ライフサイエンスコーパス: protein S

1 ted/dysregulated by elusive mechanosensitive protein(s).

2 enzymes that reduce oxidized methionines in protein(s).

3 ions can cause non-specific loss of cellular protein(s).

4 wed by catalyzing Ubl transfer to cognate E2 protein(s).

5 ropathy tissue and glomerular depositions of protein S.

6 driven by both TAM receptor ligands Gas6 and protein S.

7 e main isoform containing the beta-chain and protein S.

8 ediated inhibition of FXa compared with free protein S.

9 by the vitamin K-dependent proteins Gas6 and protein S.

10 u226 is essential for enhancement of TFPI by protein S.

11 FXa approximately 12-fold in the presence of protein S.

12 by 20-nm-long homotrimers of spike envelope protein S.

13 V) enhanced TFPI function in the presence of protein S.

14 lective small-molecular inhibitor of BET BRD protein(s), (1) decreased the levels of c-Myc mRNA and p

15 of structural biology is to understand how a protein's 3-dimensional conformation determines its capa

16 on the bilayer surface, likely impacting the protein's ability to assemble into organized pretubule s

17 8N substitution significantly diminished the protein's ability to catalyse the activation of Rac1.

18 secondary active transporter determines the protein's ability to create a substrate gradient, a feat

19 ine, in PLAA, which causes disruption of the protein's ability to induce prostaglandin E2 and cytosol

20 conformational changes can also disturb the protein's ability to interact with and adsorb onto bare

21 tacted region of the binding site alters the protein's ability to recognize contacted base sequences

22 N-glycosylation of JAM-A is required for the protein's ability to reinforce barrier function and cont

23 itors, revealing its interactions within the protein's active site.

24 otes dimerization, which is pertinent to the protein's activities and pathological aggregation, and w

25 (RbC) is necessary for the tumor suppressor protein's activities in growth suppression and E2F trans

26 same underlying mechanism, the removal of a protein's activity from a cell can have widely divergent

27 um concentrations >1 mm, consistent with the protein's activity within the intestinal and inflammator

28 hese, sequence variants in Cox7a2l alter its protein's activity, which in turn leads to downstream di

29 e Asp-His-His-Cys-Cys-rich domain-containing Protein S-Acyl Transferases (PATs) are multipass transme

30 Protein S-acylation (palmitoylation) is a reversible lip

31 rate that APE enables sensitive detection of protein S-acylation levels and is broadly applicable to

32 HC S-acyltransferases are enzymes catalyzing protein S-acylation, a common post-translational modific

33 Protein S-acyltransferases, also known as palmitoyltrans

34 es and detect even modest differences in the protein's affinities for relatively similar ligands.

35 ng and the rate of synthesis are linked to a protein's amino acid sequence is still not well defined.

36 lucidates the intricate relationship among a protein's amino acid sequence, its cotranslational nasce

37 ; and 6) the fact that a large fraction of a protein's amino acids contribute to its overall function

38 class using machine learning methods given a protein's amino-acid sequence and/or its secondary struc

39 hancement of TFPI-mediated FXa inhibition by protein S and FV depends on a direct protein S/TFPI inte

40 Tyro3, Axl, and Mer (TAMs) and their ligands protein S and Gas6 are involved in the uptake of phospha

41 of labeled microparticles in the presence of protein S and Gas6 in human aortic endothelial cells and

42 mechanism of the protein C pathway in which protein S and the aPC-cleaved form of fV are cofactors f

43 r (a) by specific recognition between capsid protein(s) and replication proteins (poliovirus), or (b)

44 onal design that allows for the digestion of protein(s) and retention of the resulting peptides with

45 ed haem is distributed by haemolymph carrier protein(s) and sequestered by vitellins in the developin

46 alcium-binding betagamma-crystallin protein, Protein S, and elaborate on its interactions with calciu

47 elet aggregates and reductions in protein C, protein S, antithrombin and A Disintegrin and Metallopro

48 ntial activities of the TAM ligands Gas6 and Protein S are poorly understood.

