ライフサイエンスコーパス: GCR

1 GCR and mercuric reductase activities were assayed using

2 GCR binding affinity was significantly reduced after inc

3 GCR correlates positively with parasitemia and is negati

4 GCR expression by CD8+ T cells from small airways correl

5 GCR expression by CD8+ T cells from small airways correl

6 GCR methylation was not associated with particulate air

7 GCR suppression by Rad5 and Rad18 appears to be exerted

8 GCR types in helicase double mutants include telomere ad

9 GCRs and CNVs underlie human genomic disorders and are a

10 GCRs are therefore likely to be produced through the res

11 GCRs are thought to be triggered by DNA double strand br

12 ng a transgene containing a PTC to trigger a GCR.

13 termination codon (PTC) promptly triggers a GCR that involves Upf3a and components of the COMPASS co

14 etylation and glucocorticoid receptor alpha (GCR alpha) translocation were evaluated.

15 GCR-beta mRNA levels; have a lower GCR-alpha/GCR-beta mRNA ratio; are less responsive to suppression

16 ation for 48 h failed to significantly alter GCR binding affinity in nonasthmatic, atopic individuals

17 ogen-induced kinase phosphatase 1, IL-8, and GCR-beta mRNA levels; have a lower GCR-alpha/GCR-beta mR

18 d no significant difference in GCR alpha and GCR beta mRNA expression were observed in both T-cell ty

19 e, i.e. the histamine synthesis enzyme), and GCR (glucocorticoid receptor), were confirmed by quantit

20 milarly, an association between response and GCR on peripheral-blood blasts was noted after standard-

21 ociated with anti-inflammatory responses and GCR agonists are widely used to treat inflammatory disea

22 ments revealed that phosphorylated STAT5 and GCR formed immune complexes.

23 w, rather than alternatives, ultraviolet and GCR are likely to be modulating Neptune's atmosphere in

24 , we assessed the same control variables and GCR in 79 subjects who were subsequently exposed to a rh

25 We conclude that large deletions and GCRs are due to excessive processing of DSBs, while most

26 reduces the frequency of large deletions and GCRs at both interstitial and subtelomeric DSBs, but has

27 t US28 is an early gene, while US27 (another GCR) is a late gene.

28 (GCR) inhibitor RU486 and a monoclonal anti-GCR, suggesting that it was mediated by a membrane (m) G

29 pair that generates point mutations to avoid GCRs and cell death during the first round of replicatio

30 ative technology solution for a ground-based GCR simulator at the NSRL to accelerate our understandin

31 The major transcript bearing GCR sequences is bicistronic, harboring coding sequences

32 Both GCR and ultraviolet mechanisms may occur more rapidly th

33 pG2 nuclear extracts that is supershifted by GCR antibody, demonstrating that this enhancer is an aut

34 screens to identify and prioritize candidate GCR-suppressing genes on the basis of the shared drug se

35 Here 2 S. cerevisiae GCR assays were used to screen a targeted collection of

36 Here multiple Saccharomyces cerevisiae GCR assays and query mutations were crossed into arrays

37 he effects of NTEs in predictions of chronic GCR exposure risk.

38 the transactivating activity of the classic GCR, termed GCR-alpha.

39 the transactivating activity of the classic GCR.

40 oth muscle fibre types expressed a cytosolic GCR.

41 the functional significance of the decreased GCR-binding affinity, monocytes were pretreated with and

42 hreatening stressful experience demonstrated GCR; and those with GCR were at higher risk of subsequen

43 y virtue of its ability to induce diminished GCR-binding affinity, may contribute to impaired GC resp

44 other cytokines could also induce diminished GCR-binding affinity.

45 Some researchers argue that enhanced GCR flux might lead to a climatic cooling by increasing

46 study 1, we assessed stressful life events, GCR, and control variables including baseline antibody t

47 In all of these species we find GCR expressed by the Muller glia.

48 We developed a simple and rapid assay for GCRs, exploiting yeast artificial chromosomes (YACs) in

49 iNOS, and the glucocorticoid receptor gene, GCR, was measured by quantitative polymerase chain react

50 B in H2AX "knockdown" cells did not generate GCRs, repair of a single engineered DNA DSB in fibroblas

51 nealing, and are therefore prone to generate GCRs.

52 e H2ax deficiency, cells no longer generated GCRs following a single engineered DNA DSB.

53 formation of either spontaneously generated GCRs or those induced by treatments with different DNA d

54 h the same controls used in study 1, greater GCR predicted the production of more local proinflammato

55 for PCNA and histone H2B, respectively, have GCR-supporting activities.

56 ele encoding H(217) are associated with high GCR, while high plasma lysophosphatidylcholine levels ar

57 othesis that allergen-induced alterations in GCR binding affinity were cytokine-induced, we examined

58 nhibition of allergen-induced alterations in GCR binding affinity.

59 riodicity was detected both at Earth, and in GCR measured by Voyager 2, then near Neptune.

