ライフサイエンスコーパス: the responsible

1 roductively focus efforts toward identifying the responsible Ag, and implementing more effective ther

2 The responsible agent, Kaposi's sarcoma-associated herpe

3 ent antibodies can be helpful in identifying the responsible agent.

4 Yet seldom have the responsible agents and their respective genes been i

5 nt neuronal network oscillations, identifies the responsible aggregation state of Abeta and proofs th

6 oman who referred to our clinic for identify the responsible antigen of anaphylaxis.

7 3 NC1 (Col4alpha3NC1) has been identified as the responsible autoantigen, it remains unknown how auto

8 amounts of sensitizing hapten suggests that the responsible B cells have increased IgM receptor gene

9 ith imaging provides possible identities for the responsible bacteria.

10 ubsequently provide evidence indicating that the responsible BFA-sensitive ADP ribosylation factor-GT

11 ear envelope ruptures during interphase, but the responsible biophysical processes remain unclear.

12 oducer of deimino-antipain was sequenced and the responsible biosynthetic gene cluster was identified

13 urce, showing that dendritic cells (DCs) are the responsible cell type for production of type I IFN,

14 However, the responsible cellular and molecular components have n

15 Probing the responsible cellular mechanisms pinpoints a disturba

16 ization, indicating that oxidative stress is the responsible cellular stimulus.

17 e-chain determinants different from those of the responsible cephalosporins and have negative pretrea

18 human insulin promoter fragment, pointing to the responsible cis element.

19 and much progress has been made in defining the responsible cis elements and transcription factors.

20 years, research has concentrated on defining the responsible cis-elements in the untranslated regions

21 The responsible clinician determined administration of s

22 The responsible clinician determined the administration

23 To schedule the blocked examinations, the responsible clinician was required to personally log

24 possible with successful treatment targeting the responsible clone.

25 blocking mAb further established factor H as the responsible cofactor.

26 the conserved lipid A portion of the LPS was the responsible component of the LPS molecule.

27 We sought to determine the responsible components of black tea and elucidate th

28 at allergic patients may lose sensitivity if the responsible compounds are avoided.

29 rrespective of the underlying mechanisms and the responsible compounds, phenolic mango peel extracts

30 r must occur between cofactor and substrate, the responsible conformational change again being that w

31 h challenges in diagnosis, identification of the responsible constituents, treatment, and prevention.

32 by Cln3 or later S- or M-phase cyclins, but the responsible cyclin interface was unknown.

33 The responsible CypD residues for this activity were map

34 w here that secretory vesicle cathepsin L is the responsible cysteine protease of chromaffin granules

35 s inhibited by ketoconazole, implying 3A4 as the responsible cytochrome P450 isoform.

36 for presentation to developing T cells, but the responsible DC subsets remained poorly defined.

37 omic nervous system balance in HRV patterns, the responsible deeper physiological, clinically relevan

38 y CNVs, and copy number gains in particular, the responsible dosage-sensitive gene(s) have been hard

39 s several neurobehavioral abnormalities, but the responsible dosage-sensitive gene(s) remain undefine

40 s a major role in glioblastoma pathogenesis, the responsible downstream mechanisms remain less clear.

41 related behaviors in humans and rodents, but the responsible downstream receptors remain poorly under

42 , is critical to limbic epileptogenesis, but the responsible downstream signaling pathways are unknow

43 ghly effective when the specific allergen is the responsible driver for the symptoms.

44 cutaneous eruption is suspected, identifying the responsible drug(s) is a complex clinical challenge.

45 alosporins and positive skin test results to the responsible drugs underwent serum specific IgE assay

46 hway by their higher affinity for binding to the responsible E3 ligase compared with proteins bearing

47 itizes IRS1 to degradation, and a screen for the responsible E3 ligase identified Fbxo40 as mediating

48 e for ubiquitin in this degradation pathway, the responsible E3 ligase is unknown.

49 l in elucidating the mammalian ERAD pathway, the responsible E3 ligase or ligases remain unknown.

50 Dictyostelium, and further identification of the responsible E3-ligase may provide a novel therapeuti

51 In addition, the responsible elastic elements must be able to stretch

52 and the E-boxes in the promoter region were the responsible element.

53 that the nonfibrillized P-tau is most likely the responsible entity for the disruption of microtubule

54 tein was cleaved within the CD4 sequence and the responsible enzymatic activity was inhibited by Comp

55 cells implicate the Src family kinase Lck as the responsible enzyme and its activity in this process

56 up-regulated by enhanced gene expression of the responsible enzyme N-acetylglucosaminyltransferase I

57 served in zygotes and primordial germ cells, the responsible enzyme(s) have been elusive.