49 y, ZAK-alpha and/or ZAK-beta transcripts and protein(s) are frequently upregulated in colorectal aden

50 PagM promotes group motility by a surface protein(s), as a pagM-expressing strain conferred motili

51 the full-length substrate protein impair the protein's assembly, implying that BamD's interaction wit

52 We explored whether additional Treg-specific protein(s) associated with GARP.TGF-beta1 complexes regu

53 Enokitake protein's band (75kDa) reacted specifically with the pat

54 tation, allowing us to tune and intermix the protein's behavior at will.

55 ome and survival, whereas serum myelin basic protein's best accuracy occurred at 48 hours.

56 e variant of C4BP lacking the beta-chain and protein S binds plasminogen much stronger than the main

57 terminal region of p17 is irrelevant for the protein's biological activity.

58 In addition, protein S bound to C4b binding protein showed greatly re

59 gating may be mediated by the membrane or by protein(s) but evidence for the latter is scarce.

60 the outer segment disk and suggests that the protein's C terminus may modulate membrane curvature-gen

61 as mapped to a 23-amino-acid sequence at the protein's C terminus.

62 ray scattering (SAXS) data revealed that the protein's C-terminal domain has a PG-binding-competent c

63 The protein's C-terminal MBT repeats bind mono and dimethyla

64 a fragment of pleiotrophin located near the protein's C-terminus.

65 h for intrinsic factors, which account for a protein's capability to act as an allergen, is ongoing.

66 ing, as the molecular signals that dictate a protein's cellular destination are often promiscuous.

67 he channel, using a relationship between the protein's charge and pH measured in a previous experimen

68 s often evolve in response to changes in the protein's chemical or physical environment (such as the

69 own to only weakly interact with scaffolding protein's coat binding domain.

70 ATPases, a substrate-specific transmembrane protein (S component) and a transmembrane protein (T com

71 , enabling the interrogation of changes in a protein's conformation required for function at varied c

72 whereas Ca(2+) binding strongly reshapes the protein's conformational dynamics by disrupting beta-she

73 By capturing the motions of a protein's constituent atoms, simulations can enable the

74 esting differences in the arrangement of the protein's core.

75 Certain "activating" fatty acids induce the protein's cytoplasmic to nuclear translocation, stimulat

76 to block HspB1 phosphorylation inhibits the protein's cytoskeletal recruitment in response to mechan

77 A conserved binding interaction between DDX protein's DEAD domain and Rev was identified, with Rev's

78 or protein C deficiency; and 1.0% (0.7%) for protein S deficiency.

79 and severity of symptoms is unrelated to the protein's dehydrogenase activity.

80 xpressing constitutively active stable DELLA proteins (S-della) displayed the opposite phenotype.

81 nstrates that the methodology can quantify a protein's disorder as well as the effects of ligand bind

82 y that is based on quantifiable metrics of a protein's disorder.

83 id head groups electrostatically capture the protein's disordered K segments, which locally fold up i

84 reciated that this method merely estimates a protein's distribution and cannot reveal changes in occu

85 Dhx9, DNA-PK and Stau1, further supports the protein's diverse functions in RNA metabolism and DNA ma

86 nd FTLD, we examined the contribution of the protein's domains to its function, subcellular localizat

87 gy is introduced that takes into account the protein's dynamic structure and maps all the cavities in

88 al theory to identify the glassy states in a protein's dynamics, and we discuss the nonnative, beta-s

89 dilational rigidity, which correspond to the protein's effective shape change.

90 raction makes an appreciable contribution to protein's energy balance, up to 2 kcal/mol.

91 some; however, most biophysical studies of a protein's energy landscape are carried out in isolation

92 To study how a protein's energy landscape changed over time, we charact

93 How exactly a protein's energy landscape is maintained or altered thro

94 l scaffold, largely ignoring the impact of a protein's energy landscape.

95 Protein S enhances FXa inhibition by TFPIalpha.

96 e with it in the abstracts referenced in the protein's entries in reliable biological databases.

97 ans that, unlike globular proteins, a repeat protein's equilibrium folding and thus thermodynamic sta

98 rotransmitter release, in agreement with the protein's established role in vesicle resupply.

