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1 nd indirect targets of SchA post-exposure to hyperosmotic stress.
2  the mechanism by which WNK1 is regulated by hyperosmotic stress.
3 he internal K+ concentration as a measure of hyperosmotic stress.
4 t are rapidly and transiently induced during hyperosmotic stress.
5 ptible to DNA (de)methylation in response to hyperosmotic stress.
6 nifest by subsequent apoptosis, to sustained hyperosmotic stress.
7 on of ERK1/2 and p38MAPalpha/beta kinases by hyperosmotic stress.
8 ot prevent FAK phosphorylation stimulated by hyperosmotic stress.
9 volved in control of apoptosis during severe hyperosmotic stress.
10  1 (SOD1) and peroxiredoxin-4 (PRDX4) during hyperosmotic stress.
11 the response partially overlaps with that to hyperosmotic stress.
12  and tyrosine phosphorylation in response to hyperosmotic stress.
13 ng that Orb6p has a role in cell response to hyperosmotic stress.
14 uited to this PKN1-positive compartment upon hyperosmotic stress.
15 ally expressed in response to dehydration or hyperosmotic stress.
16  manner to a vesicular compartment following hyperosmotic stress.
17 nd, is required for short-term adaptation to hyperosmotic stress.
18 by hypoosmotic stress, but were unchanged by hyperosmotic stress.
19 pensatory genes in response to extracellular hyperosmotic stress.
20 th of proline-overaccumulating cells in mild hyperosmotic stress.
21 ine stresses, whereas levels increased after hyperosmotic stress.
22 creased sensitivities to SDS, Congo red, and hyperosmotic stress.
23 cell growth and polarity under conditions of hyperosmotic stress.
24 nthesize phosphoinositides during periods of hyperosmotic stress.
25 pathway that may lead to plant adaptation to hyperosmotic stress.
26 mponent of the p38 MAPK-mediated response to hyperosmotic stress.
27 igated the role of p53 in mIMCD3 response to hyperosmotic stress.
28 ulons closely co-operate in the managment of hyperosmotic stress.
29 ctivated protein (MAP) kinase in response to hyperosmotic stress.
30 s environmental stress conditions, including hyperosmotic stress.
31 hanisms for regulation of gene expression by hyperosmotic stress.
32 ullary cells are uniquely exposed to extreme hyperosmotic stress.
33 tivation mechanism fail to proliferate after hyperosmotic stress.
34 ol accumulation, and enhanced survival under hyperosmotic stress.
35 lling, but does not affect MAPK responses to hyperosmotic stress.
36 serve interphase microtubules in response to hyperosmotic stress.
37  kinase II (CK2) in the cellular response to hyperosmotic stress.
38 ces a transcriptional program in response to hyperosmotic stress.
39 ich decrease under proline limitation and/or hyperosmotic stress.
40 d to maintain interphase microtubules during hyperosmotic stress.
41  its importance for the cellular response to hyperosmotic stress.
42 e rapid synthesis of glycerol in response to hyperosmotic stress.
43 om adaptation to inflammation in response to hyperosmotic stress.
44 ch becomes negative as they recover from the hyperosmotic stress.
45 ive of the in vivo changes that occur during hyperosmotic stress.
46 onal up-regulation is necessary to cope with hyperosmotic stress.
47 of SPAK to increase activity of NKCC1 during hyperosmotic stress.
48 g the response of mature collecting ducts to hyperosmotic stress.
49 nitudes after preexposure to an intermediate hyperosmotic stress.
50 l microtubules in plant cells that are under hyperosmotic stresses.
51 es plant response to abscisic acid (ABA) and hyperosmotic stresses.
52 m murine renal IM cells responds to moderate hyperosmotic stress (540 mosmol/kg) by activation of G(2
53  than the apoptotic stimulus, staurosporine, hyperosmotic stress activated caspase-3.
54                                The effect of hyperosmotic stress-activated Plk3 and increased gammaH2
55   Our results for the first time reveal that hyperosmotic stress-activated Plk3 elicited gammaH2AX.
56                                 We show that hyperosmotic stress activates the protein kinase R (PKR)
57 eased dissolved solute in their environment (hyperosmotic stress), all eukaryotic cells respond by ra
58 tment of primary cortical neurons exposed to hyperosmotic stress also decreases apoptosis.
