ライフサイエンスコーパス: modifier

1 r pathways illuminate IDO as an inflammatory modifier.

2 an Blue nanocomposite as a working electrode modifier.

3 Hz or faster or when associated with a Plus modifier.

4 p, with concomitant use of Pd as a permanent modifier.

5 gene HMGA1, encoding a multipotent chromatin modifier.

6 both as a soluble molecule and as a protein modifier.

7 ature of 2300 degrees C and Mg as a chemical modifier.

8 lygenic mechanism involving multiple genetic modifiers.

9 ravel were included as confounders or effect modifiers.

10 ing the influence of strain-specific genetic modifiers.

11 of delivery and its potential confounders or modifiers.

12 re previous knowledge of the identity of the modifiers.

13 influence from the other hypothesized effect modifiers.

14 udy, and CO methods as covariates and effect modifiers.

15 same mutation, raising interest in potential modifiers.

16 cross studies suggests influence from effect modifiers.

17 odel of cooperative inhibition by epigenetic modifiers.

18 uch as signaling pathways or immune response modifiers.

19 arcode sequencing to identify yeast toxicity modifiers.

20 uggest the possibility of mapping mutational modifiers.

21 mmed by transcription factors and epigenetic modifiers.

22 Z domains interact with small ubiquitin-like modifier 1 (SUMO-1) and Ubc9, and function as an intramo

23 e modification of proteins by ubiquitin-fold modifier 1 (UFM1) is implicated in many human diseases.

24 NA methylation in combination with chromatin modifiers able to erase H3K9me3, H3K27me3, and H2AK119ub

25 s, via the formation of individual adsorbate:modifier adducts on the surface.

26 -ICP-MS was carried out using Ca as chemical modifier/aerosol carrier in order to avoid losses of Cl,

27 However, the mechanism by which H3K4me3 modifiers affect longevity, and whether this mechanism i

28 nd LRRFIP2, raising the possibility that the modifier affects regulation of both genes.

29 Genetic modifiers alter disease progression in both preclinical

30 te immunity both as an intracellular protein modifier and as an extracellular signaling molecule that

31 ification with arbitrary linkage between the modifier and major genes under viability selection.

32 ellers, transcription factors (TFs), histone modifiers and co-factors often bind cooperatively to act

33 analyses, the influence of important effect modifiers and confounders, such as smoking status, postm

34 t these two factors are sex-specific disease modifiers and raising the possibility that aggressive an

35 nsights on how cytosine modifications, their modifiers and readers cross-regulate themselves.

36 Mutations in epigenetic modifiers and signaling factors often co-occur in myeloi

37 atin modifications, the binding of chromatin modifiers and transcription factors and cofactors, or ch

38 illustrate the ubiquitous nature of genetic modifiers and why they are relevant biological variables

39 lytic plan for exposures, covariates, effect modifiers, and analysis, and the findings were then pool

40 micronutrients, metabolic agents, signaling modifiers, and dietary regulation, while highlighting im

41 ical research, the identification of disease modifiers, and genetic counseling.

42 uses human-readable notation and wildcards, modifiers, and logical operators to define motifs of nea

43 With respect to diseases of the eye, some modifiers are an important source of phenotypic variatio

44 These modifiers are capable of influencing interpretations of

45 as a hallmark of FL, highlighting epigenetic modifiers as an attractive therapeutic target in this di

46 capable of recruiting a number of chromatin modifiers, as a crucial mediator of sexual dimorphism in

47 9 (MAP9 (del/del)) was later identified as a modifier associated with the early onset form.

48 ovided evidence that inhibition of chromatin modifiers blocks growth-promoting signaling molecules su

49 e that the poison oligomers can act as habit modifiers both during the initial crystallization and du

50 res at all frequencies with and without Plus modifier, but LRDA and GPDs were associated with seizure

51 ic analysis looking for Huntington's disease modifiers, but is hard to define and not always availabl

52 udy of mammalian genetics, it was clear that modifiers can have a striking influence on phenotypes.

