ライフサイエンスコーパス: explain how

1 A model is proposed to explain how 3'CITE-based regulation of ribosome recruitm

2 Our study provides the first model to explain how 3D motion sensitivity can arise in MT neuron

3 However, a mechanism to explain how a component of the nuclear pore complex (NPC

4 we propose a "sideways sliding" mechanism to explain how a conserved membrane-embedded alpha-helical

5 ty," but this observation does not in itself explain how a loopless structure might arise.

6 We explain how a package of culturally evolved religious be

7 Our results allow us to explain how a quasi-classical limit of helicity emerges

8 The findings provide a mechanism to help explain how a strong pOFC pathway, which is poised to mo

9 mechanism, called "ribosome drafting", that explains how a mRNA's folding kinetics and the ribosome'

10 This explains how a single Rab can coordinate recycling and f

11 Here we propose a simple mechanism that explains how a top-down attentional modulation, falling

12 ed by the tumor microenvironment and further explains how a tumor cell can coordinate many critical s

13 These functions could help explain how activin A modulates physiological signaling

14 ability of VTA DA neurons after cocaine, and explains how acute cocaine induces long-lasting remodeli

15 consequent M2 differentiation) that further explains how acute infection leads to chronic inflammato

16 Taken together, these findings explain how adaxial-abaxial polarity patterns the mediol

17 Our mathematical model explained how ADCS enhanced the inhibition of NOB growth

18 These TSP1 interactions may also explain how additional C9 subunits can be recruited to t

19 he expression of AE3 in neurons, which could explain how AE3 reduces seizure susceptibility.

20 ensitive, providing a potential mechanism to explain how ageing influences their amplitude and functi

21 These findings explain how AIF contributes to the biogenesis of respira

22 erent physiological systems of the gut could explain how all these changes are coordinated during pos

23 We explain how alterations to their profiles and functions

24 fication of numerous AMPK targets has helped explain how AMPK restores energy homeostasis.

25 These data help to explain how an enveloped virus such as NiV can infect an

26 The different LpoA structures helped explain how an outer membrane-anchored LpoA can either w

27 ce theory (NRT) provides a theoretical model explaining how an internal periodic representation of a

28 of the cleavage furrow in dividing cells-to explain how and why DE and AB models are used.

29 Neighbourhood effects also help explain how and why the benefits of interventions vary b

30 One theory that aims to explain how animals detect the magnetic field is the mag

31 The model explains how aptamer structure, ligand affinity, switchi

32 However, to explain how arousal effects are triggered, it is likely

33 Our results help explain how Arp2/3 complex is locked in an inactive stat

34 To explain how autophagic flux could exert a proviral effec

35 The structure also explains how autophosphorylation in the N lobe stabilize

36 se counteracts TacT-dependent growth arrest, explaining how bacterial persisters can resume growth.

37 This mechanism also explains how bacterial IgG-binding proteins regulate NK

38 ctively, our results provide a framework for explaining how binding events and mutations can alter in

39 ntial for specific DNA-binding by PerR, thus explaining how both the metal and DNA ligands prevent Pe

40 In this issue Ohsaki et al. explain how breastfeeding can prevent the onset of food

41 on is increasingly favored after bS16 binds, explaining how bS16 drives later steps of 30S assembly.

42 we then test which of these mechanisms best explains how burying beetles, Nicrophorus vespilloides,

43 e normal GC response, a cooperation that may explain how c-MYC and miR-155 can collaboratively functi

44 ides a structure of the Cas1-2/3 complex and explains how Cas1 and the target-bound Csy complex play

45 This study demonstrates and explains how casein-enriched retentates from microfiltra

46 Different models have been proposed to explain how Cdc48 might couple ATP hydrolysis to forcibl

47 This novel mechanism explains how CDK4 promotes anabolism by blocking catabol

48 data combine to suggest a multistep model to explain how cell intercalation can occur against a force

49 Specifically, using a common framework, we explain how cells characterized by contact inhibition of

50 The resulting dynamic equilibrium can explain how cells maintain stable, contractile connectio

51 ults resolve a long-standing controversy and explain how cells use centrosome and microtubules to mai

52 This mechanism might help explain how chaperones can facilitate the folding of var

53 These findings help to explain how chronic TLR-mediated inflammation may be per

54 ve strength for closely related groups helps explain how climbing with adhesive pads has evolved in a

55 Our findings explain how cognitive performance shifts as a function o

56 atures of this multiplexed mechanism help to explain how complex connectivity is encoded and robustly

57 social norms, are a very strong candidate to explain how complex societies function.