60 anslocation and no significant difference in GCR alpha and GCR beta mRNA expression were observed in

61 e COMPASS complex including wdr5 function in GCR.

62 growth defects and synergistic increases in GCR rates when combined with mutations affecting other D

63 ens avenues for therapeutic interventions in GCR diseases.

64 ition 5 and high (>/= median) methylation in GCR.

65 eriodicity, which occurred preferentially in GCR (not ultraviolet) during the mid-1980s.

66 The inactivation of Rad1 or Rad10 in GCR mutator strains also slightly enhanced methyl methan

67 These allergen-induced reductions in GCR binding affinity also rendered the PBMC less sensiti

68 uggesting that prolonged stressors result in GCR, which, in turn, interferes with appropriate regulat

69 t REV1 deficiency causes a major increase in GCRs.

70 Treatments that increase GCR in these lymphocyte subsets may improve graft surviv

71 IS) genes in which mutations cause increased GCR rates and 38 candidate eGIS genes that encode eGIS1

72 genes in which mutations can cause increased GCR rates are not well understood.

73 to identify mutations that caused increased GCR rates.

74 tlc1 and est2 mutants did not have increased GCR rates, but their telomeres could be joined to other

75 tants with small but significantly increased GCR rates.

76 on in RAD51 or TOP1 suppressed the increased GCR rates and/or the growth defects of rnh203Delta doubl

77 (HRS) pathway genes suppressed the increased GCR rates seen in asf1 mutants, which was independent of

78 f mutants to identify progeny with increased GCR rates.

79 t harbor truncated Brca2 spontaneously incur GCRs and genomic DNA breaks during division.

80 The cell target of IL-13-induced GCR effects was studied and found to reside in the non-T

81 d to be steroid sensitive, i.e., DEX induced GCR nuclear translocation.

82 Normal DEX-induced GCR alpha nuclear translocation and no significant diffe

83 and NFkappaB inhibition reverted TNF-induced GCR, which is in support of a cofactor reshuffle model.

84 In many instances, GCRs inactivate tumour-suppressor genes or generate nove

85 Finally, we found that foldback inversion GCRs were stabilized by secondary rearrangements, mostly

86 The 5' end of K14/GCR mRNA maps to nucleotide (nt) 127848, and its poly(A)

87 30546; a 149-nt intron is present in the K14/GCR intergenic region.

88 on and similar genetic interactions as known GCR suppressors.

89 we have examined the expression of the KSHV GCR gene in virus-infected lymphoid cells and in KS tumo

90 These results suggest that the KSHV GCR is translated by unconventional mechanisms involving

91 ct of relative drug insensitivity and of low GCR on peripheral blasts.

92 atidylcholine levels are associated with low GCR in the second study year.

93 IL-8, and GCR-beta mRNA levels; have a lower GCR-alpha/GCR-beta mRNA ratio; are less responsive to su

94 sting that it was mediated by a membrane (m) GCR.

95 or the RAD10 gene reduced GCR rates in many GCR mutator strains.

96 otein (RFA1) increase microhomology-mediated GCR formation.

97 k' for participating in duplication-mediated GCRs generated by homologous recombination.

98 nd one that suppresses non-homology-mediated GCRs (RAD50/MRE11/XRS2).

99 Rs: two that suppress microhomology-mediated GCRs (RFA1 and RAD27) and one that suppresses non-homolo

100 Extensive searches for monocistronic GCR mRNAs using nuclease mapping and reverse transcripti

101 ting the first operational run using the new GCR simulator.

102 No GCRs were detected despite dramatic decreases in spore v

103 glucocorticoid receptor (GCR) beta, but not GCR-alpha, was significantly increased in PBMCs of SR as

104 Activation of GCR signaling inhibits the formation of MGPCs and antago

105 nophil death, 2) supported the dependence of GCR phosphorylation on PP5 activity, and 3) revealed tha

106 kines (IFNgamma/TNFalpha), and expression of GCR were determined in lymphocytes subsets from cultured

107 okines (IFNgamma/TNFalpha) and expression of GCR were determined in lymphocytes subsets from cultured

108 We conclude that increased expression of GCR-beta is cytokine inducible and may account for GC in

109 ine TNF-alpha (TNF) induces an acute form of GCR, not only in mice, but also in several cell lines: e

110 ion distinct from these other major forms of GCR formation.

111 ences are available have close homologues of GCR, suggesting that there is more to be learned about t

112 The importance of GCR is further supported by the response of Neptune's at

113 By contrast, we find that inhibition of GCR signaling stimulates the formation of proliferating

114 ranzyme B, IFNgamma, TNFalpha, and a loss of GCR from these lymphocyte subsets was also found in BOS.

115 granzyme b, IFNgamma, TNFalpha and a loss of GCR from these lymphocyte subsets was also found in BOS.

