ライフサイエンスコーパス: resting cell

1 not a reservoir of exchangeable Ca2+ in the resting cell.

2 re rapidly from recently activated than from resting cells.

3 ssembly of the dense cortical actin found in resting cells.

4 estering NF-kappaB outside of the nucleus in resting cells.

5 ifferent microenvironments on the surface of resting cells.

6 gest that GSK-3beta is a C/EBPbeta kinase in resting cells.

7 al nuclear localization in differentiated or resting cells.

8 onal and have the potential to become stable resting cells.

9 e of DNA bound p50/p50 in the nuclei of most resting cells.

10 at the lower dNTP concentrations present in resting cells.

11 that the BCR is a monomer on the surface of resting cells.

12 smic RNP granules in the survival of G0-like resting cells.

13 by B cell receptor stimulation compared with resting cells.

14 uced apoptosis only in proliferating and not resting cells.

15 in actively growing bacterial cells than in resting cells.

16 sed proviral expression in latently infected resting cells.

17 are retained exclusively in the cytoplasm of resting cells.

18 romotes the nuclear accumulation of Stat3 in resting cells.

19 Lad and MEKK2 are in a complex in resting cells.

20 1 co-localizes with Nox1 in the membranes of resting cells.

21 se activity, and constitutive GTP binding in resting cells.

22 elevated extracellular UDP-glucose levels on resting cells.

23 ck PRAK to selected subcellular locations in resting cells.

24 racterize protein expression in HIV-infected resting cells.

25 cells but not tumor- or third-party-specific resting cells.

26 proteins that are usually not synthesized in resting cells.

27 would preclude a role for these proteins in resting cells.

28 complexes are localized to the cytoplasm of resting cells.

29 B-1 protein in activated eosinophils but not resting cells.

30 d it is maintained at a fairly high level in resting cells.

31 ntially no FcepsilonRI-Syk colocalization in resting cells.

32 the cell and increased levels of F-actin in resting cells.

33 molecules, co-precipitates with PKC-zeta in resting cells.

34 be associated with an IkappaBalpha kinase in resting cells.

35 cription factor NFkappaB in the cytoplasm of resting cells.

36 r to circular DNA, compared to extracts from resting cells.

37 h their relative stability in growing versus resting cells.

38 s the corresponding p235 immune complexes of resting cells.

39 and NF-kappaB interact in stimulated but not resting cells.

40 at lysine 27 (H3K27) of the HIV provirus in resting cells.

41 n is present both in actively cycling and in resting cells.

42 ch higher levels of protein p120 than normal resting cells.

43 tumor or proliferating cells than in normal resting cells.

44 tion factors that reside in the cytoplasm of resting cells.

45 ctivated macrophages while not affecting the resting cells.

46 associates with PRC2 in all cells, including resting cells.

47 PRC2-Ezh1 is required for its maintenance in resting cells.

48 a complex with p115RhoGEF in the cytosol in resting cells.

49 f WNK1 is localized on cytoplasmic puncta in resting cells.

50 L2 and turnover of p150(Sal2) in growing vs. resting cells.

51 o PKCdelta and induced its nuclear import in resting cells.

52 ts in thrombin-stimulated platelets, but not resting cells.

53 a t(1/2) of 29 min to a t(1/2) of 24 min in resting cells.

54 ription factors residing in the cytoplasm of resting cells.

55 g genes, even while the genes were silent in resting cells.

56 ylated proteins residing in the cytoplasm of resting cells.

57 used, reverse transcribed, and integrated in resting cells.

58 vented activated mast cells from stimulating resting cells.

59 where normal synaptic vesicles are found in resting cells.

60 sufficient levels of leukotriene to activate resting cells.

61 ibited a cytoplasmic localization pattern in resting cells.

