ライフサイエンスコーパス: hyperosmotic

1 umol l(-1), ouabain, the secreted saliva was hyperosmotic.

2 lis (OVLT) play a pivotal role in triggering hyperosmotic activation of SNA by recruiting neurons in

3 suggesting the primary role of TonEBP in the hyperosmotic adaptation of NP cells.

4 ococcus aureus biofilms in the presence of a hyperosmotic agent.

5 inhibiting sodium absorption, and utilizing hyperosmotic agents to rehydrate the airway surface.

6 brane transportation channels by exposure to hyperosmotic agents.

7 o alter the ability of embryos to survive in hyperosmotic and anoxic conditions and engage in the ada

8 ay system through which cells can respond to hyperosmotic and other environmental stresses.

9 gh salt on plants include Na(+) toxicity and hyperosmotic and oxidative stresses.

10 ell survival in response to proinflammatory, hyperosmotic, and cytotoxic stress and that stress-induc

11 s worms with the decision whether to cross a hyperosmotic barrier presenting the threat of desiccatio

12 Resuspension into hyperosmotic buffer lacking K+ and nutrients extracts cy

13 thermore, both calcium-dependent release and hyperosmotic (calcium-independent) dye release are reduc

14 Subjecting L6 myotubes to an acute hyperosmotic challenge (420 mosmol l(-1)) led to a 40% r

15 a membrane (or both) can withstand long-term hyperosmotic challenge by ionic and nonionic solutes wit

16 hereas AQP2 abundance decreased after 3 h of hyperosmotic challenge, it increased after 24 h of hyper

17 stemic, polymodal neurohumoral response to a hyperosmotic challenge.

18 orphology and sperm motility when faced with hyperosmotic challenges, and that Slo3 is critical for f

19 estion of water and food are major hypo- and hyperosmotic challenges.

20 microscopy, and a DNase I assay to show that hyperosmotic conditions (>400 mOsm/kg) induce chromatin

21 s the sensitivity of TRPM7 to both hypo- and hyperosmotic conditions and explored the involvement of

22 multiple residues after exposure of cells to hyperosmotic conditions and that activation is mediated

23 Moreover, hyperosmotic conditions block TORC2-dependent Ypk1-media

24 was dose-dependently induced by increasingly hyperosmotic conditions in a p38-independent manner.

25 hat exposing adult Caenorhabditis elegans to hyperosmotic conditions protects their offspring from th

26 Whereas wild-type animals exposed to hyperosmotic conditions rapidly lose body volume, motili

27 When exposed to hyperosmotic conditions through the addition of 30 mosM

28 nce of glycerol, which protects animals from hyperosmotic conditions, and glycogen, which is consumed

29 utants, Delta rrg-1 strains are sensitive to hyperosmotic conditions, and they are resistant to the f

30 devoid of the Ktr system became sensitive to hyperosmotic conditions, exhibited a hyperpolarized plas

31 phosphatidic acid (PA), occurs under various hyperosmotic conditions, including salinity and water de

32 Under hyperosmotic conditions, there is a significant activati

33 e of endogenous solutes during adaptation to hyperosmotic conditions.

34 tude, as well as under consecutive hypo- and hyperosmotic conditions.

35 ne expression changes of epimastigotes under hyperosmotic conditions.

36 on of genes critical for cell survival under hyperosmotic conditions.

37 increase LC3-II or LC3-positive puncta under hyperosmotic conditions.

38 embrane thickness and lateral pressure under hyperosmotic conditions.

39 tion, OSRE1 deletion from intron 1 abolishes hyperosmotic enhancer activity.

40 posus (NP) cells reside in a physiologically hyperosmotic environment within the intervertebral disc.

41 the kidney is the only organ that has such a hyperosmotic environment, and study provides an excellen

42 he hippocampus are parallel responses to the hyperosmotic environment.

43 ected its oxygen-limited, nutrient-poor, and hyperosmotic environment.

44 sms to sense and modulate their responses to hyperosmotic environments are poorly understood.

45 s osmosensation, adaptation, and survival in hyperosmotic environments.

46 oved after intravenous administration of 20% hyperosmotic glucose solution with dialysis and pan-reti

47 on 1 are required for precise enhancement of hyperosmotic glutamine synthetase expression.

48 While ShKif3a blocked hyperosmotic increase of TonEBP-Transactivation Domain (

49 ce plant Arabidopsis thaliana that the rapid hyperosmotic-induced Ca(2+) response exhibited enhanced

50 oroplast structure, kea3, impaired the rapid hyperosmotic-induced Ca(2+) responses.