99 l short-lived intermediate that dictates the protein's fate in a conformation-dependent manner.

100 ethod for analyzing the endogenous levels of protein S-fatty acylation and should facilitate quantita

101 To analyze the endogenous levels of protein S-fatty acylation in cells, we developed a mass-

102 describe a novel approach for quantifying a protein's flexibility in solution using small-angle X-ra

103 resolution, the distance and disorder in the protein's flexible regions using TR-FRET and DEER.

104 he knotted geometry, the interplay between a protein's fold, structure, and function is of particular

105 main interactions and calcium binding affect Protein S folding and potential structural heterogeneity

106 mportantly, these probes minimally perturb a protein's folding equilibria within cells during and aft

107 n native cysteines are required to support a protein's folding or catalytic activity.

108 The rates and energetics of a protein's folding process, which is described by its ene

109 ged approach to reveal the complexities of a protein's free-energy landscape.

110 t some mRNAs may be protected by RNA-binding protein(s) from degradation by MazFsa.

111 Given that a protein's function and role are strongly related to its

112 Hence, evolution modifies a protein's function by altering its energy landscape.

113 mechanism by which S-nitrosation modulates a protein's function is identification of the targeted cys

114 of the structure-function paradigm is that a protein's function is inextricably linked to a well defi

115 ility, suggesting they lead to a loss of the protein's function mechanism.

116 tion can come at the expense of the original protein's function, which is a trade-off of adaptation.

117 bind to the active center are central to the protein's function.

118 ed that this localization is critical to the protein's function.

119 immune cells could provide insight into the protein's function.

120 The allosteric regulation triggering the protein's functional activity via conformational changes

121 abrogate protein expression, the role of the protein's functional domains in host immunity is unknown

122 n reactions that are mediated by each of the protein's functional domains.

123 the faithful quantification of a particular protein's functional fraction are exemplified with retro

124 on of somatic missense mutations between the protein's functional regions (domains or intrinsically d

125 his modification and its contribution to the protein's functions are unknown.

126 nes of this receptor family and its ligands (protein S(+/-), Gas6(-/-), TAM(-/-), and variations of t

127 raise the concern that the prediction of the protein's gene may be incomplete.

128 In this work, unexpected protein S-GlcNAcylation on cysteine residues was observe

129 Growing evidence supports the importance of protein S-glutathionylation as a regulatory post-transla

130 Protein S-glutathionylation is a posttranslational modif

131 Of these variants, two protein S/growth arrest-specific 6 chimeras, with either

132 The original idea was that the protein's higher mass would reduce the frequency of its

133 critically dependent on the stability of the protein's hydration shell, which can dramatically vary b

134 TAM and protein S immunostaining was performed on kidney biopsy

135 We investigated TAM and their ligand protein S in patients with diabetes.

136 ity is frequently considered a question of a protein's increasing number of interactions, we found th

137 rotein-based biopharmaceutical drug due to a protein's inherent tendency to aggregate.

138 presents a convenient way of fine-tuning the protein's interaction network, by making binding sites m

139 the alpha-helices, which provide most of the protein's interactions with InsP3.

140 case specific, determined by the individual protein's interplay with the functionally optimized "int

141 iques to elucidate the role(s) played by the protein's intrinsically disordered C-terminal domain and

142 Protein S is a cofactor for tissue factor pathway inhibi

143 Protein S is a TFPI cofactor, enhancing the efficiency o

144 Protein S is more commonly known as an important cofacto

145 Axl is dispensable, and activation of Mer by Protein S is sufficient to drive phagocytosis.

146 hisms, and little is known about which viral proteins(s) is responsible for the liver tropism of JHM.

147 A protein's isoelectric point or pI corresponds to the sol

148 ration in the membrane, (ii ) control of the protein's isotopic constitution, and (iii ) control over

149 ssociation with messenger RNA export adaptor protein(s) leading to cytoplasmic repeat associated non-

150 ding MerTK receptors and associated Gas6 and protein S ligands.

151 xima shifted by up to +/-80nm, extending the protein's light absorption significantly beyond the rang

152 ociated with the catalyzed chemistry and the protein's macromolecular electrostatics at slower time s

153 regulated based on varying affinity for the protein's many binding sites.