53 nd novel factors such as REST, an epigenetic modifier central to neural differentiation and plasticit

54 w how alterations in the function of histone modifiers, chromatin remodelers, and methyl-DNA binding

55 cording to their sensitivity to 11 chromatin modifier combinations, revealing the existence of synerg

56 sons were performed against a set of related modifier compounds with targeted substitutions to help i

57 of direct TCF-SRF target genes and chromatin modifiers confirmed this and showed that H3S10ph require

58 SUMO (Small Ubiquitin-like Modifier) conjugation onto target proteins has emerged a

59 m 493 participants in the LOCCS (Leukotriene Modifier Corticosteroid or Corticosteroid-Salmeterol) tr

60 targeted inhibition of stressorins or their modifiers could serve as attractive new anti-inflammator

61 f microRNAs (miRs) in controlling epigenetic modifier-dependent transcriptional regulation in CTCL is

62 prompting consideration of sex issues in LT modifier development.

63 ct contact with the mineral phase and act as modifiers during nucleation and crystal growth.

64 with interaction terms for potential effect modifiers (e.g., age, sex, and socioeconomic status), wi

65 that PIAS3 acts as the small ubiquitin-like modifier E3 ligase for FOXP2 sumoylation.

66 ately 32% of chromosomes with the beneficial modifier effect that delays HD motor onset by 0.7 years/

67 We propose that modifier effects emerge from gene interaction networks w

68 ng those in the gene encoding the epigenetic modifier enzyme TET2, promote expansion of the mutant bl

69 it has been established that ubiquitin-like modifiers evolved from prokaryotic sulphur transfer prot

70 According to the obtained data, all four modifiers exhibited significant enhancement of peptide n

71 molecular chaperones, and post-translational modifiers facilitate collagen biosynthesis.

72 er intervention was withdrawn) was an effect modifier for both adherence to antiretroviral therapy (c

73 use and reaction mechanism of aforementioned modifiers for enhancement of peptide negative ionization

74 Our findings therefore highlight protective modifiers for FPAH that could help inform development of

75 thanal as the negative-ion-mode mobile-phase modifiers for the analysis of peptides.

76 FLG mutation and PSE were not effect modifiers for the association between IgE sensitization

77 in SMA and emphasize the power of protective modifiers for understanding disease mechanism and develo

78 tagenesis screen, we identified Smarca4 as a modifier gene that exacerbates the phenotypic severity o

79 Modifier-gene models for the evolution of genetic inform

80 r genetics and assess progress in studies of modifier genes and their targets in both simple and comp

81 Mutations in chromatin modifier genes are frequently associated with neurodevel

82 Whole-exome sequencing identified candidate modifier genes for individuals with severe FD.

83 ed pivotal roles in the expansion of histone modifier genes in F. vesca.

84 Yor1-DeltaF670 biogenesis identified several modifier genes of mRNA processing and translation, which

85 the identification of three pistil essential modifier genes unlinked to the S-locus (HT-B, 120K, and

86 s often result from the action of so-called "modifier genes" that modulate the phenotypic manifestati

87 9.9%), and unique individual factors (e.g., modifier genes, unique exposures; 6.8%) (likelihood rati

88 The protein products of USH2 causative and modifier genes, USH2A, ADGRV1, WHRN and PDZD7, interact

89 e of additional causative, contributing, and modifier genes.

90 ssociation study (GWAS) predicted additional modifier genes.

91 ore frequent mutations in RHOB and chromatin modifier genes.

92 Here, we review the principles of modifier genetics and assess progress in studies of modi

93 Genomic DNA capture and sequencing of a modifier haplotype localize the functional variation to

94 l being described; most recently, epigenetic modifiers have been of high interest as silent OR genes

95 Small molecule splicing modifiers have been previously described that target the

96 lated due to LOY, KDM5D and KDM6C epigenetic modifiers have functionally-similar X-linked homologs wh

97 Today, several modifiers have now been studied in enough detail to allo

98 Here we find that depletion of the epigenome modifier histone deacetylase 3 (HDAC3) specifically in s

99 The toxicity modifiers identified in this study may deepen our unders

100 tective SMA modifier in humans, demonstrates modifier impact in three different SMA animal models, an

101 may be achieved by using various interfacial modifiers (IMs).

102 ases the amount of utrophin, a known disease modifier in Duchenne muscular dystrophy (DMD).

103 eurocalcin delta (NCALD) as a protective SMA modifier in five asymptomatic SMN1-deleted individuals c

104 Age was reported to be an effect-modifier in four randomised controlled trials comparing

105 3 (PLS3) overexpression as an SMA protective modifier in humans and showed that SMN deficit impairs e

106 entifies a previously unknown protective SMA modifier in humans, demonstrates modifier impact in thre

107 hthyl)-ethylamine, which is used as a chiral modifier in hydrogenation catalysis, occurs through the

108 59G > C variant in SMN2 exon 7 as a positive modifier in several patients.