51 In separate preparations the hyperosmotic-induced sympathoexcitation (21 +/- 2%) was

52 Unlike for conventional enhancers, the hyperosmotic induction of glutamine synthetase by intron

53 In this study we show that hyperosmotic induction of glutamine synthetase represent

54 Hyperosmotic internalization of Ntcp was also found in l

55 Hyperosmotic internalization of Ntcp was sensitive to SU

56 ilibration between the urinary space and the hyperosmotic interstitium.

57 ated contrast material in conjunction with a hyperosmotic laxative (magnesium citrate) was associated

58 as a partial volume recovery in response to hyperosmotic loading, based on prior theoretical and bio

59 on both ionic (NaCl) and nonionic (sorbitol) hyperosmotic media.

60 corneal epithelial cells (HCECs) exposed to hyperosmotic medium at 450 mOsM.

61 Hyperosmotic medium stimulated NPR-B dephosphorylation,

62 Hyperosmotic medium was prepared by supplementing isoton

63 ay 86, OC corneas were deswelled in a common hyperosmotic medium, but not the ASM corneas, which had

64 ch could be resolved by brief treatment with hyperosmotic medium, suggesting alterations in outer ret

65 a, IL-6, MMP-2 and MMP-9 in HCECs exposed to hyperosmotic medium.

66 us (NP) cells adapt to their physiologically hyperosmotic microenvironment through Tonicity-responsiv

67 onEBP permits the disc cells to adapt to the hyperosmotic milieu while autoregulating the expression

68 The aim of this study was to analyze hyperosmotic Ntcp regulation and the underlying signalin

69 es of abiotic stress (thermal, oxidative and hyperosmotic) on two sets of nematode (Caenorhabditis el

70 In contrast, leptospiral homologues of hyperosmotic or general stress genes were not induced at

71 Water-loss dehydration (hypertonic, hyperosmotic, or intracellular dehydration) is due to in

72 Hyperosmotic, orally administered, water-soluble contras

73 rially perfused decorticate rat preparation, hyperosmotic perfusate consisted of either 135 mm NaCl,

74 Strikingly, this rapid intracellular hyperosmotic phase separation (HOPS) correlates with the

75 pheromone response, filamentous growth, and hyperosmotic resistance.

76 ve in maintaining fragmented vacuoles during hyperosmotic response and in buds.

77 The role of the hyperosmotic-response pathway in nutrient sensing may in

78 Using clr-3 mutants, we implicated the hyperosmotic-response pathway in the tunable regulation

79 Hyperosmotic responses were abolished by TRPM8 antagonis

80 oblasts (MEFs), the overall TonEBP-dependent hyperosmotic responses were preserved.

81 We examined if intravenous infusion of hyperosmotic saline affects skin sympathetic nerve activ

82 we examined if local intradermal infusion of hyperosmotic saline affects sweating and cutaneous vasod

83 In contrast, local intradermal infusion of hyperosmotic saline did not affect sweating or cutaneous

84 at RRG-1 controls vegetative cell integrity, hyperosmotic sensitivity, fungicide resistance, and prot

85 After sudden hyperosmotic shock (plasmolysis), the cytoplasm loses wa

86 In response to hyperosmotic shock and calcineurin-dependent regulation,

87 o physiological stresses that stabilize p53, hyperosmotic shock and DNA replication fork arrest, also

88 Cell shrinkage following hyperosmotic shock and energy depletion, as well as hemo

89 quired to endure various stresses, including hyperosmotic shock and hypoxia.

90 icture of the initial response of E. coli to hyperosmotic shock and offer explanations for seemingly

91 rapidly activated in response to insulin and hyperosmotic shock by distinct intracellular signalling

92 In contrast, glucose starvation or hyperosmotic shock causes cell shrinking, which results

93 Hyperosmotic shock causes water efflux and a concomitant

94 We find that hyperosmotic shock decreases SH3 stability in cells, con

95 However, Fps1 closes upon hyperosmotic shock even in hog1 cells, indicating anothe

96 sure by cuticle puncture or decreasing it by hyperosmotic shock has only a modest effect on stiffness

97 ving Escherichia coli cells before and after hyperosmotic shock in the presence and absence of the os

98 Hyperosmotic shock induces early calpain activation, Sma

99 Caspase-3 activation by hyperosmotic shock induces proteolysis of Bid and mono-u

100 Activation of Hog1 in response to hyperosmotic shock induces the rapid eviction of Rgc2 fr

101 trol of Fps1 channel activity in response to hyperosmotic shock involves a redundant pair of regulato