58 The responsible enzyme, which was recovered in the solub

59 igopeptidase B (OPB; Clan SC, family S9A) as the responsible enzyme.

60 ed for absorption, implying that CEL was not the responsible enzyme.

61 s to folate monoglutamates by the cloning of the responsible enzyme; ii) identification of the cDNA r

62 ases involved in histone ubiquitination, yet the responsible enzymes and the function of histone ubiq

63 H2B ubiquitination and histone methylation, the responsible enzymes and the functions of H2A ubiquit

64 Although the responsible enzymes are thought to be fairly well ch

65 erichia coli strains carrying genes encoding the responsible enzymes, phthalate 3,4-dioxygenase and 3

66 e assembly of ubiquitin chains is managed by the responsible enzymes.

67 7 cells, indicating that catecholamines were the responsible exercise factors.

68 produced ROS in the regenerating liver were the responsible factor for TSP-1 induction.

69 t for promoter activity in T cells; however, the responsible factor was unknown.

70 To identify the responsible factor, we tested several candidate tyro

71 The responsible factors are not fully understood, but TG

72 We put a hypothesis that one of the responsible factors is the presence of gastrointesti

73 wn stream of the muscarinic receptors may be the responsible factors.

74 that hsps rather than endotoxin or DNA were the responsible factors.

75 e identified the PE_PGRS47 protein as one of the responsible factors.

76 high collinearity between variables might be the responsible for high uncertainty values in the predi

77 account for up to 25% of the ESRD budget and the responsible for up to 25% of all hospital stays.

78 The responsible gene acts as a tumor suppressor, and tum

79 his RMD locus set the stage for isolation of the responsible gene and elucidation of a novel patho-me

80 en less robust in identifying and validating the responsible gene and/or genetic variants.

81 We provide evidence that the responsible gene at LGS1 codes for an enzyme annotat

82 We hypothesize that the responsible gene causes cortical hyperexcitability t

83 A study was undertaken to identify the responsible gene defect underlying late onset spinal

84 th such deficits is largely unknown, many of the responsible gene defects have been identified.

85 Identification of the responsible gene for SCA26 ataxia will provide furth

86 ation sequencing method, we excluded CASK as the responsible gene for the remaining family.

87 Myosin VIIa has been identified as the responsible gene for USH type 1B, and a number of mi

88 Lgn1, has been mapped to chromosome 13, but the responsible gene has not been identified.

89 Ltxs1, has been mapped to chromosome 11, but the responsible gene has not been identified.

90 requent cause of ADPHSP in UK families, that the responsible gene has not yet been mapped in a signif

91 n of risk and genetic mapping has identified the responsible gene in a few mendelian cases.

92 inked to three loci: 2p21 (GLC3A), for which the responsible gene is CYP1B1, and 1p36 (GLC3B) and 14q

93 lE7 was not identified, implying either that the responsible gene is essential for cell viability, or

94 next-generation sequencing (NGS) to identify the responsible gene mutation in the family.

95 ociated with trisomy 21 (Down syndrome), but the responsible gene or genes on chromosome 21 have not

96 henotypes followed by genotyping to discover the responsible gene or mutation.

97 -dependent retinal diseases, suggesting that the responsible gene regulates retinal aging, and its im

98 ge to our family and the new localization of the responsible gene to chromosome 2cen, together with t

99 The identification of the responsible gene will provide new insights into the

100 The responsible gene(s) therefore resides in an interval

101 netic and physical mapping efforts localized the responsible gene(s) to a well-defined region on huma

102 The responsible gene, encoding methyl-CpG binding protei

103 mutants defective in IT formation and cloned the responsible gene, ERN1, encoding an AP2/ERF transcri

104 We cloned the responsible gene, trafficking protein, kinesin bindi

105 ne locus for SSNS, as a first step to detect the responsible gene, was thus identified.

106 The responsible gene, WASP, has multiple domains, each w

107 To identify the responsible gene, we sequenced the exomes of five in

108 smooth muscle myosin heavy chain (myh11) as the responsible gene.

109 s a starting point for the identification of the responsible gene.

110 genetic form of polymicrogyria and localize the responsible gene.

111 identify the transcription factor, Usf1, as the responsible gene.

112 cholesterolemia were ruled out by sequencing the responsible genes (LDLRAP, LDLR, PCSK9, APOE and APO

113 ns can arise through several mechanisms, but the responsible genes and pathways are poorly understood

114 y now are researchers beginning to tease out the responsible genes and the underlying molecular mecha

115 astid function, yet in only a few cases have the responsible genes been cloned.