59                            Pretreatment with hyperosmotic stress also prevented the activation of S6K
60 ts were unable to accumulate ABA following a hyperosmotic stress, although their basal ABA level was
61 inase Pho85/CDK5 provides protection against hyperosmotic stress and acts before long-term adaptation
62  preferentially to OSTF1 target genes during hyperosmotic stress and compensate for reduced rates of
63 lock allows anticipation and preparation for hyperosmotic stress and desiccation that begin at sunris
64 ocation, Hrp1p redistribution is specific to hyperosmotic stress and is only reversed after stress re
65 growth (FG) pathways are activated following hyperosmotic stress and nutrient deprivation, respective
66 o rapamycin, high concentrations of calcium, hyperosmotic stress and SchA was involved in iron metabo
67 udy budding yeast in dynamic environments of hyperosmotic stress and show how the corresponding signa
68 ated tiRNAs and cell survival in response to hyperosmotic stress and suggest a novel cellular complex
69     AMPK in H-2Kb cells is also activated by hyperosmotic stress and the mitochondrial uncoupling age
70 lpha3 positively mediates plant responses to hyperosmotic stresses and that increased PLDalpha3 expre
71 efect in fibroblasts, less responsiveness to hyperosmotic stress, and reduced persistence in tissues
72  a fundamental role in protecting cells from hyperosmotic stress, and that the pathway(s) that mediat
73 une cell function and cellular adaptation to hyperosmotic stress, as a possible cause of this syndrom
74 tion of 40-kD protein kinase is specific for hyperosmotic stress, as hypotonic stress does not activa
75 s and promotes G(2)/M arrest during moderate hyperosmotic stress but not in isosmotic controls.
76 ons abolished the response to proline and to hyperosmotic stress but not to Mg(2+).
77 bcellular compartments that protects against hyperosmotic stress by generating osmolytes and metaboli
78 rst time that human ALDH7A1 protects against hyperosmotic stress by generating osmolytes and metaboli
79 ned the hypothesis that IVD cells respond to hyperosmotic stress by increasing the concentration of i
80 is known about the mechanisms of sensing the hyperosmotic stress by the innate immune system.
81   Our results for the first time reveal that hyperosmotic stress can activate the Plk3 signaling path
82 ogic implication of osmotic imbalance (i.e., hyperosmotic stress caused by intracellular over-accumul
83                                              Hyperosmotic stress caused by NaCl, LiCl, or sorbitol in
84                                    In yeast, hyperosmotic stress causes an immediate dissociation of
85                                              Hyperosmotic stress causes cell shrinkage, perturbs cell
86 y and pulsed field gel electrophoresis, that hyperosmotic stress causes DNA damage in the form of dou
87                                              Hyperosmotic stress causes growth arrest possibly via pr
88 snrk2.1/2/3/4/5/6/7/8/9/10 grew poorly under hyperosmotic stress conditions but was similar to the wi
89 udomonas aeruginosa grown under steady-state hyperosmotic stress conditions showed an up-regulation o
90 ect to partial repression by succinate under hyperosmotic stress conditions, in contrast to strong re
91 centration of glycerol within the cell under hyperosmotic stress conditions.
92 lar signal modulating solute synthesis under hyperosmotic stress conditions.
93                               In response to hyperosmotic stress, control cells from all zones decrea
94               ATF4 was not translated during hyperosmotic stress despite an increase in eIF2alpha pho
95                                              Hyperosmotic stress during G(1) phase specifically inhib
96               Salmonella seems to experience hyperosmotic stress during infection because osmotically
97  The results presented here demonstrate that hyperosmotic stress elicited increases in ATF-2 phosphor
98                           If the severity of hyperosmotic stress exceeds the tolerance limit of this
99 ivating a complex array of signaling events, hyperosmotic stress fails to up-regulate PtdIns 3,5-P(2)
100  is required for optimal invasive growth and hyperosmotic stress (high-osmolarity glycerol [HOG]) sig
101 plete loss in NKCC activation in response to hyperosmotic stress, immunoprecipitation of NKCC reveale
102 rked PtdIns 3,5-P(2) increase in response to hyperosmotic stress in differentiated 3T3-L1 adipocytes.
103 , we show that ROS production in response to hyperosmotic stress in embryonic cells of the alga Fucus
104  Skb1 homolog, Skb1Hs, is also stimulated by hyperosmotic stress in fission yeast, providing evidence
105 )-2Cl(-) cotransporter (NKCC) by insulin and hyperosmotic stress in L6 rat skeletal muscle cells.
