ライフサイエンスコーパス: LMW

1 LMW cyclin E has prognostic and predictive roles in HER2

2 LMW fraction was further purified (LWM-FP) to remove sug

3 LMW HA was a potent stimulant of AA release in a time- a

4 LMW peptides (<1kDa) were obtained by the ultrafiltratio

5 LMW thiols also preserve the transcription of Salmonella

6 LMW-E induces additional mitotic defects in cooperation

7 LMW-E upregulated ACLY enzymatic activity, subsequently

8 LMW-GS from variety C 306 brought a decrease in the doug

9 Twenty-six phenolics (13 LMW-PPs and 13 anthocyanins) were characterized and quan

10 blocked by the rfbA rffH mutations, lacks a LMW-dT pool, the initial DNA synthesis during T-starvati

11 ormation of surrounding proteins, and when a LMW ligand binds to the proteins, it can enhance protein

12 ubcellular localization may lead to aberrant LMW-E protein interactions, regulation, and activity, ul

13 ni, which was dependent on Ad-cyclin E or Ad-LMW-E expression.

14 In addition, LMW-E-overexpressing cells showed a reduction in the mit

15 if altered subcellular localization affected LMW-E degradation.

16 (-/-) mice, but not in Cd44(-/-) mice, after LMW HA stimulation.

17 implication of our findings is that altered LMW-E and LMW-E/Cdk2 subcellular localization may lead t

18 tion challenge response to HMW (n = 544) and LMW (n = 635) agents.

19 bulin 3A and 3C, chitinase, beta-amylase and LMW glutenins, were identified from the electrophoretic

20 ions found between phytoplankton biomass and LMW-DON than other N forms.

21 on of our findings is that altered LMW-E and LMW-E/Cdk2 subcellular localization may lead to aberrant

22 Here, we show that EL and LMW-E overexpression impairs the G(2)-M transition diffe

23 , we show that full-length cyclin E (EL) and LMW-E overexpression impairs the G(2)-M transition diffe

24 ties, followed by crude extract, LWM-FP, and LMW, respectively.

25 ugh by the inclusion of gluten, glutenin and LMW-GS, which lacks resemblance among different samples,

26 Decreased HER2 and LMW cyclin E expression had functional consequences, inc

27 Exposure to HMW and LMW agents by SIC induced a differential nasal airway re

28 s to determine whether OA induced by HMW and LMW agents shows distinct phenotypic profiles.

29 phenotypic profiles in OA caused by HMW and LMW agents.

30 ega-types whereas glutenins contain HMW- and LMW-types.

31 de detailed insights into how collagen I and LMW-heparin impact different stages in the aggregation o

32 ho were exposed to HMW (n = 10, Group I) and LMW (n = 10, Group II) at their workplaces were collecte

33 VSMC in a NADPH oxidase-dependent manner and LMW-HA stimulated ROS generation and cell proliferation

34 entially metal-sensitive HMW (Ag and Ni) and LMW (Tl) pools, whereas the MMW pool, which includes met

35 igher order products observed (PHA, PHQ, and LMW oxo- and dicarboxylic acids).

36 th temperature and time from FL<FG<RL<RG and LMW<WM<HMW for all pHs.

37 +) of D. radiodurans exists predominantly as LMW complexes with nitrogenous metabolites and orthophos

38 assay for screening the interactions between LMW ligands and transcription factors (TFs) and human se

39 dings establish a novel relationship between LMW-E isoforms of cyclin E and aberrant lipid metabolism

40 A2, PATJ, or Dbs (RhoGEF) expression blocked LMW-HA-mediated angiogenesis (EC proliferation, migratio

41 EphA2, PATJ, Src, or Dbs expression blocked LMW-HA-mediated RhoA activation.

42 We found that in predenitrification BNR, LMW-DON is released during the post-aerobic step followi

43 city to mount procatabolic responses to both LMW-HA and HMGB-1, demonstrated by >95% suppression of N

44 ssion, and PGE2 production were activated by LMW HA through a TLR4/MYD88 pathway.