154 to H-acceptor distance as a function of the protein's mass.

155 cellular plasma membrane is mediated by the protein's matrix (MA) domain.

156 r-weight thiol have a dramatic effect on the protein's mechanical stability.

157 To study this motor protein's mechano-chemical properties, we used a recombi

158 ible protein misfolding; when cryptic in the protein's microenvironment, it readily condenses with a

159 ght into the regulatory mechanism of the tau protein's microtubule binding activity.

160 e or domain swap variants spanning the whole protein S molecule for their TFPI cofactor function usin

161 single RNA packaging signal (PS) with capsid protein(s) (most +ssRNA viruses so far studied); step II

162 re, fold, and binding partners, point to the protein's multifaceted biological functions.

163 Mutant p53 protein(s) (mutp53) can acquire oncogenic properties tha

164 causes widespread thiol-oxidation including protein S-mycothiolation resulting in induction of antio

165 Protein S-mycothiolation was accompanied by MSH depletio

166 xICAT and RNA-seq transcriptomics to analyse protein S-mycothiolation, reversible thiol-oxidations an

167 ormation of a stable interaction between the protein's N- and C-terminal domains.

168 ein complex with the viral RNA through the N protein's N-terminal domain (N-NTD).

169 whereby upon T3SS needle assembly, the ruler protein's N-terminal end is anchored on the cytosolic si

170 ive semantically related co-occurrences of a protein's name and a molecule's name in the sentences of

171 A protein's native size in a complex, but not polypeptide

172 ch are often very important for preserving a protein's native structure and function.

173 However, the correspondence between a protein's native structure and its structure in the mass

174 inhibit the binding of other RRM-containing protein/s necessary for miR-16 processing.

175 mino acid residues within or adjacent to the protein's negative regulatory domain.

176 Although the magnitude of a protein's net charge (Z) can control its rate of self-as

177 Protein S-nitrosation (SNO-protein), the nitric oxide-me

178 A family of proteins S-nitrosylated by iNOS-S100A8/A9 were revealed

179 e results reveal an elusive parallel between protein S-nitrosylation and phosphorylation, namely, sti

180 Total cellular levels of protein S-nitrosylation are controlled predominantly by

181 Recent studies have pointed to protein S-nitrosylation as a critical regulator of cellu

182 el functional class of enzymes that regulate protein S-nitrosylation from yeast to mammals and sugges

183 ther, our data indicate that obesity-induced protein S-nitrosylation is a key mechanism compromising

184 Protein S-nitrosylation modulates important cellular pro

185 Thus, Adh6-regulated, SNO-CoA-mediated protein S-nitrosylation provides a regulatory mechanism

186 omal deletion of GSNOR results in pathologic protein S-nitrosylation that is implicated in human hepa

187 , thus favoring local NO production, nuclear protein S-nitrosylation, and induction of mitochondrial

188 ne reductase, a denitrosylase that regulates protein S-nitrosylation, exhibited decreased adipogenesi

189 -nitrosylation, we uncovered major roles for protein S-nitrosylation, in general, and for phospholamb

190 ing transgenic mice to titrate the levels of protein S-nitrosylation, we uncovered major roles for pr

191 extrinsic sialic acid intake reduced ROS and protein S-nitrosylation.

192 ) is limited by one's ability to resolve the protein(s) of interest from the proteins that are not of

193 le docking, etc. require the prediction of a protein's optimal side-chain conformations from just its

194 Different soy protein (S) or whey protein (W) blends with maltodextrin

195 We describe here results that show a protein's outer membrane regions are more heavily footpr

196 k of the fish AFP Maxi, which extends to the protein's outer surface, is remarkably similar to the {1

197 Dynamic changes in protein S-palmitoylation are critical for regulating pro

198 Protein S-palmitoylation is a reversible post-translatio

199 Palmitoyltransferase (PAT) catalyses protein S-palmitoylation which adds 16-carbon palmitate

200 ane targeting property and dynamic nature of protein S-palmitoylation.