102 ell dynamics in the Saccharomyces cerevisiae hyperosmotic shock network, which regulates membrane tur

103 physiological cell stressors ex vivo such as hyperosmotic shock or energy depletion to significantly

104 Hyperosmotic shock promotes calcineurin binding to and d

105 Inactivation of Ypk1 by hyperosmotic shock results in dephosphorylation and acti

106 Oscillatory hyperosmotic shock revealed that although plasmolysis sl

107 uced during the early phase of adaptation to hyperosmotic shock were found to be also overexpressed u

108 fluorescence imaging of single cells during hyperosmotic shock with a time resolution on the order o

109 lope material properties do not change after hyperosmotic shock, and that cell shape recovers along w

110 ) erythrocytes following ex vivo exposure to hyperosmotic shock, bacterial sphingomyelinase or C6 cer

111 ess shape changes in Escherichia coli during hyperosmotic shock, finding size heterogeneity.

112 signal transduction caused by events such as hyperosmotic shock, hormone response and response to mat

113 accharomyces cerevisiae cells are exposed to hyperosmotic shock, PI3,5P2 (phosphatidylinositol [PI] 3

114 During hyperosmotic shock, Saccharomyces cerevisiae adjusts to

115 by suppressing water-drinking behavior after hyperosmotic shock, similar to SCTR knockouts.

116 , and to cellular stresses (sorbitol-induced hyperosmotic shock, UV irradiation, and hydrogen peroxid

117 zed as a regulator of vacuole fission during hyperosmotic shock, where it interacts with the TRP Ca(2

118 enlarged vacuoles that do not fragment after hyperosmotic shock, which indicates that PtdIns(3,5)P2 l

119 ,5)P2 synthesis--for example, in response to hyperosmotic shock--remains unexplained.

120 Hyperosmotic shock-evoked 3H-glutamate was reduced by 20

121 Expression of Bcl-xL markedly reduces hyperosmotic shock-induced apoptosis.

122 Vac7p, the Vac14p-Fig4p complex controls the hyperosmotic shock-induced increase in PI3,5P2 levels.

123 ocyte Galphai2 deficiency further attenuated hyperosmotic shock-induced increase of cytosolic Ca(2+)

124 by which Hog1 regulates Fps1 in response to hyperosmotic shock.

125 ed by P. aeruginosa in immediate response to hyperosmotic shock.

126 ing the RRP, which was loaded with FM1-43 by hyperosmotic shock.

127 fluorescence imaging of single cells during hyperosmotic shocks, combined with custom made microflui

128 ved by oral administration of 600-1000 ml of hyperosmotic solution of polyetylenglycol (PEG).

129 were evoked using localized application of a hyperosmotic solution to the apical dendrites in the vic

130 controls, resist shrinkage when incubated in hyperosmotic solution.

131 as present in mouse RPE cells, the effect of hyperosmotic solutions on isolated mouse RPE cells was e

132 ctivated by drying of the ocular surface and hyperosmotic solutions, conditions that are consistent w

133 ver failure should be maintained in a mildly hyperosmotic state to minimize cerebral edema.

134 e knockdown of either gene did not alter the hyperosmotic status of proximal promoter activities and

135 our of NKCC1 are necessary components of the hyperosmotic stimulation of K(+)/K(+) exchange.

136 o 10-20 Hz and 6-10 Hz, respectively, by our hyperosmotic stimulation protocol.

137 ouse corneal epithelial layer in response to hyperosmotic stimulation.

138 ivity of Plk3 was significantly activated by hyperosmotic stimulation.

139 athoexcitation was also evoked by comparable hyperosmotic stimulation.

140 and iron can account for ROS production upon hyperosmotic stimulation.

141 observed with NKCC1, a significantly smaller hyperosmotic stimulatory effect was observed with NKCC2.

142 Remarkably, while both pheromone and hyperosmotic stimuli amplify signaling from constitutive

143 R-B phosphorylation sites is unresponsive to hyperosmotic stimuli.

144 ole in early steps mediating the response to hyperosmotic stimuli.