45 basis of inherited diseases characterized by LMW proteinuria.

46 the persistent cognitive deficit induced by LMW oligomers.

47 ollectively, the mitotic defects mediated by LMW-E induction led to failed cytokinesis and polyploidy

48 cessary for NADP(+) binding in the canonical LMW TrxRs, but also contains a 11-residue sequence which

49 less, irradiation of E. coli majorly changes LMW Mn(2+) speciation, with extensive binding of nitroge

50 atform is useful not only for characterizing LMW DOM, but also for quantifying relative variations in

51 In contrast, LMW thiols diminish the nitrosative stress experienced b

52 g potent and selective inhibitors to control LMW-PTP activity.

53 We found that cytoplasmic LMW-E/Cdk2 was less susceptible to Fbw7-mediated degrada

54 ized that aberrant localization of cytosolic LMW-E isoforms alters target binding and activation ulti

55 fferent Cdk inhibitors significantly delayed LMW-cyclin E-induced mammary tumor progression.

56 CO2 production rates from permafrost-derived LMW DOC mineralization.

57 s, resulting in the accumulation of distinct LMW peptides that promote protein aggregation in lenses

58 Even with low dosing, LMW-DS showed similar efficacy in preventing IBMIR to pr

59 f low molecular weight isoforms of cyclin E (LMW-E) overexpression on mitotic progression and its lin

60 age products, low-molecular weight cyclin E (LMW-E), is associated with poor clinical outcome in pati

61 es show that HER2-mediated signaling effects LMW cyclin E expression, which in turn deregulates the c

62 traportal and systemic treatment with either LMW-DS or heparin, targeting an activated partial thromb

63 Exogenous LMW HA fragments (average M(r) 200,000) failed to induce

64 e generated transgenic mice, which expressed LMW-cyclin E in a Cdk2-deficient background.

65 c agent) synergized to kill cells expressing LMW-E, but not full-length cyclin E.

66 We also report that breast tumors expressing LMW-E have a higher proportion of CD44(hi)/CD24(lo) tumo

67 release from chondrocytes and extracellular LMW-HA generation in normal chondrocytes.

68 ssembly into fibrils, and both extracellular LMW Tau aggregates and short fibrils, but not monomers,

69 deficient in low-molecular weight FGF2 (FGF2(LMW)) regress dependent on T cells.

70 Bone marrow derived-macrophages from Fgf2(LMW-/-) mice co-injected with cancer cells reduce tumour

71 -based protein complementation assay to find LMW-E binding proteins in breast cancer, identifying ATP

72 orrelates to GCMS data with R(2) = 0.988 for LMW and 0.998 for HMW PAHs.

73 exhibit greater than 50-fold preference for LMW-PTP over a large panel of PTPs.

74 ACLY was also required for LMW-E-mediated transformation, migration, and invasion o

75 A negative sIgE result for LMW agents does not exclude sensitization.

76 for HMW fraction, +/- 0.54 per thousand for LMW fraction, and +/-1.3 per thousand for R fraction.

77 Fourth, LMW-E-overexpressing cells fail to arrest in the presenc

78 tings where it predominates over fragmentary LMW-HA, namely, in uninflamed tissue.

79 in E readily differentiated full-length from LMW-E, respectively.

80 ctivity, correlated with shift of PDE3A from LMW to HMW peaks, and increased co-immunoprecipitation o

81 ased (p<0.05) with temperature and time from LMW>WM>HMW.

82 Furthermore, LMW-AR expression is regulated by the activation of calp

83 HMGB-1 and hyaluronidase 2 (which generates LMW-HA) to induce chondrocyte hypertrophy, which is impl

84 fic antibodies for gliadins, gamma-gliadins, LMW subunits and antigenic epitopes to gain a better und

85 and accumulation of low molecular weight HA (LMW-HA) in tumor tissue was associated with elevated pro

86 se, which generates low molecular weight HA (LMW-HA), is induced in VSMC in a NADPH oxidase-dependent