62 In resting cells, 48% +/- 3% and 61% +/- 10% of PKCdelta an

63 In resting cells, 5-LO can accumulate in either the cytopla

64 In resting cells, a flagellar signaling component [22], the

65 p maintain low levels of cytosolic cavin1 in resting cells, a prerequisite for cavins acting as signa

66 In resting cells, a subset of caspase-3 zymogens is S-nitro

67 Compared with resting cells, activated lymphocytes take up radioactive

68 ent study, we have demonstrated that, unlike resting cells, activation of cycling human mature PBT ly

69 In resting cells, AIM2 physically interacted with and limit

70 r neoplastic B cells suggests that these are resting cells analogous to memory B cells of normal lymp

71 The half-life of rp mRNA was about 11 h in resting cells and about 8 h in exponentially growing cel

72 e shown that Fas exists in monomeric form in resting cells and aggregates upon cross-linking to form

73 in mediating microglial process dynamics in resting cells and alpha2A receptors in activated cells.

74 Forms B and C are absent in resting cells and are induced up to 20-fold after stimul

75 In general, patterns of chemotaxis in the resting cells and calcium responses in the activated cel

76 in TNF-alpha 3'UTR luciferase expression in resting cells and CARHSP1 knockdown LPS-stimulated cells

77 vely and positively regulate Lck activity in resting cells and CD45 versus TCR clustering and signali

78 Expression levels of Qa-2 were monitored in resting cells and cells stimulated with interferon-gamma

79 onas putida B2) in the pH range 6.1-8.6 with resting cells and crude cell extracts.

80 These findings show that resting cells and CSCs are irresponsive to the drug, and

81 Golgi and adjacent to the plasma membrane in resting cells and does not redistribute appreciably afte

82 ession, while E2F-1 induced DNA synthesis of resting cells and DP-1 arrested cells in G1.

83 e levels of BRCA1 gene products are found in resting cells and early G1 cycling cells and high levels

84 Using resting cells and extracts of Streptomyces clavuligerus

85 IgG BCRs are more clustered than IgM BCRs on resting cells and form larger protein islands after anti

86 ls of CtIP polypeptides, which remain low in resting cells and G(1) cycling cells, increase dramatica

87 ufficient to render MRTF-A inactive, both in resting cells and in cells with exogenously activated Rh

88 a membrane expression of the EGF receptor in resting cells and increased EGF-induced phosphorylation

89 2 negatively regulates basal IKK activity in resting cells and inhibits TNFalpha-induced cell death b

90 protein can be directly detected in infected resting cells and occurs with simultaneous loss of CD4,

91 Pase activity from both specific granules of resting cells and plasma membranes of GM-CSF-treated cel

92 sm that retains PKCdelta in the cytoplasm of resting cells and regulates its nuclear import in respon

93 stic model whereby DISC1 sequesters PDE4B in resting cells and releases it in an activated state in r

94 t yielded 10-fold less progeny from infected resting cells and serum-deprived or contact-inhibited hu

95 p47phox, which is located in the cytosol of resting cells and translocates to the plasma membrane wh

96 ly demonstrate channel-CaM preassociation in resting cells and underscore the potential of three-cube

97 p50 acetylation was detected in resting cells and was increased by TNFalpha or lipopolys

98 l-length SRAG protein levels were highest in resting cells and were reduced in proliferating cells.

99 S) does so at the low levels of free Ca2+ in resting cells and when almost all Ca2+ is chelated in ce

100 PE is generally sequestered inside a normal resting cell, and the mechanism by which circulating ant

101 n interactions are present on the surface of resting cells, and antigen activation induces these to c

102 ndoplasmic reticulum Ca(2+) concentration in resting cells, and for the refilling of Ca(2+) stores af

103 Fodrin has a highly punctate distribution in resting cells, and insulin causes a dramatic remodeling

104 From A exists in resting cells, and its activity is increased threefold a

105 cytoskeleton may stabilize NADPH oxidase in resting cells, and its binding of PtdIns (3)P potentiate

106 ar Tat distributed widely, entered nuclei of resting cells, and specifically transactivated the HIV L

107 fector Th cells may differ from the level on resting cells, and that a change in receptor expression

108 ocalized to the nucleus in differentiated or resting cells, and to the cytoplasm in advanced tumor ce

109 nsible for their subcellular localization in resting cells; and 3) the N-terminal folding domain of E

110 of phospho-Thr(286)-alphaCaMKII can occur in resting cells (approximately 100 nM [Ca(2+)]).