106 d p38 demonstrated activation of p38 MAPK by hyperosmotic stress in vitro and in vivo.
107                     The adaptive response to hyperosmotic stress in yeast, termed the high osmolarity
108                             In intact cells, hyperosmotic stress increased phosphorylated PKCdelta, i
109                                              Hyperosmotic stress increases phosphoinositide levels, r
110 in NMuMg mammary epithelial cells exposed to hyperosmotic stress induced by the organic osmolyte sorb
111                                              Hyperosmotic stress induced by treatment of Swiss 3T3 ce
112                                We found that hyperosmotic stress induced DNA-double strand breaks and
113      Our study results here demonstrate that hyperosmotic stress induced H2AX phosphorylation (gammaH
114  the authors explore the mechanism involving hyperosmotic stress-induced activation of c-Jun/AP-1 thr
115                                The effect of hyperosmotic stress-induced activation of Plk3 on ATF-2
116 ation of H2AX at serine 139 was catalyzed by hyperosmotic stress-induced activation of Plk3.
117 lternative signaling mechanism that involves hyperosmotic stress-induced activation of the Plk3 pathw
118 ylation of c-Jun by Plk3 was responsible for hyperosmotic stress-induced apoptosis, which was indepen
119 k3 mRNA effectively diminished the effect of hyperosmotic stress-induced ATF-2 phosphorylation.
120 rexpression of Plk3 and its mutants enhanced hyperosmotic stress-induced ATF-2 phosphorylation.
121                                              Hyperosmotic stress-induced c-Jun phosphorylation was en
122  colocalized with gammaH2AX in the nuclei of hyperosmotic stress-induced cells.
123 n Plk3 mRNA effectively reduced gammaH2AX in hyperosmotic stress-induced cells.
124 , a transcription factor reported to mediate hyperosmotic stress-induced cytoprotection in renal medu
125 tridium difficile toxin B potently inhibited hyperosmotic stress-induced FAK tyrosine phosphorylation
126                                  We found in hyperosmotic stress-induced HCE cells that Plk3 transfer
127                            It was found that hyperosmotic stress-induced increases in the phosphoryla
128 he contribution of ArPIKfyve-PIKfyve for the hyperosmotic stress-induced rise in PtdIns 3,5-P(2).
129 of Ssh1p as two early successive events in a hyperosmotic stress-induced signaling cascade in plants.
130 ssion of K+ channel activity did not prevent hyperosmotic-stress-induced JNK activation.
131                          Unlike yeast, where hyperosmotic stress induces a dramatic increase in phosp
132                                              Hyperosmotic stress induces a rapid rise in intracellula
133                   However, severe or chronic hyperosmotic stress induces apoptosis, which involves cy
134                            In budding yeast, hyperosmotic stress induces Ca(2+) release from the vacu
135                                              Hyperosmotic stress induces rapid redistribution of WNK1
136                            Here we find that hyperosmotic stress induces strong phosphorylation of Ss
137 l cell line, we originally demonstrated that hyperosmotic stress induces transcription of the aldose
138                   These results suggest that hyperosmotic stress induces volume change in IVD cells a
139            Activation of Pak2 in response to hyperosmotic stress inhibits cap-dependent, but not IRES
140                     The cellular response to hyperosmotic stress involves rapid efflux of water and c
141       Here we show that the response to mild hyperosmotic stress involves regulation of the phosphory
142 cts and show that as a cell is compressed by hyperosmotic stress it becomes progressively more rigid.