201 However, the molecular identity of the protein(s) participating in the basolateral Pi efflux re

202 ults may be attributed to differences in the protein's partition depth, the membrane's hydrophobic th

203 RNA in cells was mediated exclusively by the protein's peptide-binding domain.

204 titrations to monitor interactions from the protein's perspective.

205 Their utility is validated in examining protein S-persulfidation.

206 Optimization of a protein's pharmaceutical properties is usually carried o

207 nteraction site on protein S, we screened 44 protein S point, composite or domain swap variants spann

208 ntrality score, which is related both to the protein's position within a module and to the module's r

209 n to lower temperatures, consistent with the protein's postulated function in cold stress.

210 However, the BLNK protein's precise function in human B-cell differentiati

211 sional structure, which is determined by the protein's primary amino acid sequence.

212 ssumed to select their substrates based on a protein's primary sequence, but a consensus sequence has

213 e various methods to predict disorder from a protein's primary sequence, they all were developed usin

214 degradation via a reaction that requires the protein's prior ubiquitination and the presence of the I

215 that provides a quantitative assessment of a protein's probability to function in chromatin.

216 es that are activated by endogenous ligands, protein S (PROS1) and growth arrest-specific gene 6 (GAS

217 YjhX was expressed well with an N-terminal protein S (PrS) tag in soluble forms.

218 ent Cas9 variant engineered by replacing the protein's REC2 domain with the BCL-xL protein and fusing

219 ity and provide functional insights into the protein's recognition pattern with respect to regulators

220 Exonic genetic variation near each protein's respective gene (cis) was identified using seq

221 meno presto model of prestin, influences the protein's responsiveness to chloride binding and provide

222 it further enhanced TFPI in the presence of protein S, resulting in an approximately 8-fold reductio

223 tual screening; this inhibitor reduced the N protein's RNA-binding affinity and hindered viral replic

224 For example, the pistil SI proteins S-RNase and HT protein function in a pistil-sid

225 g-term studies are needed to clarify dietary protein's role in bone health.

226 h about JAM-A, little is known regarding the protein's role in mechanotransduction or as a modulator

227 isease causing mutations in GDAP1 impede the protein's role in mitochondrial dynamics.

228 le attention has recently focused on dietary protein's role in the mature skeleton, prompted partly b

229 ystatin-C[rs2424577] and Vitamin K-Dependent Protein S[rs6123] in the schizophrenia group; Interleuki

230 ssecting kinase catalytic functions from the protein's scaffolding functions.

231 Cu(2+), Mg(2+), and Zn(2+)), a proxy for the protein's selectivity over these ions.

232 his is done not only within the context of a protein's sequence and structure but also the relationsh

233 rotein function occur through changes to the protein's shape, or conformation.

234 The importance of the protein S SHBG-like domain (and its laminin G-type 1 sub

235 We show that binding of TFPI to the protein S SHBG-like domain enables TFPI to interact opti

236 tical temperature T( *)cr, is related to the protein's single-chain average radius of gyration <Rg>.

237 erent locations within the SLB based on each protein's size and charge.

238 helices of most type II single-span membrane proteins (S-SMPs) of Escherichia coli occur near the N-t

239 lies on the ability to use light to change a protein's solubility.

240 way subtle structural modifications affect a protein's stability and enable it to function in diverse

241 ovalently bound, SUMO can alter a conjugated protein's stability and/or function.

242 s for posttranslational control of the model protein's stability, we tested the ability of various Ch

243 ost common method for determining an unknown protein's structural class is to perform expensive and t

244 ic age, it is possible to predict an unknown protein's structural class using machine learning method

245 FtsN, but the importance of this bond to the protein's structural integrity is unclear.

246 he Met20 catalytic loop region and study the protein's structural motion at this site.

247 nt understanding of the relation between the protein's structural properties and its pathologic behav

248 rsible posttranslational modification of the protein's structure and biological function.

249 ill illustrate how such mutations modify the protein's structure and consequently its pH stability.

250 consistent with existing knowledge about the protein's structure and function, and can be used to cre

251 instability in vivo and adversely affect the protein's structure and function.