145 tenuated the increase in LSNA induced by the hyperosmotic stimulus (control: 25 +/- 2%; after isoguva

146 reduced the increase in LSNA elicited by the hyperosmotic stimulus (control: 29 +/- 6%; after blocker

147 These results suggest that a physiological hyperosmotic stimulus produces sympathetically mediated

148 Remaining experiments used the NaCl hyperosmotic stimulus.

149 m murine renal IM cells responds to moderate hyperosmotic stress (540 mosmol/kg) by activation of G(2

150 is required for optimal invasive growth and hyperosmotic stress (high-osmolarity glycerol [HOG]) sig

151 than the apoptotic stimulus, staurosporine, hyperosmotic stress activated caspase-3.

152 We show that hyperosmotic stress activates the protein kinase R (PKR)

153 tment of primary cortical neurons exposed to hyperosmotic stress also decreases apoptosis.

154 inase Pho85/CDK5 provides protection against hyperosmotic stress and acts before long-term adaptation

155 preferentially to OSTF1 target genes during hyperosmotic stress and compensate for reduced rates of

156 lock allows anticipation and preparation for hyperosmotic stress and desiccation that begin at sunris

157 s) phase-separates in mammalian cells during hyperosmotic stress and dissolves upon isosmotic rescue

158 growth (FG) pathways are activated following hyperosmotic stress and nutrient deprivation, respective

159 o rapamycin, high concentrations of calcium, hyperosmotic stress and SchA was involved in iron metabo

160 udy budding yeast in dynamic environments of hyperosmotic stress and show how the corresponding signa

161 ated tiRNAs and cell survival in response to hyperosmotic stress and suggest a novel cellular complex

162 ons abolished the response to proline and to hyperosmotic stress but not to Mg(2+).

163 bcellular compartments that protects against hyperosmotic stress by generating osmolytes and metaboli

164 rst time that human ALDH7A1 protects against hyperosmotic stress by generating osmolytes and metaboli

165 is known about the mechanisms of sensing the hyperosmotic stress by the innate immune system.

166 Our results for the first time reveal that hyperosmotic stress can activate the Plk3 signaling path

167 ion difference of the samples in response to hyperosmotic stress can potentially provide us with a un

168 Hyperosmotic stress caused by drought and salinity is a

169 In yeast, hyperosmotic stress causes an immediate dissociation of

170 Hyperosmotic stress causes cell shrinkage, perturbs cell

171 liquid-liquid phase separation (LLPS) under hyperosmotic stress conditions allows cells to react to

172 snrk2.1/2/3/4/5/6/7/8/9/10 grew poorly under hyperosmotic stress conditions but was similar to the wi

173 udomonas aeruginosa grown under steady-state hyperosmotic stress conditions showed an up-regulation o

174 ect to partial repression by succinate under hyperosmotic stress conditions, in contrast to strong re

175 lar signal modulating solute synthesis under hyperosmotic stress conditions.

176 e accumulation of glycerol in the absence of hyperosmotic stress conditions.

177 ATF4 was not translated during hyperosmotic stress despite an increase in eIF2alpha pho

178 Hyperosmotic stress during G(1) phase specifically inhib

179 Salmonella seems to experience hyperosmotic stress during infection because osmotically

180 The results presented here demonstrate that hyperosmotic stress elicited increases in ATF-2 phosphor

181 If the severity of hyperosmotic stress exceeds the tolerance limit of this

182 ivating a complex array of signaling events, hyperosmotic stress fails to up-regulate PtdIns 3,5-P(2)

183 the present study, we highlight the role of hyperosmotic stress in inducing human alpha-syn to aggre

184 )-2Cl(-) cotransporter (NKCC) by insulin and hyperosmotic stress in L6 rat skeletal muscle cells.

185 In intact cells, hyperosmotic stress increased phosphorylated PKCdelta, i

186 Hyperosmotic stress increases phosphoinositide levels, r

187 We found that hyperosmotic stress induced DNA-double strand breaks and

188 Our study results here demonstrate that hyperosmotic stress induced H2AX phosphorylation (gammaH

189 Unlike yeast, where hyperosmotic stress induces a dramatic increase in phosp

190 Hyperosmotic stress induces a rapid rise in intracellula

191 However, severe or chronic hyperosmotic stress induces apoptosis, which involves cy

192 In budding yeast, hyperosmotic stress induces Ca(2+) release from the vacu

193 Hyperosmotic stress induces rapid redistribution of WNK1

194 Here we find that hyperosmotic stress induces strong phosphorylation of Ss

195 Activation of Pak2 in response to hyperosmotic stress inhibits cap-dependent, but not IRES

196 Hyperosmotic stress inhibits translocation through Rck2-

197 The cellular response to hyperosmotic stress involves rapid efflux of water and c

198 Here we show that the response to mild hyperosmotic stress involves regulation of the phosphory

199 cts and show that as a cell is compressed by hyperosmotic stress it becomes progressively more rigid.