58 and implausible: incomplete, as it does not explain how continuous magnitudes are calculated; implau

59 The existing model explains how core PCP proteins, including Van Gogh (Vang

60 Here, we elucidate crucial steps that explain how CRC favors SGG colonization.

61 This streamlined type I-C system explains how CRISPR pathways can evolve compact structur

62 ar organization mechanisms of E1 cells could explain how CSF flow contributes to brain function and m

63 These findings at least partially explain how Ct infection could result in adverse pregnan

64 provide the genetic and mechanistic basis to explain how cystine deprivation triggers necrosis by act

65 d heterogeneity in origin firing and help to explain how defined replication timing profiles emerge f

66 To date, however, a unified theory explaining how deltas self-organize to distribute water

67 omical knowledge of MSO neurons to plausibly explain how dendrite-targeting excitation and soma-targe

68 elop a model based on the TREM2 structure to explain how different TREM2 ligands might interact with

69 ppraisal is and why it plays a major role in explaining how different individuals consider food suppl

70 model to describe transfection activity, we explain how dimensions of amyloid fibrils are able to mo

71 pare competing trophic cascade hypotheses to explain how dingoes could influence shrub recruitment.

72 The structure explains how diphthamide, a eukaryotic and archaeal spec

73 In this Quick Guide, Votier and Sherley explain how diverse seabirds play important roles in eco

74 These findings explain how DLK specifically mediates nerve injury respo

75 This discovery helps explain how Dlx mutations result in abnormal forebrain d

76 The current data therefore explain how duration of antigen presentation affects the

77 This overlap explains how DX-2507 blocks IgG binding to FcRn and ther

78 Our model explains how dynactin binding to the dynein-1 tail direc

79 (TMT) is a generic sociological theory that explains how emergent projects of collective action are

80 become a core concept in community ecology, explaining how environmental fluctuations can promote co

81 ts attraction to a different chromatin type, explaining how enzymes that act on histones, which often

82 comitant with chromosome 'condensation', and explains how enzymes a few nanometers in size are able t

83 nism that maintains TE silencing, but cannot explain how epigenetic silencing is first initiated.

84 Several mechanisms explain how epilepsy and comorbidities are associated, i

85 Therefore, the current findings not only explain how ESC-specific miRNAs are preserved and accumu

86 Two models are proposed to explain how Escherichia coli pyruvate kinase type 1 is a

87 this paper provides a molecular framework to explain how EspG disrupts recycling whilst also reportin

88 e propose a model for U6 snRNP assembly that explains how evolutionarily divergent and seemingly anta

89 sterior superior temporal sulcus (pSTS) best explained how face selectivity arises in both controls a

90 However, this alone is not enough to explain how false memories can arise naturally in the co

91 mediates their stepwise unfolding, but also explain how FANCJ chooses between supporting DNA repair

92 stream of FGFRs could therefore in principle explain how FGFs play several distinct roles in other de

93 ain interface, and we can for the first time explain how fructose 1,6-bisphosphate affects the active

94 y neuron subtypes has not been sufficient to explain how GABAergic neurotransmission sculpts principa

95 g revealed a broad HLA-DR cross-restriction, explaining how Gag293-specific public clonotypes could b

96 analyzed to determine the possible mechanism explaining how GAGs promote iron uptake by the Caco-2 ce

97 the two kinds of photoreceptors and help to explain how gene duplication and the formation of rod-sp

98 ation within the bacitracin network can also explain how gene expression noise propagates between res