87 In order to explore how LMW-E enriches cancer stem cells in breast tumors, we co

88 yaluronidase (Hyal) and low m.w. hyaluronan (LMW HA) fragments have been widely reported to stimulate

89 Low m.w. hyaluronan (LMW HA) has been shown to elicit the expression of proin

90 R-4 ligands low molecular weight hyaluronan (LMW-HA) and high mobility group box chromosomal protein

91 trated that low molecular weight hyaluronan (LMW-HA, approximately 2500 Da) promotes endothelial cell

92 findings establish a requirement for Cdk2 in LMW-cyclin E-mediated mammary tumorigenesis, arguing tha

93 pecifically test the requirement for Cdk2 in LMW-cyclin E-mediated mammary tumorigenesis, we generate

94 nd that Cdk2 silencing induced cell death in LMW-overexpressing breast cancer cell lines, but not in

95 icroRNAs in primary T cells were enriched in LMW-RISC.

96 While memory impairment in LMW oligomer-injected mice was associated with decreased

97 , each log unit (roughly 3-fold) increase in LMW metabolites was associated with 21% and 22% increase

98 -APH in vitro resulted in a >20% increase in LMW peptides.

99 Notably, in LMW-PTPs, the phosphorylation status of two well conserv

100 phloroglucinol polymerisation are present in LMW fractions of the three brown macroalgal species.

101 oduction plays a negative regulatory role in LMW HA (200 kDa) induced lung inflammation.

102 evel explanation for the function of TLR4 in LMW HA (200 kDa)-induced lung inflammation, as inhibitio

103 also for quantifying relative variations in LMW DOM availability across space, revealing hotspots of

104 tive and relative-quantitative variations in LMW DOM with depth using water extracts from a soil core

105 Taken together, these results indicate LMW-HA-mediated transactivation of EphA2 is required for

106 Lastly, downregulation of Cdc25C inhibits LMW-E-mediated chromosome missegregation, anaphase bridg

107 associated with modestly increased internal LMW phthalate and paraben exposure in 4-9 year old child

108 ession of the low molecular weight isoforms (LMW-E) of cyclin E induces chromosome instability; howev

109 ; MMW: medium molecular weight, 40-<1.3 kDa; LMW: low molecular weight, <1.3 kDa).

110 er cell lines, but not in cell lines lacking LMW expression.

111 Lastly, LMW-E expression in human breast cancer tissues correlat

112 C for 30, 60, 120min, and dialysed into low (LMW) and high molecular weight (HMW) fractions.

113 inguish between and metabolize the two major LMW-SNO signaling molecules GSNO and SNO-CoA, allowing f

114 act mainly through IgE-mediated mechanisms, LMW agents appear to act through both immunological and

115 y and the multiligand receptors that mediate LMW protein uptake in PT cells, how these are regulated

116 , implying condensation of low MW molecules (LMW) to form high MW (HMW) molecules.

117 NMR structure of the free form of the MptpA LMW-PTP.

118 ese findings indicate that AKR1A1 is a multi-LMW-SNO reductase that can distinguish between and metab

119 d to aggregate and subsequently form low MW (LMW) oligomers, high MW (HMW) aggregates such as protofi

120 of low-molecular-weight dissolved organic N (LMW-DON), which is highly bioavailable and stimulates ph

121 of other low-molecular weight nitrosothiols (LMW-RSNOs) in biological samples.

122 n order to gain more information on nonlipid LMW metabolites.

123 On the other hand, HMW oligomers, but not LMW oligomers, induced oxidative stress in hippocampal n

124 mutant (6G11) that degrades HMW PAHs but not LMW PAHs.

125 the de novo lipogenesis pathway, as a novel LMW-E-interacting protein in the cytoplasm.

126 ands after synthesis, producing the observed LMW intermediates.

127 l specimens of breast cancer, the absence of LMW-E and low expression of adipophilin (PLIN2), a marke

128 cells as key players in the accumulation of LMW-HA in the tumor microenvironment and cancer-related

129 report that intratracheal administration of LMW HA (200 kDa) causes inflammation in mouse lung.

130 rification systems produced larger amount of LMW-DON than CAS.