200 increasing levels of cytoplasmic K(+) during hyperosmotic stress latter via its C-terminal domain and

201 neous exposure of L6 myotubes to insulin and hyperosmotic stress led to an additive increase in NKCC-

202 Stimulating transgenic cells with hyperosmotic stress led to another 2-fold increase, sugg

203 Hyperosmotic stress of rat brain slices, produced by add

204 The effect of hyperosmotic stress on rose bengal staining in vitro was

205 work reveals a novel CK2 function during the hyperosmotic stress response that promotes cell-to-cell

206 mbers, and the function of PLD activation in hyperosmotic stress responses has remained elusive.

207 Exposure of immature T-cells to hyperosmotic stress resulted in a rapid, synchronous, an

208 Hyperosmotic stress resulted in cell shrinking within a

209 Here we show that hyperosmotic stress signaling induced by sorbitol disrup

210 Thus, the Ran system is a target of hyperosmotic stress signaling, and cells use protein loc

211 M2-MEKK3 pathway that has been implicated in hyperosmotic stress signaling.

212 s more sensitive to ABA and more tolerant to hyperosmotic stress than wild-type plants.

213 These results reveal hyperosmotic stress to be a potent activator of caspase-

214 Plk3 was activated by extracellular hyperosmotic stress to directly phosphorylate c-Jun in t

215 These effects correlate with the ability of hyperosmotic stress to interfere with protein traffickin

216 In the present study, we determined if hyperosmotic stress to rat hippocampal slices activates

217 ce to translational inhibitors, and enhanced hyperosmotic stress tolerance.

218 s activated through hormonal stimulation and hyperosmotic stress via a protein kinase C (PKC) delta-m

219 [PP](2)-InsP(4) levels normally seen during hyperosmotic stress were attenuated by 2-(2-chloro-4-iod

220 Plants experience hyperosmotic stress when faced with saline soils and pos

221 Elevated extracellular solute concentration (hyperosmotic stress) perturbs cell function and stimulat

222 eased dissolved solute in their environment (hyperosmotic stress), all eukaryotic cells respond by ra

223 ts were unable to accumulate ABA following a hyperosmotic stress, although their basal ABA level was

224 efect in fibroblasts, less responsiveness to hyperosmotic stress, and reduced persistence in tissues

225 T cells under oxidative stress but not under hyperosmotic stress, and they were high and unchanging i

226 une cell function and cellular adaptation to hyperosmotic stress, as a possible cause of this syndrom

227 plete loss in NKCC activation in response to hyperosmotic stress, immunoprecipitation of NKCC reveale

228 tein kinase Hog1 is activated in response to hyperosmotic stress, inducing the production and retenti

229 C1 and functional activation of NKCC1 during hyperosmotic stress, measured as bumetanide-sensitive ba

230 such as protein misfolding and aggregation, hyperosmotic stress, membrane fracturing, and changes in

231 ally sumoylated proteins during heat stress, hyperosmotic stress, oxidative stress, nitrogen starvati

232 d to improve bacterial growth recovery under hyperosmotic stress, partly through stabilization of the

233 Hyperosmotic stress, produced by addition of sorbitol to

234 For such cells to survive hyperosmotic stress, systematic genetic analysis ruled o

235 When cells were exposed to hyperosmotic stress, the MORN peptide redistributed from

236 physiological changes resulting from imposed hyperosmotic stress, thereby offering a clear visualizat

237 function of the inflammasome as a sensor of hyperosmotic stress, which is crucial for the induction

238 el role of c-Rel in the adaptive response to hyperosmotic stress, which is inhibited via a PACT/PKR-d

239 Formed within seconds of hyperosmotic stress, YAP condensates compartmentalized t

240 rast, caffeine had no effects on melphalan-, hyperosmotic stress-, or IL-1beta-induced activation of

241 The effect of hyperosmotic stress-activated Plk3 and increased gammaH2

242 Our results for the first time reveal that hyperosmotic stress-activated Plk3 elicited gammaH2AX.

243 the authors explore the mechanism involving hyperosmotic stress-induced activation of c-Jun/AP-1 thr

244 The effect of hyperosmotic stress-induced activation of Plk3 on ATF-2

245 ation of H2AX at serine 139 was catalyzed by hyperosmotic stress-induced activation of Plk3.