99 s are needed to test whether appetite traits explain how genetic risks accelerate growth earlier in d

100 in the arginine vasopressin-oxytocin pathway explains how genetic diversity at Avpr1a and Oxtr could

101 At present, limited evidence explains how genetic risk for schizophrenia is manifest

102 Our theorem explains how GKS band gaps from metageneralized gradient

103 These findings serve to explain how GlcNAc-1-phosphotransferase recognizes a lar

104 thways, providing an underlying mechanism to explain how glucose utilization is increased to support

105 ed sampling of an open Skp1 conformation can explain how glycosylation enhances interactions with F-b

106 ique features of its catalytic machinery and explain how GTP binding induces conformational changes t

107 Our findings explain how GTP hydrolysis controls septin assembly, and

108 9-2.4 A resolution structures presented here explain how HcaR recognizes four ligands (ferulate, 3,4-

109 To explain how high Cut7 occupancy causes this reversal, we

110 ulated (p)ppGpp synthesis, our model did not explain how hipBA induced persistence.

111 Our results explain how HIV-1 IN, which self-associates into higher-

112 SLiMs and provide an alternative concept to explain how Hox interactome specificity could be achieve

113 ribe how these approaches can be utilized to explain how human genetic variation can modulate the eff

114 ial reasoning and reproductive pressures and explains how human intelligence may have become so disti

115 This finding may explain how humans can develop an enduring sense of agen

116 They may explain how humans overcome the allure of short-term gai

117 activities of XPF-ERCC1, RPA and SNM1A might explain how ICL unhooking is achieved in vivo.

118 The Turing reaction-diffusion model explains how identical cells can self-organize to form s

119 active T cells targeting hybrid peptides may explain how immune tolerance is broken in T1D.

120 We present a model to explain how impaired iron localization in leaf veins res

121 From a control perspective, we explain how improvements in reducing post-death transmis

122 Furthermore, we can explain how, in both single and mixed alkali composition

123 To explain how intervention processes interact with context

124 ocyanate-induced inhibition of DUBs may also explain how isothiocyanates affect inflammatory and DNA

125 he filament, to determine its kinematics, to explain how it is linked to nearby sources, or to accoun

126 fer an update to Maynard Smith's analogy and explain how it might be developed into an exploratory an

127 he TAR complex despite not touching the RNA, explaining how it enhances TAR binding to the SEC 50-fol

128 The model also naturally explains how KaiA, by acting as a nucleotide exchange fa

129 Two models have been proposed to explain how kinesin-1 functions to move nuclei in myotub

130 coupling mechanisms of CcO mutants, but also explains how kinetic gating in the D-channel is imperati

131 HIFI explains how labor can progress despite paradoxical meta

132 ing the abundance of somatic mutations might explain how larger organisms could overcome the burden o

133 To explain how learning achieves this, we provide analysis

134 combining information across modalities, and explaining how learnt associations modulate taxis.

135 es can hijack host replication processes and explain how loader activity is internally regulated to p

136 ticity of large-scale chromatin organization explains how localized changes in DNA topology allow DNA

137 nced early cellular fitness, and potentially explains how longer coded peptides, that is, proteins, c

138 eed, this alternative mechanism might better explain how low-abundance lncRNAs transcribed from nonco

139 ill no consensus on a mechanistic model that explains how magmatism leads to the turnover of terrestr

140 We explain how major types of MRI probes work and how they

141 urrent study provides a mechanistic basis to explain how matrix controls the antifungal effector func

142 This model explains how mechanical strain on cutaneous wounds might

143 In addition, we explain how metabolic modelling may be used to conduct i

144 lution between TCR and MHC genes, helping to explain how MHC compatibility and bias can be encoded wi

145 ways may develop in non-B HIV-1 subtypes and explain how "minor" polymorphisms and substitutions in H

146 These findings help explain how mTORC1 selects its substrates, how its kinas

147 d Jez reveals critical domain movements that explain how multiple methylation reactions are uniquely