109 deletion (Scn2a+/-) as a protective genetic modifier in the Kcna1 knockout mouse (Kcna1-/-) model of

110 the use of Molecularly Imprinted Polymers as modifiers in bulk optodes, Miptode, for the determinatio

111 Special emphasis is given to ophthalmic modifiers in mice, especially those relevant to selectio

112 he potential role of dysregulated epigenetic modifiers in normal aging hematopoiesis, which may inclu

113 nt terms, the method can learn new names and modifiers in order to generate synonyms for the descenda

114 patterns, but the role of specific chromatin modifiers in regulating the replication process is yet u

115 Possible phenotypic modifiers include the type and location of mutation and

116 Effect modifiers included sex, low job control, high demands, a

117 The proposed mechanism of action of the modifiers includes proton transfer reactions through oxo

118 rences persisted after controlling for known modifiers, including low birth weight, maternal educatio

119 There were a number of significant effect modifiers, including public insurance, panel reactive an

120 mitochondrial turnover, while covalent Keap1 modifiers, including sulforaphane (SFN) and dimethyl fum

121 How chromatin modifiers instrumental to its activity are recruited to

122 ne method by which ROM1 may act as a disease modifier is by contributing to the large variability in

123 oteins, including Sin3a and other epigenetic modifiers known to alter Runx1 transcriptional function

124 found that the SUMO (small ubiquitin-related modifier) ligase ZATT (ZNF451) is a multifunctional DNA

125 f PIAS3, an E3-SUMO (small ubiquitin-related modifier) ligase.

126 This study aimed to identify modifier loci associated with an earlier AAO of schizoph

127 Although natural crossover recombination modifier loci have been detected in plants, causal genes

128 To genetically map modifier loci in Atp6v1b1vtx/vtx mice, we analysed ABR t

129 the genetic linkage between a cue locus and modifier loci influences the evolutionary interest of mo

130 f HD onset age provided initial evidence for modifier loci on chromosomes 8 and 15 and suggestive evi

131 s, establishing that fundamentally important modifier loci remain unelucidated.

132 a seasonally selected trait and a plasticity modifier locus that modulates the effects of target-locu

133 Here, we report that the chromatin modifier LSD1, an important regulator of AR transcriptio

134 dence as CRPC-NE, suggesting that epigenetic modifiers may play a role in the induction and/or mainte

135 type can be modulated by common disease risk modifiers (metformin and pravastatin).

136 We found that the SUMO (small ubiquitin-like modifier)-modification and ubiquitin-proteasome systems

137 NEDD8 is a ubiquitin-like modifier most well-studied for its role in activating th

138 andard-of-care cytotoxic drugs or epigenetic modifiers, NE and ML cell populations converged toward t

139 l modification with the small ubiquitin-like modifier nedd8.

140 licate a protein factor as a gender-specific modifier of a mild mouse model of SMA.

141 nt an important, incremental insult and risk modifier of acute and longer-term outcome, but it does n

142 hop participants also considered gender as a modifier of biology.

143 ance of an MDM2 splice variant as a critical modifier of both p53-dependent and -independent tumorige

144 proof of concept for CD5-2 as a therapeutic modifier of cancer immunotherapy via effects on the tumo

145 2-hydroxypropyl-beta-cyclodextrin (CYCLO), a modifier of cholesterol efflux from cellular membrane an

146 udies suggest that ACTN3 R577X genotype is a modifier of clinical phenotype in DMD patients.

147 c region on Chr11p13 that is implicated as a modifier of cystic fibrosis airway disease.

148 c variability within DNM3 as an age-of-onset modifier of disease (n=232; rs2421947; haplotype p=1.07

149 here recognize an inherent role of MTA1 as a modifier of DNMT3a and IGFBP3 expression, and consequent

150 Sixteen lines, referred to as "modifier of Factor 5 Leiden (MF5L1-16)," exhibited trans

151 DNA methylation is a common epigenetic modifier of gene expression.

152 NA polymerases, thereby acting as a positive modifier of global gene expression.

153 surface serine protease matriptase, a known modifier of intestinal epithelial physiology.

154 e show that group IIA sPLA2, a known genetic modifier of mouse intestinal tumorigenesis, is expressed

155 The prolyl isomerase PIN1, a critical modifier of multiple signalling pathways, is overexpress

156 drift, and ultimate elimination of a genetic modifier of mutation rate.