111 When resting cells are induced to proliferate, the steady-sta

112 ation increases as pH(i) rises, such as when resting cells are induced to proliferate.

113 step is performed because it is thought that resting cells are resistant to transduction by lentivira

114 actors are increased transiently when normal resting cells are stimulated to proliferate.

115 le for up to 12 h, [gamma-(32)P]ATP added to resting cells as a radiotracer was completely degraded w

116 ferentiation, later forming a stable pool of resting cells as viral load decreases during chronic inf

117 th assays, neutralization was greater in the resting-cell assay than in the blast assay on day 7, but

118 ary isolates was 25 to 30 times lower in the resting-cell assay than in the PBMC blast assay.

119 hemagglutinin 1 day after virus inoculation (resting-cell assay) or 2 days prior to virus inoculation

120 e of antibody was delayed 2 to 3 days in the resting-cell assay.

121 lates replicated poorly or not at all in the resting-cell assay.

122 e activity of the reductive dehalogenases in resting cell assays of strain CBDB1 with brominated arom

123 ocalized uniformly on the plasma membrane of resting cells, at active protrusions and cell-cell conta

124 n I kappa B alpha exists in the cytoplasm of resting cells bound to the ubiquitous transcription fact

125 The oxidase is dormant in resting cells but acquires activity when the cells are s

126 The enzyme is dormant in resting cells but becomes active when the cells are expo

127 ATM exists in an inactive state in resting cells but can be activated by the Mre11-Rad50-Nb

128 -affinity conformation of LFA-1 is mobile on resting cells but immobile on phorbol-12-myristate-13-ac

129 e-3 is a Ser/Thr kinase, tonically active in resting cells but inhibited by phosphorylation of an N-t

130 This multicomponent enzyme is dormant in resting cells but is activated on exposure of the cells

131 typically 'resting' cells that, unlike truly resting cells, but like the first cells mainly infected

132 abilized monoubiquitylated p53, generated in resting cells by basal levels of Mdm2-type ligases, is s

133 ha(q) x Gbetagamma complexes are observed in resting cells by fluorescence resonance energy transfer

134 ctor complex that is negatively regulated in resting cells by its physical assembly with a family of

135 clear factor-kappaB (NF-kappaB) signaling in resting cells by targeting NF-kappaB-inducing kinase (NI

136 on, Sin was constitutively phosphorylated in resting cells by the Src kinase Fyn and bound to signali

137 logy of the three subunits at the surface of resting cells can be best described by a "triangular mod

138 found in resting CD4+ T cells even when the resting cell compartment was analyzed with assays that d

139 ghly up-regulated in activated compared with resting cells, concomitant with an increase in KCa curre

140 ne consequence of the weaker binding is that resting cells containing these mutants show incomplete i

141 sites, but, unlike the complex that typifies resting cells, cyclin A and CDK2 are also present.

142 Although absent in resting cells, cytoplasmic tristetraprolin protein was d

143 Ultrastructural analysis of resting cells demonstrated that rough endoplasmic reticu

144 ficant portion (50%) of basal proton leak in resting cells depended on UCP2.

145 vitro LPS activation into the cycle, because resting cells did not divide.

146 Although resting cells did not express Hili, its expression was r

147 In resting cells, eIF4E-binding protein 1 (4E-BP1) binds to

148 Pbeta prevented C/EBPbeta phosphorylation in resting cells, enhanced C/EBPbeta DNA binding, and led t

149 ation following receptor stimulation, but in resting cells, eNOS is tonically inhibited by its intera

150 Resting cell experiments showed that methane production

151 pproaches show that both SH-SY5Y and SK-N-AS resting cells express comparable levels of DFF40/CAD.