148 It helps explain how multiscale cooperation from the community to

149 of-function mechanisms have been proposed to explain how mutant FUS leads to motor neuron degeneratio

150 Here we present two mechanisms that help to explain how mutations in one VGSC gene, Scn8a, contribut

151 , there are conflicting conceptual models to explain how N availability influences the decomposition

152 ween evolution and machine learning can help explain how natural selection across fluctuating environ

153 activity and nucleic acid binding assays to explain how naturally occurring mutations within this po

154 ms that account for spatial selectivity also explained how neural responses changed with degraded sig

155 linical onset of most agents and the need to explain how neurochemical changes reverse the many diffe

156 tion of a mammalian mtDNA genetic bottleneck explains how new germline variants can increase to high

157 We explain how non-canonical splicing can lead to aberrant

158 model proposed by Mather et al. attempts to explain how norepinephrine enhances processing in highly

159 4, ADMA, and mitochondrial dysfunction could explain how obesity and IL-4 can synergize to exacerbate

160 Our analysis explains how observed gradients of host specialism and g

161 lyses supporting the seed-bank hypothesis to explain how oceanic viral communities maintain high loca

162 strate channels in a T-shaped configuration, explaining how OleA coordinates its two substrates and p

163 It helps explain how oocytes respond to a highly prevalent human

164 ermediate endpoint) is a third variable that explains how or why >/=2 other variables relate in a put

165 ochemical responses in membrane dynamics may explain how organelles orderly cohabit in the crowded cy

166 studies elucidate active-site features that explain how orthologs can generate rigid macrocyclic sca

167 This simple but elegant mechanism explains how oxalate, a molecule that humans and most an

168 Our results explain how p58C participates in RNA synthesis and prime

169 e model: the replication fork model that can explain how passage of a replication fork and regulation

170 erstanding of mechanobiology has advanced to explain how passive and active forces induce similar sig

171 latory features discovered in animal genomes-explains how patched/Ptch1 can drive dramatic adaptation

172 The structure of TcPINK1 explains how PD-linked mutations that lie within the kin

173 near and into the exponential regimes, which explains how PDADMA can mysteriously "pass through" laye

174 coding theories provide a unified framework explaining how perception is shaped by the integration o

175 In this Primer, I will explain how perceptual learning is transformative in gui

176 how no apparent structural change that could explain how phosphorylation could enable catalytic activ

177 ce domain binding the L-selectin tail and to explain how phosphorylation of the L-selectin tail abrog

178 This tutorial review explains how photo-initiated polymerization reactions ha

179 se results reveal an endogenous mechanism to explain how physical exercise leads to the induction of

180 ubulin contacts in microtubules, this result explains how pironetin inhibits the formation of microtu

181 Moreover, the structure explains how Pno1 coordinates the 3'end cleavage of the

182 onalisation of MHC alleles into 'supertypes' explains how polymorphisms persist during rapid host-par

183 tamine binds to the fibrin clot, which could explain how protamine instigates clot lysis and increase

184 s and in elucidating general mechanisms that explain how quaternary structure tends to evolve.

185 Our data explain how R696 is accommodated in the middle of the me

186 The ternary complex architecture explains how Rab11 vesicles support coordinated F-actin

187 ased on these data we propose a mechanism to explain how Rad53 enhances the specificity of FHA1-media

188 l mixing of the lipids have been proposed to explain how raft-like microstructures involving choleste

189 erlaps in Serpin1 and WSCP accumulation that explain how RD21 contributes to the innate immunity of m

190 These results help explain how reproduction of HSV-1, a ubiquitous, medical

191 g the essential features of this interaction explains how resource availability modulates the interac

192 The goal of this study is to explain how RNA can remain soluble and available for int

193 Our findings explain how RNAP thermal motions control the promoter se

194 determined, to develop a detailed model that explains how RNase R digests structured RNA and how this

195 in recognition mechanisms in the nucleosome, explaining how RNF168, RNF169, and RAD18 regulate 53BP1