116 dence is well established; identification of the responsible genes has proved challenging.

117 s it is absent from humans and disruption of the responsible genes has shown a lethal phenotype for E

118 ured from primary cilia of kidney cells, but the responsible genes have not been identified.

119 The identification of the responsible genes is providing scientists a window i

120 The identification of the responsible genes may lead to insights into the path

121 n persons with schizophrenia and then mapped the responsible genes onto transcriptome profiles of nor

122 uman disease loci may help identification of the responsible genes, and is thus a topic of considerab

123 To identify the responsible genes, we mapped virulence in F(1) proge

124 two genetic loci, within which we identified the responsible genes: one locus contains a known xylose

125 None of the 'responsible' genes have previously been identified.

126 compare closely related strains to identify the responsible genetic determinants.

127 Identification of the responsible genetic factors will greatly enhance the

128 Identification of the responsible genetic locus in those mutants significa

129 ees of humans with congenital TTP and mapped the responsible genetic locus to chromosome 9q34.

130 al component in linking phenotypic traits to the responsible genetic variation in the genomes of plan

131 Nearly all of the responsible gram-negative bacilli possess capsular p

132 However, the responsible growth factor(s) has not yet been identi

133 oliferation in crypt stem cell compartments, the responsible growth factors regulating this continuou

134 ent specificities limited our exploration of the responsible HDAC member to HDAC1, HDAC2, or HDAC3.

135 e E3 ligase that mediates the proteolysis of the responsible HDACs (see the related article beginning

136 fter Caesarean section and, if so, to define the responsible hemodynamics.

137 However, the responsible histone acetyltransferase enzymes are ye

138 Many chemicals were identified by GC-MS, but the responsible individual compounds could not be exactl

139 induction of transplantation tolerance, but the responsible inflammatory mediators have not been ide

140 ecular levels permits mechanistic studies of the responsible interactions relevant to the inherited h

141 The responsible interplanetary meteoroids were initially

142 e timely adoption of innovative methods, and the responsible interpretation of research findings.

143 However, the responsible intracellular signaling pathways trigger

144 These will support the responsible introduction of surgical innovations.

145 ubiquity of this common excitable property, the responsible ion channels have not been identified.

146 specific function, our algorithm identifies the 'responsible' isoform(s) of a gene and generates cla

147 functionalities and experimentally validated the 'responsible' isoforms using data from mammary tissu

148 The responsible justice department and ethics committee

149 However, the responsible kinase has remained elusive.

150 tion, but the nature of the phosphorylation, the responsible kinase in vivo, and its physiological si

151 own to be a phosphoprotein in vivo; however, the responsible kinase(s) have not been determined.

152 y targets S451 and we have identified Akt as the responsible kinase.

153 ic treatment modalities, which may eliminate the responsible malignant clone.

154 tering a "bottom-up" stewardship approach to the responsible management of risks from engineered nano

155 ignaling, imposed by nuclear plakoglobin, is the responsible mechanism for the pathogenesis of ARVC.

156 ist around the acetylene bridging unit to be the responsible mechanism generating a partial to an alm

157 nstrated in patients with schizophrenia, but the responsible mechanism has not been identified.

158 The responsible mechanism involves an increased nuclear

159 The responsible mechanism is the breakdown of the aforem

160 menon is due to an expansion of T cells, but the responsible mechanism is unknown.

161 bone loss induced by ovariectomy (ovx), but the responsible mechanism is unknown.

162 one loss induced by estrogen deficiency, but the responsible mechanism is unknown.

163 n cellular stress and apoptosis, were likely the responsible mechanism of action.

164 nephropathy and retinopathy in diabetes, but the responsible mechanism remains unclear.

165 ine is a potent elicitor of GLP-1 secretion, the responsible mechanism remains unclear.

166 Analysis of the responsible mechanism using neutrophils from beta2 n

167 Cellular origin of excess adipocytes, the responsible mechanism(s) and the basis for predomina

168 To delineate the responsible mechanism, we generated transgenic mice

169 inkage between polar and tropical regimes as the responsible mechanism: the interplay of northward mi

170 ture of the pathology of chronic asthma, but the responsible mechanisms and main sources of angiogeni

171 ptual framework to help the understanding of the responsible mechanisms and, when available, an updat

172 The responsible mechanisms are multifarious, but effects

173 d as a risk factor for beta-amyloidosis, but the responsible mechanisms are not clear.

174 The responsible mechanisms are not completely understood

175 ardial infarction and thrombotic events, but the responsible mechanisms are not fully understood.