152 Further analysis reveals that while resting cells express only SHIP, B cell blasts also expr

153 endently of the cytokine milieu, although on resting cells, expression was maintained preferentially

154 In resting cells, Fc gammaRI colocalized with the Src famil

155 Akinetes are spore-like resting cells formed by certain filamentous cyanobacteri

156 In resting cells G beta gamma localized predominantly at th

157 These data suggest that resting cells have a [Ca2+] gradient with [Ca2+]pm > [Ca

158 Resting cells have few assembled microtubules.

159 In resting cells, HK-ATPase is contained within cytoplasmic

160 In resting cells, however, only about half was associated w

161 on overexpression studies suggested that in resting cells, human PLD1 localized primarily to the Gol

162 alpha was found to associate with FLIP(S) in resting cells in a manner dependent on the ATP-binding N

163 levels were elevated 10-20-fold relative to resting cells in contrast to the other isoforms.

164 accinia virus is significantly attenuated in resting cells in vitro and demonstrates tumor-specific r

165 ising ability of SIV and HIV to replicate in resting cells in vivo, in contrast to propagation of inf

166 of 5-lipoxygenase can be rapidly altered in resting cells, independent of 5-lipoxygenase activation.

167 rai1-YFP results in a high degree of FRET in resting cells, indicating that Orai1 exists as a multime

168 To better understand the kinetics by which resting cell infection (RCI) is established, we develope

169 eservoir of resting CD4(+) T-cell infection (resting cell infection [RCI]).

170 The frequency of resting cell infection was stable before addition of enf

171 stimulation, lymphocytes develop from small resting cells into highly proliferative and secretory ce

172 In resting cells, Irbit was sequestered by InsP3 receptors

173 In resting cells, IRF8 was mainly bound to composite sites

174 ese findings suggest that the contour of the resting cell is not normally dependent on the elasticity

175 he positioning of 5-LO within the nucleus of resting cells is a powerful determinant of the capacity

176 The survival of these resting cells is also dependent upon autophagy, a membra

177 B-dependent nuclear accumulation of Stat3 in resting cells is independent of tyrosine phosphorylation

178 ct that the turnover of free IkappaBalpha in resting cells is S293-dependent.

179 ction of p40(phox), which binds p67(phox) in resting cells, is incompletely understood.

180 n shares considerable homology with NEMO, in resting cells, it is not present in the high-molecular-w

181 Ca(2+)](SR) that is close to that present in resting cells, it is possible that the activator-inhibit

182 umenal GFP fusion protein and shown that, in resting cells, large molecules can rapidly diffuse acros

183 dies targeting circRNAs have been limited to resting cells, leaving their role in dynamic cellular re

184 (10 microM) mimicked the effects of DEA/NO (resting cell length and time to 50 % relaxation were 100

185 ng level of intracellular calcium falls, the resting cell length increases and the amplitude of short

186 ncreased (11.6 +/- 0.5% versus 10.2 +/- 0.6% resting cell length), whereas the time to peak shortenin

187 (DEA/NO, 10 microM) significantly increased resting cell length, reduced twitch amplitude and accele

188 women, in association with a 14% increase in resting cell length.

189 1 hour of linear pulsatile stretch (110% of resting cell length; 3 Hz), expression of connexin43 (Cx

190 s of HIV transcripts are detectable in these resting cells, little to no viral protein is produced, r

191 Both GRB2-SH3 and SH2 domains bind CBL in resting cell lysates; upon Fc gammaRI stimulation, phosp

192 unaltered, suggesting that UCP2 function in resting cells may be concerned with the control of ATP p

193 wide range of hypoxia at different levels of resting cell membrane potential (Em ).

194 nses to a wide range of hypoxia at different resting cell membrane potential (Em ).

195 In contrast to resting cells, mitogen-activated macrophages, NK cells,

196 In resting cells, most of the eNOS is localized at the cell

197 In resting cells, Munc18-2, but not STX3, interacted with t

198 Instead, we made a novel discovery that in resting cells myoferlin was bound to EHD2 protein and wh

199 ion from an infected resting cell to another resting cell nearby.