252 e type and magnitude of hydrodynamic flow, a protein's structure and stability, and the resultant agg

253 rable interest, mostly for investigating the protein's structure and transport mechanism.

254 tanding of the general principles by which a protein's structure determines its function.

255 We find that changes in a protein's structure due to a mutation influences protein

256 onal challenge of exploring the breadth of a protein's structure space.

257 - to millisecond-timescale fluctuations of a protein's structure.

258 modeling is a powerful tool for predicting a protein's structure.

259 refore underlines the reshaping potential of protein's structures and functions but also limits prote

260 Urinary and plasma levels of protein S, sTyro3, sAxl, and sMer were determined in 126

261 tides were observed regardless of the target protein's subcellular localization.

262 ediated inhibition of FXa in the presence of protein S, suggesting a functional contribution of the B

263 Protein S-sulfenylation is the reversible oxidative modi

264 Mapping the specific sites of protein S-sulfenylation onto complex proteomes is crucia

265 s global, in situ, site-specific analysis of protein S-sulfenylation using sulfenic acid-specific che

266 "tag-switch" method which can directly label protein S-sulfhydrated residues by forming stable thioet

267 Protein S-sulfhydration (forming -S-SH adducts from cyst

268 dy emphasizes the importance of CBS-mediated protein S-sulfhydration in maintaining vascular health a

269 -synthase regulates endothelial function via protein S-sulfhydration.

270 Protein S-sulfinylation (R-SO2(-)) and S-sulfonylation (

271 that lead to localized perturbations of the protein's surface, hydration, electrostatics, and dynami

272 a three-dimensional map or footprint of the protein's surface.

273 ed regions that serve to present them on the protein's surface; (2) ISDs generally have a hydrophobic

274 igh versus low" protein intake or 2) dietary protein's synergistic effect with Ca+/-D intake on bone

275 of G9a activity depends on yet unknown novel protein(s) synthesis.

276 The shorter isoform of the human protein (S-tetherin) lacks the first 12 amino acids of t

277 tion by protein S and FV depends on a direct protein S/TFPI interaction and that the TFPI C-terminal

278 ed a yeast two-hybrid screen to identify the protein(s) that could directly interact with human FTO p

279 To do so, viruses encode dedicated protein(s) that facilitate this process.

280 We hypothesized that ui1.1 encodes an SLF protein(s) that interacts with CUL1 and Skp1 proteins to

281 However, the G protein(s) that is involved in MC4R-mediated suppression

282 Our aim is to identify the protein(s) that may be important for snake venom neutral

283 ained with lupin, and aiming to identify the protein(s) that release(s) the peptides responsible for

284 In contrast to protein S, the other TAM ligand, which was constitutivel

285 ivatable, electrophiles are matched with the protein(s) they react with in cells or cell lysate.

286 characterized for the ability to perform the protein's three known functions: participation in partic

287 overcoming this problem is to tag the target protein(s) to allow for rapid removal from the mixture f

288 t that Ctp may interact with a Hippo pathway protein(s) to exert inverse transcriptional effects on Y

289 th SatPC and specific phospholipid transport protein(s) to initiate trafficking of SatPC from the end

290 presumably making them dependent on partner proteins(s) to provide this function.

291 erfacial region, potentially adjacent to the protein's transmembrane domains.

292 Using TFPI and protein S variants, we show further that the enhancement

293 ity as well as nuclear-localization of PgMPK protein(s) was only detected in the S. graminicola resis

294 complementary functional interaction site on protein S, we screened 44 protein S point, composite or

295 t procofactor V (cleaved by aPC at R506) and protein S were necessary cofactors for the aPC-mediated

296 coagulants (ie, antithrombin, protein C, and protein S), were assessed, and data on risk factors and

297 known ligands, growth arrest-specific 6 and Protein S, were downregulated in classically activated c

298 nces that can selectively target GAG-binding protein(s), which may lead to chemical biology or drug d

299 owing engagement with their ligands Gas6 and Protein S, which recognize phosphatidylserine on apoptot

300 the association between an mRNA and binding protein(s) within a neuron was significant or accidental