176 stimulation protects cells from anoikis, but the responsible mechanisms are not well known.

177 However, the responsible mechanisms are not well understood.

178 the ischemic myocardium from infarction, but the responsible mechanisms are unclear.

179 atic nucleus (SCN) have been implicated, but the responsible mechanisms have not been clearly delinea

180 Although the responsible mechanisms have not been well defined, n

181 The responsible mechanisms involve cis-trans interaction

182 Clues to the responsible mechanisms may lie with the discovery of

183 plication results in chronic-phase AIDS, but the responsible mechanisms remain controversial.

184 However, the responsible mechanisms remain elusive.

185 gression of cardiovascular disease, although the responsible mechanisms remain unclear.

186 r CD4-mediated rejection responses, however, the responsible mechanisms remain unclear.

187 tation are well studied in maize (Zea mays), the responsible mechanisms remain unclear.

188 EAK1 is known to promote cell migration, but the responsible mechanisms remain unclear.

189 e processing and oncogenic ability, although the responsible mechanisms remain unknown.

190 ression is increased in tissue ischemia, but the responsible mechanisms remain unknown.

191 However, the responsible mechanisms remain unresolved.

192 The responsible mechanisms, however, are not well unders

193 The responsible mechanisms, however, remain unclear and

194 To investigate the responsible mechanisms, we studied the regulatory ef

195 d aging in cancer survivors and to determine the responsible mechanisms.

196 and turnover rates are useful in elucidating the responsible mechanisms.

197 ratum corneum integrity/cohesion, as well as the responsible mechanisms.

198 icity and mechanical durability, and reveals the responsible mechanisms.

199 The responsible metabolic lesion appears to involve a po

200 ereby implicating hexosamine biosynthesis as the responsible metabolic pathway.

201 To identify the responsible methyltransferase(s) and to gain insight

202 dification has been hindered by ignorance of the responsible methyltransferase.

203 ver, for the majority of these methylations, the responsible methyltransferases (MTases) remain unkno

204 ver been shown in a longitudinal design, and the responsible milk components are still unknown.

205 The responsible miRNAs function by suppressing multiple

206 However, the responsible mitochondrial lysine-specific methyltran

207 de useful platforms from which to search for the responsible modulators.

208 n the last two decades has aimed to decipher the responsible molecular and cellular mechanisms for re

209 early events in muscle differentiation, but the responsible molecular mechanisms are unknown.

210 lain this fundamental biological phenomenon, the responsible molecular mechanisms have not been deter

211 in response to mechanical loading; however, the responsible molecular mechanisms remain largely unkn

212 To begin dissecting the responsible molecular mechanisms, we set out to iden

213 e of maintaining HSCs ex vivo long-term, but the responsible molecular players remain unknown.

214 netic mosaics, present evidence that Slit is the responsible molecule.

215 This provides the basis for identifying the responsible molecules and developing strategies to a

216 tion and endocrine inhibition, implying that the responsible molecules are not unique to pancreatic m

217 in the fourth to fifth postnatal weeks, but the responsible molecules are unknown.

218 vities have been recorded in many cells, but the responsible molecules have not been identified.

219 Identification of the responsible mutant genes and of the functional conse

220 Map-based identification of the responsible mutation identified a G-->A transition,

221 roduce the same cellular phenotype, although the responsible mutations are located in different funct

222 s were formed of neuroserpin aggregates, and the responsible mutations in neuroserpin were identified

223 f identifying families with XLID and finding the responsible mutations, as well as the determined and

224 nced their host attachment genes to identify the responsible mutations.

225 The responsible neuronal circuitries show lifetime plast

226 learning because it is difficult to identify the responsible neurons when a mistake is made.

227 The responsible non-ribosomal peptide-polyketide hybrid

228 n or loss of sensation and to CPSP, although the responsible nuclei have not been identified.

229 y, we identify the Yersinia urease enzyme as the responsible oral toxin.

230 found in mammalian cells, including kidney, the responsible organ for osmolyte regulation, posing th

231 the conclusion that heat-processing was not the responsible parameter for that distortion, but the s

232 and laboratorians to continue the search for the responsible pathogen.

233 However the responsible pathogenic mechanisms are still far to b

234 or to this threat, but little is known about the responsible pathogens.

235 ted the role of ceramide versus caspase, and the responsible pathway for ceramide generation in ultra

236 o define the final steps in this pathway and the responsible peptidases, we fractionated by size the

237 We hypothesized that the responsible permeability barrier to CO(2) resides in

238 to the intervention group (n=1238), in which the responsible physician was alerted by another hospita

239 patients to an intervention group, in which the responsible physician was alerted to a patient's ris

240 se guidelines, the committee recognizes that the responsible physician's judgment remains paramount.

