of products and in the presence of the dead end inhibitor sulfite are most consistent with a se

178 yl-L-alanine in the absence or presence of a dead-end inhibitor (pyrrole-2-carboxylate) indicate that

179 The dead-end inhibitor analog desulfo-CoA was competitive ve

180 ty patterns in the presence and absence of a dead-end inhibitor and two triarylimidazole p38 inhibito

181 s for 1-phosphono-(E,E,E)-geranylgeraniol, a dead-end inhibitor for GGPP, gave a competitive double r

182 beta-Fluoropyruvate was investigated as a dead-end inhibitor for pyruvate.

183 enylyl cyclase by use of [32P]2'-d-3'-AMP, a dead-end inhibitor that binds to the post-transition con

184 Desulfo-CoA, a dead-end inhibitor, also demonstrated simple competitive

185 but supports no kinase activity, acting as a dead-end inhibitor.

186 te binding was confirmed by using AMP-PCP, a dead-end inhibitor.

187 s in the absence and presence of product and dead end inhibitors in both reaction directions.

188 We utilized product and dead end inhibitors of prenylcysteine lyase to probe the

189 Inhibitor studies were conducted with dead-end inhibitors for GGPP and the peptide substrate.

190 omplex mechanism, and the response of SAT to dead-end inhibitors indicates a random order for the add

191 agnitude of the inhibition constants for the dead-end inhibitors may provide insight into the catalyt

192 We propose that P-site analogs act as dead-end inhibitors of product release, stabilizing an e

193 dy state kinetics of AKT1 in the presence of dead-end inhibitors supported the finding and suggested

194 procal plots, in the presence and absence of dead-end inhibitors, argues that interconversion of tern

195 ocity studies in the absence and presence of dead-end inhibitors, suggests random addition of NAD and

196 ined using fosmidomycin and dihydro-NADPH as dead-end inhibitors.

197 TP substrates were varied in the presence of dead-end inhibitors.

198 an increased tendency for the catalytically dead-end intermediate compound III to form.

199 alpha5 or beta3, stable, partially degraded, dead end intermediates accumulated within the cells.

200 ded DNA invading strand, which may represent dead end intermediates of homologous recombination in vi

201 r program, SQID-XLink, searches all regular, dead-end, intra and inter cross-linked peptides simultan

202 In addition, dead-end, intra-, and inter-cross-linked peptides can be

203 Because tissue invasion is an evolutionary dead end, it is likely that amebic pathogenicity is coin

204 Dead-end JNK inhibitors were then used to differentiate

205 t into how homing endonucleases may escape a dead-end life cycle in a population of saturated target

206 groups multiplied the opportunities for many dead-end lineages to iteratively evolve developmental ho

207 Many fluid-transporting epithelia possess dead-end, long, and narrow channels opening in the direc

208 The structure suggests a noncovalent, dead-end mechanism of inhibition.

209 ansported intracellularly and reduced to the dead-end metabolite xylitol.

210 Hence, dead-end metabolites and blocked reactions can arise tha

211 ing reactions that are indirectly related to dead-end metabolites but of biological importance to the

212 iJR904 model, for instance, about 42% of the dead-end metabolites were fixed by our proposed method.

213 ent of information gaps for E. coli, such as dead-end metabolites.

214 l of four intermolecular cross-links and two dead-end modifications were identified using IRCX and LC

215 asexuality is supposed to be an evolutionary dead end, morphological, cytogenetic, and genomic data s

216 cyanobacteria are widely regarded as trophic dead-ends mostly inedible for zooplankton, but substanti

217 der binding combined with the formation of a dead-end mRNA-Hfq complex causes high concentrations of

218 of the enzyme, because of the formation of a dead-end N-5 formylflavin adduct, is more than 100-fold

219 The maternal RNAs vasa, dead end, nanos1, and daz-like all become localized to t

220 lass of germ plasm components, which include dead end, nanos1, and vasa RNAs, are initially present i

221 n of weak adaptability drives species into a dead end of evolution.

222 The recalls of reactions and dead ends of DEF reach around 73% and 86%, respectively.

223 ed prion forming capability and representing dead ends of the prion replication cycle.

224 he presence and type (i.e., inter, intra, or dead-end) of the cross-linked products to be readily det

225 The non-swapped oligomers likely represent a dead-end offshoot of the amyloid pathway and must dissoc

226 tribution of carbonate minerals that form in dead-end one-dimensional diffusion-limited zones that ar

227 ed that this empty capsid was an off-pathway dead end or at best served for storage of pentameric sub

228 Any obvious problems in the network, such as dead end or disconnected reactions, can, therefore, be s

229 indicate that the enzyme may be resistant to dead-end organophosphate aging reactions that permanentl

230 ate model which describes the time course of dead-end, partial HA ultrafiltration.

231 mation of Co(4)(CO)(12) is not necessarily a dead end pathway in the Co(2)(CO)(8)-catalyzed Pauson--K

232 y converts Mtb's methylcitrate cycle into a "dead end" pathway that sequesters tricarboxylic acid (TC

233 ut and leading to the formation of apparent "dead-end" pathways.

234 This finding allowed the dead-end peptide inhibitor EDNEFTA to be characterized a

235 e formation of the experimentally observed ''dead-end'' phosphohistidine product (PDB Code = 1V0W ).