196 ged to form the pyrenoid matrix, potentially explaining how Rubisco packaging into a pyrenoid could h

197 bly strong, up to approximately 500 pN, thus explaining how SasG can withstand physiological shear fo

198 cells in combination with bacterial genetics explains how Shigella evades a broad spectrum of immune

199 Thus, our study provides a framework explaining how signals from different activating recepto

200 Furthermore, analysis of these structures explained how single nucleotide mutations and methylatio

201 These new observations explain how slings form from tethers and provide insight

202 icotine reward-related behavior and may help explain how smokers of menthol cigarettes exhibit reduce

203 This work explains how spatial patterning in the ectoderm controls

204 tural and biochemical insights that start to explain how specific proteins recognize DNA replication

205 cation promotes efficient DNA processing and explains how SSB stimulates rather than inhibits RecQ ac

206 This may help explain how stress contributes to substance abuse and ho

207 cells, no existing quantitative model fully explains how structural differences between kinesins alt

208 rmational changes induced by leukotriene C4, explaining how substrate binding primes the transporter

209 A compressed film model explains how surface tension depression by interfacial o

210 rganization of SVs into a liquid phase could explain how SVs remain tightly clustered without being s

211 This helps to explain how T. brucei escapes 'wholesale deamination' of

212 ell as cell and ovary culture experiments we explain how TAp63alpha is kept inactive in the absence o

213 We propose a model explaining how TARPs stabilize the activated state of AM

214 scribe a cell-autonomous signaling mechanism explaining how tenascin-C promotes cancer cell migration

215 isual hierarchy, and our computational model explains how that hierarchy might be built.

216 These results explain how the Cas1-Cas2 CRISPR integrase recognizes a

217 Overall, our model can explain how the combination of temporally regulated sens

218 We explain how the components of inheritance can influence

219 tion, assessment and management do not fully explain how the decision process occurs in clinical prac

220 A theoretical model was developed to explain how the denaturation of an individual, adsorbed

221 constellation of deprivation (BCD) needs to explain how the development of personal control, trust,

222 We explain how the device works through several examples an

223 Several theories can explain how the distributions of BMP and Chordin are reg

224 Our findings explain how the effects of an HCM mutation in the C-doma

225 These results explain how the glycosyltransferase modifies a progressi

226 This phenomenon might explain how the high rate of infection is maintained in

227 Here, we show and explain how the layer stacking and physical properties o

228 interactions among neighbouring archaellins explain how the long but thin archaellum maintains the s

229 Our results explain how the molecular size and chemical nature of N-

230 To explain how the network's neuronal properties encode tim

231 Our findings explain how the outer segment structure evolved from the

232 We also explain how the presence of links affects the folding pa

233 economic theories suggest causal pathways to explain how the prevalence of rule violations in people'

234 IM and the cytoplasm, and current ideas that explain how the Psp response keeps bacterial cells alive

235 Ecologists have long sought a way to explain how the remarkable biodiversity observed in natu

236 Together, our findings help explain how the spatial and temporal behaviors of the FM

237 NA circularisation and ribosome drop-off, we explain how the transcript length may play a central rol

238 full account of search will probably need to explain how the two interact to find visual targets.

239 nization and desynchronization mechanisms to explain how the two systems interact in the service of e

240 our model, we propose testable hypotheses to explain how the viral shell becomes destabilized, leadin

241 It remains to be explained how the apparent complete loss of YCF1 can be

242 o evade previously elicited antibodies, thus explaining how the GII.4 genotype can persist over long

243 triggers the formation of the active state, explaining how the HNH domain exerts a conformational co

244 to altered distributions of CHS siRNAs, thus explaining how the k1 mutation reverses the phenotype of

245 itochondrial proteins to the 26S proteasome, explaining how the whole sperm mitochondria are degraded

246 Predictive coding explains how the brain might perform Bayesian inference

247 The mechanism that emerges from our analysis explains how the Cas9/sgRNA complex is able to locate th

248 and growth between the different conformers explains how the change in incubation condition could le