131 We report the discovery of a novel class of LMW-PTP inhibitors derived from sulfophenyl acetic amide

132 The maximum concentrations of LMW-PPs corresponded to the flavanols (+)-catechin and (

133 r future studies with more optimal dosing of LMW-DS for the prevention of IBMIR in islet transplantat

134 of this study was to determine the effect of LMW HA on cPLA2alpha activation, arachidonic acid (AA) r

135 ggest that targeting downstream effectors of LMW-HA could be a useful therapeutic intervention for an

136 ites, respectively, inhibited the effects of LMW-FGF-2 and HMW-FGF-23 to stimulate FGF-23 promoter ac

137 On the contrary, the effects of LMW-GS extracted from variety PBW 550 were more strong a

138 lability of mercury through the exudation of LMW thiols, and thus they may play a key role in the pro

139 ggesting that neither PH20 nor generation of LMW HA fragments in situ stimulates cytokine and chemoki

140 and demonstrate the potential importance of LMW DOC in driving the rapid metabolism of Pleistocene-a

141 l lysates, representing a 9-fold increase of LMW proteins due to prefractionation.

142 44 or EphA2 siRNA and observed inhibition of LMW-HA-induced angiogenesis in implanted Matrigel plugs.

143 ation of PDGF receptor with no inhibition of LMW-PTP.

144 ite of phosphate, a competitive inhibitor of LMW-PTPs, on MptpA and elucidated the involvement of bot

145 single intracerebroventricular injection of LMW AbetaOs (10 pmol) induced rapid and persistent cogni

146 Levels of LMW thiols of presumed algal origins were highly correla

147 ERK phosphorylation and increased levels of LMW-AR.

148 hese results suggest that the high levels of LMW-E isoforms found in breast cancer may contribute to

149 suggest that the heightened oncogenecity of LMW-E relates to its ability to promote CSC properties,

150 crease in the dough strength in the order of LMW-GS < gluten < glutenin.

151 uch as that of SodA, with a minority pool of LMW Mn(2+) complexes that show negligible coordination b

152 time of fibril formation in the presence of LMW-heparin and slowing the rate at higher concentration

153 in sediments enables the rapid processing of LMW DOC, particularly during high C enrichment events an

154 ystem with the pleiotropic responsibility of LMW PAH-centric hydroxylation, and its epistatic functio

155 Sequences of LMW-peptides either from doughs and breads were determin

156 there is otherwise no sequence similarity of LMW-PTPs to other classes of PTPs, the phosphate binding

157 there have been no ligand-free structures of LMW-PTPs described, and hence the dynamics of the D-loop

158 d ROS because it lacks an adequate supply of LMW Mn antioxidants.

159 nd MMW (42%) were more abundant than that of LMW (24%) in a diabetic patient with macroalbuminuria.

160 42) were significantly greater than those of LMW-Abeta(1-42).

161 d significantly higher urinary levels of one LMW phthalate and two parabens, respectively, when compa

162 f cyclin E (low molecular weight cyclin E or LMW-E) in complex with CDK2 are preferentially mislocali

163 found that in strains lacking PBP5 and other LMW PBPs, higher FtsZ concentrations increased the frequ

164 trations with R(2) = 0.976 and overestimates LMW PAHs.

165 Transgenic mice overexpressing LMW-cyclin E have increased incidence of mammary tumors

166 uing that human breast tumors overexpressing LMW-cyclin E are prime candidates for anti-Cdk2 therapy.

167 lecular weight protein tyrosine phosphatase (LMW-PTP) is a regulator of a number of signaling pathway

168 lecular weight protein tyrosine phosphatase (LMW-PTP).

169 n the redox-sensitive tyrosine phosphatases, LMW-PTP and SHP-2, which in turn results in increased ph

170 Low molecular weight polyphenols (LMW-PPs) and anthocyanins, along with the antioxidant ca

171 conjugate made with the LMW polysaccharide (LMW-TT).

172 1, and PLK1 in a G(2)-M-enriched population, LMW-E overexpression causes premature inactivation of Cd

173 ge but introduce larger quantities of potent LMW-DON into coastal systems.