200 However, in the resting cell, net flux through the transporter is often

201 In resting cells, NF-kappa B is retained as an inactive cyt

202 We propose that, in resting cells, NFAT is targeted to a region of the calci

203 In resting cells, NFAT proteins are heavily phosphorylated

204 ed stoichiometrically to 4-fluorobenzoate by resting cells of strain KZ-4, compatible with a reductiv

205 Resting cells of VC1 degraded NQ effectively (54 mumol h

206 ole in the ring expansion of penicillin G by resting cells or cell-free extracts.

207 In a resting cell, our results support a model where RhoA is

208 We found that in resting cells p53 is present in a mix of oligomeric stat

209 In resting cells, PDK1(A280V) localized in the cytosol and

210 Live confocal imaging revealed that in resting cells, PH-GFP is localized predominantly on the

211 ate that vaccinia-related kinase 1 (VRK1) in resting cells plays an important role in the formation o

212 constitutively activated GTP-bound state in resting cells, possibly because of impaired GTPase activ

213 ly regulated in peripheral T cells such that resting cells predominantly express the larger CD45 isof

214 of cysteinyl leukotriene type I receptors on resting cells prevented them from responding to the para

215 t the pre-BCR is expressed on the surface of resting cells primarily in a nonaggregated state.

216 However, activating resting cells prior to transduction alters their physiol

217 depressed all the responses without altering resting cell properties.

218 localization of the Rho family G proteins in resting cells; Rac isoforms partially exist as a GDI-fre

219 Upon exposure to gamma radiation, resting cells rapidly underwent apoptotic death.

220 ration or to a phenotypic change of existing resting cells remains controversial.

221 the high homeostatic turnover of IkappaB in resting cells renders the NF-kappaB system remarkably re

222 IFRD1 mRNA instability in resting cells requires translation of an upstream open r

223 It is generally believed that NFAT in resting cells resides in the cytoplasm, and its nuclear

224 HSPA1B expression following heat shock or in resting cells, respectively.

225 CSF-stimulated neutrophils with cytosol from resting cells resulted in a time- and temperature-depend

226 Conversely, addition of [gamma-(32)P]UTP to resting cells resulted in transient formation of [gamma-

227 In the resting cell, RhoA suppresses Cdc42 activation, IkappaBa

228 In resting cells, RIG-I is maintained as a monomer in an au

229 terminal RyR2 domains, we determined that in resting cells, RyR2 interdomain interaction remained una

230 In resting cells, SNAP-25 is at the apical plasma membrane

231 In resting cells, STATs, including Stat3, reside largely in

232 In resting cells, STIM1 diffusion is Brownian, while Orai1

233 llel with viral clearance, but a spectrum of resting cell subsets reflecting the pattern at the peak

234 1 to initiate its productive growth cycle in resting cells, such as latently infected neurons.

235 c genes that were previously up-regulated in resting cells, suggesting a potential new mechanism by w

236 mal naive VH3 IgM and IgD mRNA repertoire in resting cells supports the prospect that with proper sti

237 thraquinone-2,6-disulfonate, and fumarate by resting cell suspensions and to be essential for growth

238 Analyses of metabolites in spent media and resting cell suspensions confirmed that CBB5 initially N

239 ing the tetrapyrrole pigments accumulated by resting cell suspensions of R. sphaeroides, we demonstra

240 d for the study of the behaviour of EEI with resting cell suspensions of Saccharomyces cerevisiae.

241 The addition of 25 mM NaCl to resting cell suspensions stimulated ATP synthesis driven

242 idize formaldehyde, which was confirmed with resting cell suspensions.