249 referred orientations is demonstrated, which explains how the conversion reaction occurs in alpha-MnO

250 Moreover, the complex structure explains how the DX-2507 interaction is pH-insensitive u

251 It explains how the evidence that is available from randomi

252 It also explains how the machinery that regulates vesicle fusion

253 y defines YabA as a novel structural hub and explains how the protein tetramer uses independent CTDs

254 utionary time to be highly pathogen-specific explains how the risks of autoreactivity in this system

255 e review the 'tumor hotspot' hypothesis that explains how the tissue-intrinsic local microenvironment

256 Shin Yim et al. (2017) identify a pathway to explain how these aspects of our physiology are deeply a

257 g an 'imperfect' photon counting machine, we explain how these constraints give rise to adaptive quan

258 We propose several models to explain how these mechanisms are integrated with each ot

259 were developed in agricultural science, and explain how these methods can minimize bias in quantitat

260 role/N-methylimidazole polyamides that helps explain how these molecules locate rare target sites.

261 reate a need for theoretical principles that explain how these networks shape neural communication.

262 To attempt to explain how these observed effects might support enhance

263 We explain how these processes enable the tendon to geometr

264 n its wild-type counterpart, thus helping to explain how these single-nucleotide polymorphisms contri

265 To help explain how these small structural differences can have

266 Computations explain how these structural elements contribute to reve

267 a from studies in vivo we propose a model to explain how these two activities contribute to the funct

268 itive than nearly all previous upper limits, explaining how these jets, if common, could thus far hav

269 Currently, there is no model that explains how these different spatial patterns arise and

270 ere, we present a theoretical framework that explains how these larger fluctuations in archaeal cell

271 ct metabolic signatures of key immune cells, explains how these metabolic setups facilitate immune fu

272 In this review, we define ECVs, explain how they are generated using the CLSI methodolog

273 osolically exposed transmembrane domains and explain how they use ubiquitin to triage clients for deg

274 e benefits and harms of aspirin therapy, and explain how they would incorporate shared decision makin

275 ere mutations that escape germline selection explains how they can contribute to the risk of late-ons

276 o the variable domains of gp120 and begin to explain how this could be exploited to enhance the immun

277 Here we explain how this discrepancy may be due to englacial sol

278 I also explain how this edge-detection computation is done.

279 l walls was the first proposed hypothesis to explain how this element reduced the severity of plant d

280 teractions coupled with catalytic deficiency explain how this mutant nuclease prevents dsDNA degradat

281 creation of ICU liberation philosophy and to explain how this patient- and family-centered, quality i

282 ver, current models of canonical RdDM cannot explain how this self-perpetuating mechanism is initiate

283 f location in feature binding, and the model explains how this special role could be realized in the

284 ers into higher-order oligomers, potentially explaining how Tie2 is differentially clustered followin

285 We explain how to establish the immune organoid culture to

286 We explain how to establish these cultures in the fully def

287 In this protocol, we explain how to generate Parkin-expressing, mitochondria-

288 We explain how to quantify and design CO2 resistant membran

289 ring certain types of data, this Perspective explains how to work through the general intellectual pr

290 This mechanism explains how transcription activation cycles, lasting fo

291 ZG cells provides a unifying mechanism that explains how transiently activating CaV 3.2 channels can

292 nly form during transcription elongation and explains how translation can prevent transcriptional pau

293 The identification of this compatible solute explains how Trichodesmium spp. can thrive in the marine

294 This mechanism explains how twitches, although self-generated, trigger

295 corneal epithelial cell differentiation, and explains how two SNPs may contribute to corneal diseases

296 This could in principle explain how Ub-Fancd2 promotes ICL repair, but we show t

297 In this Quick Guide, Steven Buck explains how, uniquely among the bright primary perceptu

298 TJ and paracellular permeability, which may explain how various drugs, chemicals, and metabolic stat

299 mes localized during regeneration would help explain how wounds establish pattern in new tissue.

300 f pheromone molecules, have been proposed to explain how yeast cells filter fluctuations and detect s