174 nd its low-molecular-weight partner protein (LMW SLP).

175 olecular weight penicillin-binding proteins (LMW PBP) have been difficult to discern in Gram-negative

176 olecular-weight penicillin-binding proteins (LMW PBPs) exhibit morphological alterations that also ap

177 ulosis, secretes a low molecular weight PTP (LMW-PTP), MptpA, which is required for its survival upon

178 -mediated decrease of ERK expression reduces LMW-AR levels in R1 cells.

179 low molecular weight thioredoxin reductases (LMW TrxRs), is an NADP(+)-independent dithiol oxidase.

180 due to the rffC defect, maintains a regular LMW-dT pool, but cannot recover dTTP from it, and thus s

181 s of microRNAs in low molecular weight RISC (LMW-RISC) not bound to mRNA, suggesting that these micro

182 DacA-1 alone among V. cholerae's LMW PBPs is critical for bacterial growth; mutants lacki

183 Second, LMW-E-overexpressing cells are binucleated or multinucle

184 ve no phenotype, and cells lacking all seven LMW PBPs remain viable.

185 , reaching statistical significance for some LMW phthalates and parabens.

186 With this AuNP method, two strong LMW binders are identified for FoxA1 and AP-2gamma; liga

187 fied low molecular weight glutenin subunits (LMW-GS) using a 4 g sample Microdoughlab (MDL).

188 Low molecular dextran sulfate (LMW-DS) has been shown in experimental settings to inhib

189 nit of P-TEFb, forming a distinct Tax/P-TEFb LMW complex.

190 Moreover, we demonstrated that LMW HA activated the M1 macrophage phenotype with the un

191 , analyses of human tumor samples found that LMW-AR levels are higher in tumors that have an increase

192 We found that LMW-FGF-2 induced NFAT and Ets1 binding to conserved cis

193 Therefore, we hypothesized that LMW-E isoforms have altered subcellular localization.

194 Here we report that LMW-E expression in human mammary epithelial cells induc

195 Our results reveal that LMW-E isoforms preferentially accumulate in the cytoplas

196 Our results revealed that LMW-heparin strongly promotes WT-hbeta(2)m fibrillogenes

197 These results suggest that LMW-E overexpression leads to higher centrosome numbers

198 cytokinesis and polyploidy, suggesting that LMW-E expression primes cells to accrue chromosomal inst

199 The LMW fraction displayed a dose-dependent decrease in NO p

200 The LMW phenolics of the commercial cultivar, 'July Prince',

201 The LMW-E/CDK2 complex phosphorylated Hbo1 at T88 without af

202 weight (MMW) (28%) adiponectin, although the LMW level was still high (52%).

203 Thus, a relationship between the LMW PBPs and cytoplasmic FtsZ ultimately affects cell di

204 y of the Pdo system to oxidize biphenyl, the LMW PAHs naphthalene, phenanthrene, anthracene, and fluo

205 The data support a model for the LMW overlap complex that is homologous to the striated m

206 MR was induced by heating the LMW peptides in the presence of sucrose for 2h at 90 deg

207 itial weak TPC, RSA and FRAP observed in the LMW fractions relative to the HMW fractions were substan

208 is that the overlap spans 16 residues in the LMW tropomyosin complex compared to 11 residues in the H

209 uces a striking conformational change in the LMW-PTP active site, leading to the formation of a previ

210 Intriguingly, the LMW form was more abundant in synovial fluid than in ser

211 Antioxidant capacities of the LMW and HMW fractions were determined using in vitro ass

212 pain 2 plays a role in the generation of the LMW-AR in R1 cells.

213 tivated ERK to promote the generation of the LMW-AR.

214 ) thiol glutathione, but it does produce the LMW thiol bacillithiol (BSH).

215 trand-specific targets demonstrates that the LMW replication intermediates come from both the lagging

216 sal challenge than a conjugate made with the LMW polysaccharide (LMW-TT).