236 lly unstable, the reactions proceeded via a "dead-end" polymerization mechanism, and only low to mode

237 Importantly, it is shown that addition of dead-end pores increases tortuosity in proportion to the

238 sity decrease in ischemic brain slices where dead-end pores were partially occluded by large macromol

239 tected thiols can undergo isomerization to a dead-end product (a 4-methylcoumarin-3-yl thioether) upo

240 te, the dinitrosyl complex is converted to a dead-end product after the dissociation of the proximal

241 The hydroquinone detected in vitro is a dead-end product most likely resulting from chemical or

242 of 0.2 to 0.8 V using acetic acid, a typical dead-end product of glucose or cellulose fermentation.

243 ast for bovine enterovirus, but are either a dead-end product or direct precursor into which viral RN

244 g that this is a true intermediate and not a dead-end product.

245 b forms in vivo, it will not accumulate as a dead-end product.

246 epine and 10,11-dihydroxy carbamazepine as a dead-end product.

247 et, rather than promote the formation of the dead-end product.

248 susceptible to Cannizzaro reduction to give dead end products.

249 Based on the identification of dead-end products (i.e., a cross-link modification conta

250 cells, suggesting that these RNAs represent dead-end products normally destined for decay by TbDSS-1

251 strate that these immature particles are not dead-end products of assembly, but progress into mature

252 grated viral genomes are largely considered "dead-end products" of reverse transcription.

253 stream from the PPT is predicted to generate dead-end products.

254 s to the 3' exon of the precursor, producing dead-end products.

255 dentified as both intermediates and apparent dead-end products.

256 can be ascribed to the presence of inactive dead-end promoter complexes with features similar to tho

257 S strongly, and these oligomers rapidly form dead-end protofilaments.

258 quent to substrate binding by formation of a dead-end quaternary complex consisting of enzyme, coenzy

259 DNA and inhibits TAR-induced self-priming, a dead-end reaction that competes with minus-strand transf

260 Dead-end reactions with oxidized folate are avoided by t

261 ity benefits the bacteria because males are "dead ends" regarding bacterial transmission, and their a

262 This method is capable of finding indirectly dead-end-related reactions with biological importance fo

263 pid release of tight-binding inhibitors from dead-end ribulose-bisphosphate carboxylase/oxygenase (Ru

264 Analyses of dead end RNAi and mutant embryos reveal that the lumen f

265 mber of operations required to eliminate the dead-ending segments and segment pairs grows quadratical

266 Although often considered as evolutionary dead ends, selfing taxa may make an important contributi

267 er, this pathway represents a thermodynamic "dead end" since the radical pairs generated by homolysis

268 By contrast, dead-end species tend to be disulfide-insecure, in that

269 as des[26-84] and des[58-110] are metastable dead-end species that preferentially reshuffle.

270 bserved incomplete chains are non-obligatory dead-end species, in that their formation is not mandato

271 Thus, it is a dead-end species, neither oxo group acceptance nor e(-)-

272 nsfer, respectively, than previously studied dead-end species.

273 at can misfold to form an aggregation-prone, dead-end species.

274 to distinguish on-pathway intermediates from dead-end species.

275 ation of this four-coordinate cob(II)alamin "dead-end" species in the His759Gly variant illustrates t

276 CF3)3], are stable and unreactive, remaining dead-end spectators throughout the coupling process.

277 Most emerging infections result in dead-end "spillover" events in which a pathogen is trans

278 ggregates or inclusion bodies that represent dead-end static structures.

279 Evolutionary dead-end strategies are characterized by short-term prod

280 Here, I detail a real-time dead-end strategy associated with the behavioural traits

281 er promote the formation of a nonproductive "dead-end" ternary complex, protected the lid from trypsi

282 ction loops sequentially while isolating or "dead-ending" the remaining nonactive loops.

283 that functional locationism is a theoretical dead end; their proposed mechanistic framework is a firs

284 ion, from trapping pathogens in evolutionary dead ends, through slowing or inhibiting the process of

285 in forms of conformational freedom, and also dead ends to further saturation.

286 whether nuclear eIF4E also binds nascent but dead-end transcripts is unclear.

287 An SmTK crystal was soaked with the dead end transition state analog (TSA) components tauroc

288 s are productive on-pathway intermediates or dead-end traps.

289 Using dead-end ultrafiltration (UF) and batch ozonation tests,

290 , to fill gaps by finding the most efficient dead-end utilization paths in a constructed quasi-endosy

291 We characterized dead-end vesicles using a combination of membrane capaci

292 nts, indicating they were permanently docked dead-end vesicles.

293 sing open-syntaxin increased the fraction of dead-end vesicles.

294 Munc18-2 or SNAP-25 reduced the fraction of dead-end vesicles.

295 nes incubated with anti-GAPDH and Rab2 form "dead end" vesicles that are unable to transport and fuse

296 e essential PPT and att site and generated a dead-end viral DNA product.

297 th century, lactate was largely considered a dead-end waste product of glycolysis due to hypoxia, the

298 ny of these interspecies transfer events are dead end, where transmission is confined only to the ani

299 In between are ancestors and dead ends, which functionally correspond to stem and non

300 be mathematically shown to be inconsistent (dead-ending) with the globally optimal alignment.