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 cyclin E overexpression in mammary epithelial cells

3 LMW derivatives of cyclin E1 have been proposed to be ge

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

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

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

7 LMW thiols also preserve the transcription of Salmonella

8 LMW-E induces additional mitotic defects in cooperation

9 LMW-E upregulated ACLY enzymatic activity, subsequently

10 LMW-PTP colocalizes with Nox4 both in PaCa cells and in

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

12 We determined the structure of a LMW tropomyosin N-terminal model peptide complexed with

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

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

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

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

17 if altered subcellular localization affected LMW-E degradation.

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

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

20 ammatory mediator, cleaves HMW FGF-2 into an LMW FGF-2-like form that stimulates endothelial cell mig

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

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

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

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

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

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 onal and translational regulation of HMW and LMW FGF-2 has been extensively investigated, little is k

29 d in high- and low-molecular-weight (HMW and LMW, respectively) fractions; however, only the LMW form

30 example is the opposing effects of HMW- and LMW-HA on the proliferation of vascular smooth muscle ce

31 rm and lower molecular weight form (HMW- and LMW-HA, respectively).

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

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

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

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

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

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

38 r dissect the mechanisms that produce the AR LMW forms using Rv1 cells and the related CWR22-R1 (R1)

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

40 ation results in inhibition of PTPs, such as LMW-PTP, leading, in turn, to enhanced and sustained pho

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

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

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

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

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

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

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

48 basis of inherited diseases characterized by LMW proteinuria.

49 the persistent cognitive deficit induced by LMW oligomers.

50 oA blocked the barrier disruption induced by LMW-HA.

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

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

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

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

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

56 Conversely, LMW FGF-2 upregulates both cell proliferation and migrat

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

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

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

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

61 l lines and found that the ability to detect LMW derivatives of cyclin E1 correlates only with the le

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

63 s tumorigenic low molecular weight cyclin E (LMW-E) isoforms that lack a portion of the EL amino-term

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

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

66 Compared with full-length cyclin E, LMW cyclin E overexpression induces delayed mammary grow

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 ion and metastasis were markedly enhanced in LMW cyclin E transgenic mice.

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

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

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

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

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

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

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

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

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

105 Growth factors inhibited LMW-PTP through its oxidation by NADPH oxidase.

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 weight HA (HMW-HA, approximately 1,000 kDa; LMW-HA, approximately 2.5 kDa) effects on human transend

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

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

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

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

114 Heart failure plasma contained both low- (LMW-BNP) and high-molecular-weight (HMW-BNP) forms.

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

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

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

118 Moreover, LMW cyclin E overexpression selects for inactivation of

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

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 n E1 levels on Western blots are normalized, LMW derivatives of cyclin E1 were observed at roughly eq

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

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

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

127 ands after synthesis, producing the observed LMW intermediates.

128 In addition, metastasis was seen in 25% of LMW cyclin E tumor-bearing animals compared with only 8.

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

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

131 Alignment of LMW SLPs, which exhibit high sequence diversity, reveals

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

133 ll cycle progression, whereas the binding of LMW-HA to CD44 stimulates cell cycle progression.

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

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

136 Therefore, the detection of LMW derivatives of cyclin E1 is likely a function of cyc

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

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

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

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

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

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

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

144 44 or EphA2 siRNA and observed inhibition of LMW-HA-induced angiogenesis in implanted Matrigel plugs.

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

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

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

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

149 ERK phosphorylation and increased levels of LMW-AR.

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

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

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

153 The production of LMW succinoglycan can be generated by direct synthesis o

154 biosynthesis as well as in the production of LMW succinoglycan.

155 Reduction of LMW-PTP expression with the ASO in cultured mouse hepato

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

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

158 28 candidate peaks from MALDI-TOF spectra of LMW enriched sera.

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

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

161 port that cyclin D1 is the primary target of LMW-HA in human vascular smooth muscle cells, as it is f

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

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

164 gested that overexpression of full-length or LMW derivatives of cyclin E1 are independent variables a

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

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

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

168 lecular weight protein-tyrosine phosphatase (LMW-PTP) in glucose metabolism and insulin action, a spe

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

170 lecular weight-protein tyrosine phosphatase (LMW-PTP), and apoptosis.

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

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

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

174 1, and PLK1 in a G(2)-M-enriched population, LMW-E overexpression causes premature inactivation of Cd

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

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

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

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

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

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

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

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

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

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

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

186 In doing so, LMW HA acts as an endogenous danger signal alerting the

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

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

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

190 In this report, we demonstrate that LMW HA activates the innate immune response via TLR-2 in

191 Finally, we demonstrate that LMW HA can act as an adjuvant promoting Ag-specific T ce

192 These data demonstrate that LMW-PTP is a key negative regulator of insulin action an

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

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

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

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

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

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

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

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

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

202 The LMW-BNP migrated similarly to a 32-amino acid BNP standa

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

204 Additionally, the LMW forms of cyclin E strongly correlate with decreased

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

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

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

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

209 Transfection experiments identified the LMW-PTP as a negative regulator of sustained JAK2 phosph

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

211 er activity in young human lenses was in the LMW fractions.

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

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

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

215 However, the oncologic role of the LMW forms of cyclin E in breast cancer tumorigenesis is

216 l structure of a truncated derivative of the LMW SLP reveals two domains.

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

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

219 , respectively) fractions; however, only the LMW forms of either succinoglycan or EPS II are active i

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

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

222 tic versus nondiabetic subjects, whereas the LMW form did not significantly differ.

223 Therefore, LMW cyclin E overexpression strongly selects for spontan

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

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

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

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

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

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

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

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

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

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

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

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

236 x component, is broken down into lower m.w. (LMW) fragments, which in turn activate an innate immune

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

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

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

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

241 Many cognate low molecular weight (LMW) agonists bind to seven transmembrane-spanning recep

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

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

244 ion, and generation of low molecular weight (LMW) derivatives.

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

246 cular weight (HMW) and low-molecular weight (LMW) fractions of adiponectin in 11 type 2 diabetic and

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

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

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

250 the appearance of five low molecular weight (LMW) isoforms.

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

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

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

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

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

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

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

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

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

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

261 exon, tropomyosins are low molecular weight (LMW), found in the cytoskeleton and predominant in trans

262 dicarboxylic acids of low molecular weight (LMW).

263 The fgf-2 gene encodes low molecular weight (LMW, 18 kDa) and high molecular weight (HMW, 22-24 kDa)

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

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

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

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

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

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

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

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

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

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

274 aks in mass spectra of low-molecular-weight (LMW) enriched sera, a systematic method is needed to sel

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

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

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

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

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

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

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

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

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

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

290 due to a reduction of the HMW form, whereas LMW forms were not significantly affected.

291 ent signaling to the cyclin D1 gene, whereas LMW-HA binding to CD44 selectively stimulates ERK activa

292 in-enriched lipid raft microdomains, whereas LMW-HA induced brief CD44s association with S1P1 followe

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 HMW-HA increased TER, whereas LMW-HA induced biphasic TER changes ultimately resulting

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

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

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

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

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