157 findings indicate UDP-sugar balance is a key modifier of neurological outcomes in all three interacti

158 hese studies support ABCB6 role as a genetic modifier of porphyria and suggest that porphyrin-inducin

159 e-dependent protein kinase 1 (PDK1) as a key modifier of ribociclib sensitivity in estrogen receptor-

160 s implicate disruption in ZnT2 function as a modifier of secretory capacity and lactation performance

161 kinson disease (PD), because it is a genetic modifier of sensitivity to l-DOPA and of nicotine neurop

162 timulation was ameliorated by the allosteric modifier of Sirt1 deacetylase, SRT3025, in association w

163 In Arabidopsis, MODIFIER OF snc1-1 (MOS1) modulates a number of processe

164 n2a gene deletion acts as protective genetic modifier of SUDEP and suggest measures of brain-heart as

165 n-induced PTB to determine whether Nrf2 is a modifier of susceptibility to PTB and prematurity-relate

166 MEM106B genotype has also been found to be a modifier of the age at disease onset in frontotemporal d

167 Overweight was assessed as a potential modifier of the association between LGA and asthma.

168 SMN2 copy number is a key positive modifier of the disease, but it is not always inversely

169 we report that Lunatic fringe (Lfng), a key modifier of the Notch receptor, is selectively expressed

170 n and plasmin-mediated fibrinolysis is a key modifier of the onset of neuroinflammatory demyelination

171 We conclude that H2O2 is a biological modifier of the structure and ligand recognition functio

172 he Na(+)/H(+) exchanger NHE1 is an important modifier of the tumour nanoenvironment.

173 evaluated aldosterone as a potential effect modifier of these associations.

174 ausibilities that obesity might be an effect modifier of treatment, but supporting evidence from clin

175 and microglial cells in gliomas as a pivotal modifier of tumor neovascularization and immunosuppressi

176 BRPF1 encodes a protein modifier of two histone acetyltransferases associated wi

177 ion models, Y1 vaccine was not a significant modifier of Y2 VE (P= .43), whereas Y2 IIV-HD remained s

178 YP27B1, GC, and RXRA were analyzed as effect modifiers of 25(OH)D.

179 nome-wide association study detected genetic modifiers of age at onset in Huntington's disease.

180 disease pathogenesis and identify epigenetic modifiers of Alzheimer's disease.

181 hepatocyte nuclear factor 4A (Hnf4a), known modifiers of bile acid transporters and metabolic traits

182 entified features of UMC iPSC-ECs related to modifiers of BMPR2 signaling or to differentially expres

183 implications for drug discovery and genetic modifiers of chemotherapy-induced cardiomyopathy.

184 ted clefts, suggesting that several loci are modifiers of cleft risk in both isolated and nonisolated

185 onal studies will require stratification for modifiers of disease progression identified in this stud

186 rivers genetically interact, we searched for modifiers of epidermal growth factor receptor (EGFR) dep

187 Whereas there are fewer examples of modifiers of eye disorders in humans with a molecular id

188 , we review progress in the study of genetic modifiers of eye disorders, with examples from mice and

189 ide association analysis to discover genetic modifiers of HD onset age provided initial evidence for

190 ablishes an approach for identifying genetic modifiers of human disease.

191 effect of the metagenome and exposome as key modifiers of immune-system aging and discuss a conceptua

192 Pharmacologic agents are critical modifiers of leukocyte diversity in healing mechanisms t

193 uppressor/enhancer screen to uncover genetic modifiers of LRRK2.

194 k analyses identified ERG, IL6R, and LDLR as modifiers of MMP9, with a direct interaction between ERG

195 Thus, identifying modifiers of mutant huntingtin-mediated neurotoxicity mi

196 ssed nitrate interactions with TTHM and with modifiers of NOC formation (smoking, vitamin C).

197 nown and previously unidentified GIs between modifiers of ricin toxicity.

198 We show that epistatic modifiers of the cue polymorphism can evolve to make opt

199 We aimed to identify individual-level modifiers of the effect of multiple micronutrient supple

200 ith KCTD13, MVP, and MAPK3, major driver and modifiers of the proximal 16p11.2 600 kb BP4-BP5 syndrom

201 We sought to identify the genetic modifiers of the relation between cortical beta-amyloid

202 at the human orthologs of the yeast toxicity modifiers of these ALS genes are enriched for several bi

203 er research is needed to understand possible modifiers of these associations and develop intervention

204 results show that crocodiles were important modifiers of these bone assemblages.