217 Therefore, LMW-HA and HMGB-1 act as innate immune cytokine-like sig

218 Third, LMW-E overexpression causes mitotic defects, chromosome

219 on, and activity, ultimately contributing to LMW-E tumorigenicity.

220 ng and activation ultimately contributing to LMW-E-induced tumorigenicity.

221 tation (1.76 [1.07-2.91]), whereas OA due to LMW agents exhibited a higher risk of severe exacerbatio

222 By contrast, OA due to LMW agents was associated with chest tightness at work (

223 olecular weight than in those with OA due to LMW.

224 ways inflammatory response after exposure to LMW and HMW agents by specific inhalation challenge test

225 -deficient mice were completely resistant to LMW-cyclin E-mediated mammary tumors.

226 g is essential for procatabolic responses to LMW-HA and HMGB-1, and MyD88 drives chondrocyte hypertro

227 mation on protein conformational change upon LMW ligand loading as can be observed from AuNPs' UV-vis

228 xplore our hypothesis, we compared EL versus LMW-E localization in cell lysates and in vivo using fra

229 eight of the agent (high molecular weight vs LMW) was the only factor associated with an increase in

230 ition [% decrease from the baseline (HMW vs. LMW) was 36.9 vs. 74.1% (Abeta40, P<0.05) and 25.4 vs. 8

231 generated fractions of low molecular weight (LMW) (<3.5 kDa) and of high molecular weight (HMW) (3.5-

232 as lysozyme and also a Low Molecular Weight (LMW) ACE effector, bilirubin, which act in concert to re

233 nal asthma (OA) due to low molecular weight (LMW) agents is not well established compared to classica

234 nant Tau misfolds into low molecular weight (LMW) aggregates prior to assembly into fibrils, and both

235 However, for low molecular weight (LMW) allergens, pooled sensitivity is generally lower (0

236 ionated for elution of low-molecular weight (LMW) and high-molecular weight (HMW) fractions.

237 in four cases it was a low molecular weight (LMW) chemical.

238 Characterizing low molecular weight (LMW) dissolved organic matter (DOM) in soils and evaluat

239 ence of (14)C-labelled low molecular weight (LMW) DOC at a wide range of concentrations (0.1 uM to 10

240 e approximately 80,000 low molecular weight (LMW) form.

241 Low molecular weight (LMW) forms and monomers were the major components (93%)

242 in the accumulation of low molecular weight (LMW) HA and activation of monocytes and macrophages.

243 itions in vivo, are of low molecular weight (LMW) independently of the organism, suggesting discontin

244 in E, particularly the low molecular weight (LMW) isoforms.

245 oughput screening of small molecular weight (LMW) ligands for protein and sensitive determination of

246 me characterization of low molecular weight (LMW) ligands that induce conformational changes.

247 h comprises a range of low molecular weight (LMW) molecules (molecular mass < 150 Da) that differ fro

248 ect of addition of the low-molecular weight (LMW) organic compounds, easily ionized elements (EIEs),

249 cular weight (HMW) and low molecular weight (LMW) peaks.

250 (MR), induced between low molecular weight (LMW) peptides and sucrose, was studied.

251 reased accumulation of low molecular weight (LMW) peptides, similar to those found in aging human and

252 Low-molecular weight (LMW) phthalate diesters function as plasticizers, fixati

253 such that little to no low-molecular weight (LMW) products are externally released to the environment

254 his pathway results in low molecular weight (LMW) proteinuria that can progress to end-stage kidney d

255 iol (MSH) is the major low molecular weight (LMW) thiol in Actinomycetes.

256 elevated abundance of low molecular weight (LMW) thiols, including glutathione (GSH) and coenzyme A

257 dicarboxylic acids of low molecular weight (LMW).

258 olecular size [25 kDa, low molecular weight (LMW)].

259 rations of PAHs with lower molecular weight (LMW, 126 < MW < 202) and higher molecular weight (HMW, 2

260 We used low molecular weight (LMW, 18 kDa) FGF-2 and high molecular weight (HMW) FGF-2

261 ly more toxic than the low molecular weight (LMW, 2-3 ring) PAHs.