241 epression and a decrease in return visits to the responsible physician.

242 to structured and open-ended interviews with the responsible physicians, nurses, social workers, and

243 integrin alpha(IIb)beta(3) in platelets, but the responsible PKC isoforms and mechanisms are unknown.

244 The responsible point mutation affects expression of the

245 For each quantitative trait locus, the responsible polymorphism is rare among a diverse set

246 ciated with 2 main haplotypes in VKORC1, but the responsible polymorphisms remain unknown.

247 hich pigments have been discolored, what are the responsible processes, and which (environmental) con

248 quencing of the encoding gene indicates that the responsible processing enzyme is a member of the pro

249 cells to activation induced cell death, and the responsible products had the features of ganglioside

250 s in brain inflammation and injury, although the responsible prostaglandin receptors have not been fu

251 However, the identity of the responsible protease and its role in the pathophysio

252 hought, raising questions on the identity of the responsible protease(s).

253 The responsible protease, tumor necrosis factor-alpha co

254 by incubation with synovial fluid, although the responsible proteases could not be identified.

255 This study was undertaken to identify the responsible proteases.

256 loci more frequently than to loci for which the responsible protein coding gene is known, thus sugge

257 r cellular phenotype and the inactivation of the responsible protein due to the off-target effect of

258 The simulations identify the responsible protein residues, the arginine finger al

259 The responsible protein was identified as a P450 monooxy

260 data regarding the structure and function of the responsible protein, ATP7B, and the importance of it

261 The responsible proteins for the transport of 5-azacytid

262 However, the responsible quality control (QC) mechanisms remain p

263 report the in vitro reconstitution of TbtI, the responsible radical S-adenosyl-methionine (rSAM) C-m

264 the cause and determine, in cooperation with the responsible radiologist, whether these doses are jus

265 The responsible receptors and signaling pathways are inc

266 The responsible regions of Dmp1 gene were located in the

267 In order to define the responsible regulatory elements within the Ig lambda

268 nthesis of their membrane phospholipids, but the responsible regulatory mechanisms are incompletely u

269 To delineate the responsible regulatory motifs, luciferase reporter c

270 The responsible residue is usually identified by site-sp

271 To find the responsible residue, all cysteines, Cys(7), Cys(379)

272 volatile hexanoic acid and characterize how the responsible sensory receptor (the variant ionotropic

273 from cell membranes and, if so, to identify the responsible sheddase and determine whether activatio

274 lpha, providing a strong incentive to define the responsible sheddases.

275 chimeras, hSkM1P1 and hH1P1, indicated that the responsible sialic acids are localized to the hSkM1

276 sive research, many parts and subroutines of the responsible signal transduction networks have been i

277 ectrolyte efflux to restore cell volume, but the responsible signaling pathways are incompletely defi

278 was shown to induce leukocyte migration but the responsible signaling receptors were not characteriz

279 However, the responsible soy component or components and the magn

280 sterol in hypercholesterolemic subjects, but the responsible soy components and the effects in normoc

281 We identified the responsible species and the produced toxins as well

282 More data are needed to inform next steps in the responsible stewardship of this process, from the pe

283 The identification of the responsible substitutions and elucidation of the und

284 sease; however, the differentiation state of the responsible T cells is unclear.

285 but the underlying mechanisms of action and the responsible target genes are largely unknown.

286 However, the responsible trans-factors and the mechanism by which

287 and identified nuclear factor Y (NFY) to be the responsible transcription factor as assessed by over

288 indicated that an ATF4/c-Jun heterodimer was the responsible transcription factor.

289 ial gene expression, because the identity of the responsible transcription factors (TFs) often cannot

290 diagnosis and treatment require excision of the responsible tumor.

291 istry testing, and difficulty in identifying the responsible tumor.

292 nstrate that elevated NEDD4 is implicated as the responsible ubiquitin E3 ligase for HSF1 degradation

293 high prevalence of cognitive impairment but the responsible underlying pathological mechanisms are u

294 the reproductive setting is needed to inform the responsible use of these technologies to decrease th

295 well-informed public discussions to explore the responsible use of this currently theoretical techno

296 an only be removed effectively by correcting the responsible valvular lesion.

297 Both the responsible variant and the molecular mechanism caus

298 action of the familial risk, perhaps because the responsible variation arises by somatic mutation (SM

299 Identification of gG as the responsible vCKBP was achieved by repeating similar

300 5), and possibly both, due to an increase in the responsible Wee1 and Myt1 kinases.