205 ir household contacts and examined potential modifiers of this relationship.

206 n tumor drivers and mitochondria as critical modifiers of tumorigenicity and metastasis.

207 genitor genes suggested earlier; 'epigenetic modifiers' of the mediators, which are frequently mutate

208 stic as well as adverse effects of chromatin modifiers on removal of resistance.

209 ut by the differential clustering of neutral modifiers onto different ions and can be explained by a

210 ifiers such as SUMO (small ubiquitin-related modifier) or NEDD8 (neural precursor cell expressed, dev

211 relative to mutations in SETBP1, epigenetic modifiers, or the spliceosome has been determined only i

212 w that the TALE TF MEIS recruits the histone modifier PARP1/ARTD1 at promoters to decompact chromatin

213 Whereas the wGSCRP was not a modifier ( Pinteraction = 0.8) on the multiplicative sca

214 In contrast, the human genetic modifier plastin 3 (PLS3), an actin-binding and -bundlin

215 l modification by SUMO (small ubiquitin-like modifier) plays important but still poorly understood re

216 e by antagonizing formation of the chromatin modifier PRC2 and by epigenetically activating NOTCH sig

217 fied A-44G as an additional positive disease modifier, present in a group of patients carrying 3 SMN2

218 ics, such as pattern frequency (hertz), Plus modifier, prevalence, and stimulation-induced patterns,

219 f the Medicare Physician Value-Based Payment Modifier Program, physician practices that served more s

220 Conjugation of SUMO (Small Ubiquitin-like Modifier) protein to cellular targets is emerging as a v

221 y launched the Physician Value-Based Payment Modifier (PVBM) Program, a mandatory pay-for-performance

222 l combination, pairing the estrogen response modifier raloxifene with the c-Met/VEGFR2 kinase inhibit

223 Histone modifiers regulate proper cellular activities in respons

224 Chromatin modifiers regulate the expression of genes involved in m

225 otential clinical relevance and also disease modifiers related to coexisting medical conditions.

226 Other modifiers represent an opportunity for new therapeutic t

227 pressive complex 2 (PRC2) is a key chromatin modifier responsible for methylation of lysine 27 in his

228 Since both protective modifiers restore endocytosis, our results confirm that

229 ing to, and nitrosylation of, the epigenetic modifier ring finger protein 1A (RING1A) as assessed by

230 matic, suggesting protection through genetic modifier(s).

231 Here, we identify a chromatin modifier, Satb1, with a distinct role in this decision.

232 rmacodynamics properties of the SMN splicing modifier SMN-C1.

233 composition, flow-through microvial chemical modifier solution composition, and modifier solution flo

234 chemical modifier solution composition, and modifier solution flow rate were carefully optimized.

235 standing experiments with multiple levels of modifier species and the distributions of modifications

236 mechanisms for how alterations in epigenetic modifiers, specifically histone and DNA methylases and d

237 e part of mixed polymers with ubiquitin-like modifiers such as SUMO (small ubiquitin-related modifier

238 eparative mechanisms-translational leukocyte modifiers, such as aging, the source of leukocytes, and

239 Mutations in genes encoding epigenetic modifiers, such as DNMT3A, ASXL1, TET2, IDH1, and IDH2,

240 mportance for axon outgrowth are microtubule modifiers, such as SCG10 (Stathmin-2).

241 nding of both ubiquitin (Ub) and the Ub-like modifier SUMO.

242 h the conjugation of small ubiquitin-related modifier (SUMO) and comprises an important regulator of

243 ionally modified by the small ubiquitin-like modifier (SUMO) and functionally interacts with the PIAS

244 Small ubiquitin-like modifier (SUMO) conjugation is a reversible post-transla

245 Small ubiquitin-like modifier (SUMO) modification regulates numerous cellular

246 n cultured cells by the Small ubiquitin-like modifier (SUMO) on two independent sites: K169, within a

247 hat knockdown of the small ubiquitin-related modifier (SUMO) pathway components Ubc9 (a SUMO-conjugat

248 zing the conjugation of small ubiquitin-like modifier (SUMO) proteins (SUMO1, SUMO2, and SUMO3) to ly

249 ovalent modification by small ubiquitin-like modifier (SUMO) proteins.

250 s of the E1 for the Ubl small ubiquitin-like modifier (SUMO) revealed a single active site that is tr

251 tiviral response is the small ubiquitin-like modifier (SUMO) signaling pathway.