262 duce breads from which low molecular weight (LMW-) peptides were extracted.

263 ationally cleaved into low molecular weight (LMW-E) isoforms, which are tumor-specific and accumulate

264 t PAHs identified were low molecular weight (LMW-PAH) (liver > muscle) with 2-3 aromatic ring.

265 ght (HMW; 0.4-10 kDa), low molecular weight (LMW; 50-400 Da), and retained (R) fraction.

266 parated into low- and high-molecular-weight (LMW and HMW) fractions by Sephadex LH-20 column chromato

267 to the accumulation of low-molecular-weight (LMW) "antioxidant" Mn(2+)-metabolite complexes that prot

268 cular-weight (HMW) and low-molecular-weight (LMW) Abeta oligomers in the brain ISF of living animals,

269 s were only exposed to low-molecular-weight (LMW) agents.

270 Here, we report that low-molecular-weight (LMW) and high-molecular-weight (HMW) Abeta oligomers dif

271 Low-molecular-weight (LMW) and high-molecular-weight (HMW) agents have been re

272 ght (HMW) proteins and low-molecular-weight (LMW) chemicals can cause occupational asthma (OA) althou

273 were fractionated, and low-molecular-weight (LMW) components were separated from the proteins by filt

274 s in either an active, low-molecular-weight (LMW) form or an inactive, high-molecular-weight (HMW) fo

275 istered anticoagulant, low-molecular-weight (LMW) heparin, in the initiation and subsequent aggregati

276 cancer and appears as low-molecular-weight (LMW) isoforms that correlate strongly with decreased sur

277 More lower-molecular-weight (LMW) n-alkanes (C9-C18) were partitioned in MOS than in

278 e was derived from the low-molecular-weight (LMW) organic acids acetate and butyrate.

279 MS analyses of various low-molecular-weight (LMW) organic compounds, including alkaloids, saccharides

280 ior(s) responsible for low-molecular-weight (LMW) PAHs in HMW PAH-metabolic networks remain poorly un

281 including protein and low-molecular-weight (LMW) S-nitrosothiols (S-nitroso-GSH (GSNO) and S-nitroso

282 rent dissociation into low-molecular-weight (LMW) species after RNase A treatment.

283 starting material, and low molecular-weight (LMW) species.

284 ytoplasmic pool of the low-molecular-weight (LMW) thiol glutathione (GSH) is readily oxidized in Salm

285 s does not produce the low-molecular-weight (LMW) thiol glutathione, but it does produce the LMW thio

286 s-127 reacted with the low-molecular-weight (LMW) thiol mycothiol, protecting it from overoxidation.

287 ercury complexation by low-molecular-weight (LMW) thiols can affect its bioavailability and thus the

288 stitutive secretion of low-molecular-weight (LMW) VWF is targeted basolaterally, toward the subendoth

289 olar concentrations of low-molecular-weight (LMW), high-molecular-weight (HMW), and di-2-ethylhexylph

290 ere we identify such a low-molecular-weight (LMW)-dT source as mostly dTDP-glucose and its derivative

291 Low-molecular-weight (LMW, <26kDa) unique alkaline proteins comprise 75% of th

292 ography into low- and high-molecular-weight (LMW/HMW) fractions.

293 W peaks contained PDE3A1 and PDE3A2, whereas LMW peaks contained PDE3A1, PDE3A2, and PDE3A3.

294 s cell cycle arrest in prometaphase, whereas LMW-E overexpression reduces the length of mitosis and a

295 When coexpressed with LMW-E/CDK2, wild-type Hbo1 promoted enrichment of cancer

296 ata indicate that treatment of human EC with LMW-HA induced CD44v10 association with the receptor-tyr

297 solated from a human lens water-soluble (WS)-LMW fraction on a reversed-phase column and were identif

298 A human lens WS-LMW fraction contained two major peaks of activity.

299 An action spectrum for the WS-LMW fraction from human lens showed activity throughout

300 cellular enzymes (external hydrolysis) yield LMW products available to the wider bacterioplankton com