243 logical and genetic manipulations we find in resting cells that both Gli2 and Smo appear to shuttle i

244 an oxidase subunit located in the cytosol of resting cells that during oxidase activation migrates to

245 pathway leading to basal Ly49E expression in resting cells that is induced by Pro2-mediated Ly49e tra

246 ssion from integrated proviruses occurred in resting cells that lacked surface CD4, likely resulting

247 Subcellular fractions of resting cells that were positive for immunoreactive PIKf

248 vated but were instead immunophenotypically 'resting' cells that, unlike truly resting cells, but lik

249 In resting cells the B-cell surface antigen CD20 is associa

250 In untransformed, resting cells, the ARE targets GM-CSF mRNA for rapid deg

251 In resting cells, the level of p27Kip1 provides an inhibito

252 In resting cells, the majority of OSR1, like WNK1, is on cy

253 In resting cells, the NFAT1 transcription factor is kept in

254 In resting cells, the preexisting nuclear RelA has already

255 In resting cells, the protein is present in the cytoplasm,

256 consensus TEFRE, is regulated by TEF in the resting cell; the second class, represented by icerTEFRE

257 Steady state ATP release was measured in resting cells; then mechanical stimulation was delivered

258 Our results indicate that in resting cells there is a pool of activated PKC near the

259 level of bona fide NFkappaB activity in most resting cells, this interaction between Sp-factors and k

260 oken chains of transmission from an infected resting cell to another resting cell nearby.

261 -IX shifts from the membrane skeleton of the resting cell to the cytoskeleton of the activated cell i

262 fe of nucleolin mRNA increased from 1.8 h in resting cells to 3.2 h with phorbol ester activation, su

263 ffuse pattern with a few small aggregates in resting cells to large isolated clusters after antigen s

264 viruses exploit the greater availability of resting cells to maintain unbroken chains of transmissio

265 de exchange factor located in the cytosol of resting cells, translocated to the plasma membranes of s

266 f CD45 exon 4 in the final mRNA; however, in resting cells, TRAP150 binds PSF and prevents access to

267 In resting cells, TRPC3 exists in TRPC3-H1b/c-IP(3)Rs compl

268 Although uPAR co-caps with CR3 on resting cells, uPAR was found to dissociate or "uncap" c

269 Finally, resting cell volume of glaucomatous TM cells was found t

270 was monitored using immunoblot analysis, and resting cell volume was measured by forward light scatte

271 Similar effects of AQP1 expression on resting cell volume were observed in TM monolayers.

272 volume decrease (RVD) and the resumption of resting cell volume.

273 ity in the partitioning of these proteins in resting cells was confirmed by immunoelectron microscopy

274 CAD in resting cells was cytosolic and unphosphorylated.

275 -state rate of ERK entry into the nucleus in resting cells was energy-independent and greater than th

276 First, CTLA-4 engagement on resting cells was found to indirectly block ICOS costimu

277 Interestingly, the DNA methylation status of resting cells was highly predictive of transcriptional c

278 The absence of puncta in resting cells was required to prevent spontaneous store

279 the quantitative distribution of calponin in resting cells was statistically indistinguishable from t

280 In resting cells, WASP exists in a complex with WIP, which

281 ATP concentrations on resting cells were 1-10 nm.

282 st frequencies of spontaneous Ca2+ sparks in resting cells, were denoted 'eager sites'.

283 hosphorylated and reside in the cytoplasm of resting cells; when cells are stimulated by a rise in in

284 y decreased biotin production by B. subtilis resting cells whereas a strain having a cerulenin-resist

285 exist as a GDI-free pool at the membrane of resting cells, whereas RhoA is trapped in the cytosol by

286 tudies show that CR3 associates with uPAR on resting cells, whereas uPAR associates with CR4 at lamel

287 DNA polymerase prevent viral replication in resting cells, which contain low dNTP concentrations, bu

288 In resting cells, which make essentially no cytokines, the

289 ed the formation of LC3(+) autophagosomes in resting cells, while other isoforms promoted autophagoso

290 lating their availability and/or activity in resting cells, while Sin is required for targeting these

291 utively expressed and predominates in normal resting cells, while Type II is selectively up-regulated

292 hosts, they survive and rapidly become small resting cells with a memory phenotype.

293 he persisting T cells were exclusively small resting cells with a memory phenotype: CD44high CD62L+/-

294 Methanogenesis by resting cells with pyruvate as the electron donor was al

295 In resting cells, Y(216) phosphorylation was restricted to