246 lternative signaling mechanism that involves hyperosmotic stress-induced activation of the Plk3 pathw

247 ylation of c-Jun by Plk3 was responsible for hyperosmotic stress-induced apoptosis, which was indepen

248 k3 mRNA effectively diminished the effect of hyperosmotic stress-induced ATF-2 phosphorylation.

249 rexpression of Plk3 and its mutants enhanced hyperosmotic stress-induced ATF-2 phosphorylation.

250 Hyperosmotic stress-induced c-Jun phosphorylation was en

251 colocalized with gammaH2AX in the nuclei of hyperosmotic stress-induced cells.

252 n Plk3 mRNA effectively reduced gammaH2AX in hyperosmotic stress-induced cells.

253 , a transcription factor reported to mediate hyperosmotic stress-induced cytoprotection in renal medu

254 tridium difficile toxin B potently inhibited hyperosmotic stress-induced FAK tyrosine phosphorylation

255 We found in hyperosmotic stress-induced HCE cells that Plk3 transfer

256 It was found that hyperosmotic stress-induced increases in the phosphoryla

257 he contribution of ArPIKfyve-PIKfyve for the hyperosmotic stress-induced rise in PtdIns 3,5-P(2).

258 ression of N17 Rac only slightly altered the hyperosmotic stress-mediated localization of phosphoryla

259 ression of the N17 mutant of Cdc42 disrupted hyperosmotic stress-stimulated FAK Tyr-397 localization

260 lling, but does not affect MAPK responses to hyperosmotic stress.

261 serve interphase microtubules in response to hyperosmotic stress.

262 kinase II (CK2) in the cellular response to hyperosmotic stress.

263 ces a transcriptional program in response to hyperosmotic stress.

264 ich decrease under proline limitation and/or hyperosmotic stress.

265 d to maintain interphase microtubules during hyperosmotic stress.

266 its importance for the cellular response to hyperosmotic stress.

267 ch becomes negative as they recover from the hyperosmotic stress.

268 ive of the in vivo changes that occur during hyperosmotic stress.

269 onal up-regulation is necessary to cope with hyperosmotic stress.

270 of SPAK to increase activity of NKCC1 during hyperosmotic stress.

271 g the response of mature collecting ducts to hyperosmotic stress.

272 the second messengers in plant responses to hyperosmotic stress.

273 the mechanism by which WNK1 is regulated by hyperosmotic stress.

274 he internal K+ concentration as a measure of hyperosmotic stress.

275 t are rapidly and transiently induced during hyperosmotic stress.

276 nifest by subsequent apoptosis, to sustained hyperosmotic stress.

277 on of ERK1/2 and p38MAPalpha/beta kinases by hyperosmotic stress.

278 ot prevent FAK phosphorylation stimulated by hyperosmotic stress.

279 volved in control of apoptosis during severe hyperosmotic stress.

280 le of RBOH-dependent ROS, specifically under hyperosmotic stress.

281 tivation mechanism fail to proliferate after hyperosmotic stress.

282 e rapid synthesis of glycerol in response to hyperosmotic stress.

283 om adaptation to inflammation in response to hyperosmotic stress.

284 nitudes after preexposure to an intermediate hyperosmotic stress.

285 nd indirect targets of SchA post-exposure to hyperosmotic stress.

286 ptible to DNA (de)methylation in response to hyperosmotic stress.

287 1 (SOD1) and peroxiredoxin-4 (PRDX4) during hyperosmotic stress.

288 creased sensitivities to SDS, Congo red, and hyperosmotic stress.

289 duced cytosolic Ca(2+) signal in response to hyperosmotic stress.

290 ol accumulation, and enhanced survival under hyperosmotic stress.

291 rophosphates also responded within 30 min of hyperosmotic stress: levels of bisdiphosphoinositol tetr

292 lpha3 positively mediates plant responses to hyperosmotic stresses and that increased PLDalpha3 expre

293 l microtubules in plant cells that are under hyperosmotic stresses.

294 es plant response to abscisic acid (ABA) and hyperosmotic stresses.

295 The ME/CFS samples' response to the hyperosmotic stressor observed as a unique characteristi

296 lls from sickle trait patients (deoxygenated hyperosmotic sucrose solutions at pH 6) supported their

297 r, terrestrial mammals produce urine that is hyperosmotic to plasma.

298 in reduced vacuolar efflux was observed upon hyperosmotic transfer.

299 ree of phosphorylation is rapidly altered by hyperosmotic treatment.

300 he formation of primary cilia did not affect hyperosmotic upregulation of TonEBP.