252 lants rapidly attach small ubiquitin-related modifier (SUMO) to a large collection of nuclear protein

253 Conjugation of the small ubiquitin-like modifier (SUMO) to protein substrates is an important di

254 , thioredoxin (Trx), small ubiquitin-related modifier (Sumo), glutathione S-transferase (GST), maltos

255 member of the Ub-like family, small Ub-like modifier (SUMO), has also been recognised as integral fo

256 ere we demonstrate that small ubiquitin-like modifier (SUMO)- and folate-dependent nuclear de novo th

257 ns could be modified by small ubiquitin-like modifiers (SUMOs) and what roles this modification may h

258 tional modifications by small ubiquitin-like modifiers (SUMOs) regulate many cellular processes, incl

259 al modification with small ubiquitin-related modifier (SUMOylation) in Sox11, which suppresses Sox11'

260 suggest the existence of additional genetic modifiers, supporting expanded, comprehensive genetic an

261 play of the 5-methylcytosine reader Mbd1 and modifier Tet1 by analyzing their dynamic subcellular loc

262 some proteins (SRSF2, U2AF1), and epigenetic modifiers (TET2, ASXL1).

263 Ubiquitin (Ub) is a protein modifier that controls processes ranging from protein de

264 TD) is a voltage-gated sodium channel (VGSC) modifier that is used as an "agonist" in functional scre

265 e results identify Hdac3 as a key epigenetic modifier that maintains blood-lymph separation and integ

266 identifies estrogens as a potential disease modifier that underlie sex-related differences in FSHD b

267 , suggesting that genetic variation provides modifiers that alleviate the disease.

268 ion provides a paradigm for other epigenetic modifiers that bind RNA without canonical RNA-binding mo

269 To uncover biochemical modifiers that exacerbate CL deficiency, we carried out

270 inum surface and their performance as chiral modifiers that impart enantioselectivity to the hydrogen

271 These differences likely reflect genetic modifiers that provide resistance or predisposition to h

272 Polycomb proteins are critical chromatin modifiers that regulate stem cell differentiation via tr

273 variability is partly attributed to genetic modifiers that regulate the disease process.

274 By varying the concentration of the neutral modifier, the separation factor of the respective cluste

275 ic variation can interact with an epigenetic modifier to produce differences in gene expression, esta

276 riptional factor conveys a general chromatin modifier to specific genes, thereby allowing the executi

277 erated metabolites are utilized by chromatin modifiers to affect epigenetic modification.

278 and its interaction with repressive histone modifiers to inhibit BA synthetic genes.

279 ature and recent research describing genetic modifiers to risk for the more common late effects of ch

280 anscription factors and recruiting chromatin modifiers to the promoters of E2F target genes.

281 inding properties, demonstrating that gating-modifier toxins can bind to Cav channels in a domain spe

282 Few gating-modifier toxins have been reported to target low-voltage

283 n, the covalent binding of the small protein modifier ubiquitin to a target protein, is an important

284 fication of cellular proteins with the small modifier, ubiquitin (Ub), regulates virtually every know

285 a motley crew of nuclear proteins, chromatin modifiers, ubiquitin ligases, and a few kinases to regul

286 E1 enzymes for ubiquitin (Ub) and Ub-like modifiers (Ubls) harbor two catalytic activities that ar

287 phatic valve development; yet the epigenetic modifiers underlying lymphatic valve morphogenesis remai

288 The percentage of modifier used was proportional to the amount of polar co

289 We further demonstrate that the chromatin modifier USP21 reduces resistance through its H2AK119 de

290 nd the association was greater when the Plus modifier was present (58%; odds ratio [OR], 2.00, P < .0

291 Increased use of ICSs and leukotriene modifiers was observed just after the regulatory activit

292 Influences of modifiers were examined for nonpolar and polar compounds

293 Prespecified effect modifiers were tested using multivariable hierarchical l

294 ytic graphite tube without use of a chemical modifier, which acts as an advantage considering this ty

295 and 'epigenetic modulators' upstream of the modifiers, which are responsive to changes in the cellul

296 ssive complexes (PRCs) are important histone modifiers, which silence gene expression; yet, there exi

297 play of transcription factors and epigenetic modifiers, which together determine cellular identity.

298 loci influences the evolutionary interest of modifiers, with tighter linkage leading to greater diver

299 as determined that neither naphthalene-based modifiers without amine groups nor those with tertiary a

300 were performed in consideration of potential modifiers (world region, national income, sample size, y