143 increasing levels of cytoplasmic K(+) during hyperosmotic stress latter via its C-terminal domain and
144 neous exposure of L6 myotubes to insulin and hyperosmotic stress led to an additive increase in NKCC-
145            Stimulating transgenic cells with hyperosmotic stress led to another 2-fold increase, sugg
146        In contrast to isoosmotic conditions, hyperosmotic stress led to the proper folding and proces
147                 Exposure of plant tissues to hyperosmotic stress led to the rapid phosphorylation of
148 rophosphates also responded within 30 min of hyperosmotic stress: levels of bisdiphosphoinositol tetr
149 C1 and functional activation of NKCC1 during hyperosmotic stress, measured as bumetanide-sensitive ba
150 ression of N17 Rac only slightly altered the hyperosmotic stress-mediated localization of phosphoryla
151    Overexpression of N17 RhoA did not reduce hyperosmotic stress-mediated localization of phosphoryla
152  such as protein misfolding and aggregation, hyperosmotic stress, membrane fracturing, and changes in
153        Reductions in turgor caused by either hyperosmotic stress, nystatin, or removal of cell wall a
154                                              Hyperosmotic stress of rat brain slices, produced by add
155                                The effect of hyperosmotic stress on rose bengal staining in vitro was
156 Identification of [PP]2-InsP4 as a sensor of hyperosmotic stress opens up a new area of research for
157 rast, caffeine had no effects on melphalan-, hyperosmotic stress-, or IL-1beta-induced activation of
158 d to improve bacterial growth recovery under hyperosmotic stress, partly through stabilization of the
159 Elevated extracellular solute concentration (hyperosmotic stress) perturbs cell function and stimulat
160                                              Hyperosmotic stress, produced by addition of sorbitol to
161 nuous 6-base pair substitutions identified a hyperosmotic stress-regulated element that is GC-rich an
162 fied four major DNA-protein complexes in the hyperosmotic stress-regulated element that, by competiti
163      These results strongly suggest that the hyperosmotic stress resistance of renal inner medullary
164 nstrate a new role for Skb1 as a mediator of hyperosmotic stress response in fission yeast.
165 work reveals a novel CK2 function during the hyperosmotic stress response that promotes cell-to-cell
166 le for Skb1-related proteins as mediators of hyperosmotic stress response, as well as mechanisms invo
167 ogression with morphological changes, and in hyperosmotic stress response.
168 otein kinase (Sgk) is a new component of the hyperosmotic stress response.
169 d MEK1 are involved in the regulation of the hyperosmotic stress response.
170 lar turgor-sensing mechanisms might regulate hyperosmotic stress responses both in yeast and plants.
171 mbers, and the function of PLD activation in hyperosmotic stress responses has remained elusive.
172              Exposure of immature T-cells to hyperosmotic stress resulted in a rapid, synchronous, an
173                                              Hyperosmotic stress resulted in cell shrinking within a
174 own of storage oil and are more resistant to hyperosmotic stress, salt stress, oxidative stress, free
175                            Here we show that hyperosmotic stress signaling induced by sorbitol disrup
176          Thus, the Ran system is a target of hyperosmotic stress signaling, and cells use protein loc
177 M2-MEKK3 pathway that has been implicated in hyperosmotic stress signaling.
178                                              Hyperosmotic stress-stimulated FAK phosphorylation at Ty
179 ression of the N17 mutant of Cdc42 disrupted hyperosmotic stress-stimulated FAK Tyr-397 localization
180  the p38 MAPK signaling pathway mediates the hyperosmotic stress stimulation of sgk gene expression.
181 Cdc42 inhibits both processes in response to hyperosmotic stress, suggesting that Cdc42 has a role in
182                    For such cells to survive hyperosmotic stress, systematic genetic analysis ruled o
183 s more sensitive to ABA and more tolerant to hyperosmotic stress than wild-type plants.
184                   After a 10 min exposure to hyperosmotic stress the levels of PtdIns(3,5)P(2) rise 2
185                              In fact, during hyperosmotic stress the vacuole morphology of wild-type
186                   When cells were exposed to hyperosmotic stress, the MORN peptide redistributed from
187      Organisms, almost universally, adapt to hyperosmotic stress through increased accumulation of or
188                         These results reveal hyperosmotic stress to be a potent activator of caspase-
189          Plk3 was activated by extracellular hyperosmotic stress to directly phosphorylate c-Jun in t
190  These effects correlate with the ability of hyperosmotic stress to interfere with protein traffickin
191       In the present study, we determined if hyperosmotic stress to rat hippocampal slices activates
192 ce to translational inhibitors, and enhanced hyperosmotic stress tolerance.
193  when the transfected cells are subjected to hyperosmotic stress (total approximately 30-fold).
194 s activated through hormonal stimulation and hyperosmotic stress via a protein kinase C (PKC) delta-m
195  of activation, the response of gamma-PAK to hyperosmotic stress was examined.
196  [PP](2)-InsP(4) levels normally seen during hyperosmotic stress were attenuated by 2-(2-chloro-4-iod
197                            Plants experience hyperosmotic stress when faced with saline soils and pos
198  function of the inflammasome as a sensor of hyperosmotic stress, which is crucial for the induction

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