116 This mechanism of GCR opens avenues for therapeutic interventions in GCR d

117 propose that the functions and mechanisms of GCR signaling are highly conserved and are mediated thro

118 A number of GCR isoforms are created from the same pre-mRNA transcri

119 ciated with a significantly higher number of GCR-beta-immunoreactive cells in peripheral blood than G

120 e primary amino acid sequence and pattern of GCR expression in the retina is highly conserved across

121 Given the conserved expression pattern of GCR in different vertebrate retinas, we propose that the

122 In this assay, the rate of GCR formation was increased 600-5, 000-fold by mutations

123 e-wide pool of mutants for elevated rates of GCR.

124 The restriction of GCR expression to the lytic cycle has important implicat

125 This association may lead to retardation of GCR nuclear translocation because IL-2 was not able to i

126 factors that control alternative splicing of GCR pre-mRNA are of great importance.

127 Rad1-Rad10 functions at different stages of GCR formation and that there is an alternative pathway f

128 onstrated many mechanisms for suppression of GCR formation in yeast.

129 onded normally with nuclear translocation of GCR in response to steroids, but failed to translocate G

130 reases the de novo telomere addition type of GCR.

131 To further our understanding of GCR formation, we have developed a novel mutator assay i

132 evisiae does not prevent the accumulation of GCRs, and interestingly, its loss causes subunit-specifi

133 eriphery causes substantial accumulations of GCRs and elevated sumoylation of most proteins except fo

134 ever, pathways that promote the formation of GCRs are not as well understood.

135 DNA damage while promoting the formation of GCRs.

136 0 heterodimer and monitored the formation of GCRs.

137 arted forks contributes to the generation of GCRs and gene amplification in cancer, and to non-recurr

138 methanesulfonate increased the induction of GCRs compared with that seen for a wild-type strain.

139 Moreover, the breakpoint junctions of GCRs from these GCR mutator mutants were determined with

140 nactivate these pathways cause high rates of GCRs and show synergistic interactions, indicating that

141 c28 is required for formation or recovery of GCRs.

142 studying genes implicated in suppression of GCRs in other studies, we found that inverted repeat fus

143 repair (PRR) pathways in the suppression of GCRs, checkpoint function, sensitivity to hydroxyurea (H

144 e proteins functioning in the suppression of GCRs.

145 the rate of accumulating different types of GCRs including translocations and deletion of chromosome

146 eptune's brightness suggests nucleation onto GCR ions.

147 d lead to diverse outcomes (proper repair or GCR formation) through different regulation of DNA repai

148 rearranges to form a translocation and other GCRs.

149 In vitro effects of allergen on PBMC GCR Kd were also examined by incubating PBMC from atopic

150 ive dosimetry; however, the ever penetrating GCR will continue to pose the most significant health ri

151 Multiple pathways that prevent GCRs, including S-phase cell cycle checkpoints, homologo

152 ination repairs, has a novel role to produce GCRs.

153 In a screen for genes that promote GCR, we identified MPH1, which encodes a 3'-5' DNA helic

154 s (DSBs), which suggests that Mph1p promotes GCR by partially suppressing HR.

155 Therefore, Mph1p promotes GCR formation by partially suppressing HR, likely throug

156 GRE half-site 1) specifically binds purified GCR, 2) can displace binding of the GCR to a consensus G

157 We purified GCR from Halobacterium sp. NRC-1 and identified the sequ

158 the difficulty in reliably using qualitative GCR assays to detect mutants with small but significantl

159 of radiation from galactic cosmic radiation (GCR) and the possibility of a large solar particle event

160 cose production, and glucose clearance rate (GCR).

161 h either ultraviolet or galactic cosmic ray (GCR) effects on atmospheric particles.

162 n important concern for galactic cosmic ray (GCR) exposures, which consist of a wide-energy range of

163 d causes an increase in galactic cosmic ray (GCR) flux.

164 t of only minimal germinal center reactions (GCR) in Peyer's patches and more robust GCR in mesenteri

165 hanges indicating germinal center reactions (GCRs) and the activation of CD4(+) T cells in PP were de

166 Gross chromosomal rearrangement (GCR) is a type of genomic instability associated with ma

167 g increased gross chromosomal rearrangement (GCR) rates in Saccharomyces cerevisiae are hampered by t

168 s leads to gross chromosomal rearrangements (GCR).

169 and induces gross chromosome rearrangements (GCR).

170 to induce gross chromosomal rearrangements (GCRs) and copy-number variations (CNVs).

171 Gross chromosomal rearrangements (GCRs) are frequently observed in many cancers.

172 Gross chromosomal rearrangements (GCRs) are large scale changes to chromosome structure an

173 Gross chromosomal rearrangements (GCRs) have been observed in many cancers.

174 tions, and gross chromosomal rearrangements (GCRs) in sch9Delta mutants is associated with increased

175 ulation of gross chromosomal rearrangements (GCRs) is characteristic of cancer cells.

176 generates gross chromosomal rearrangements (GCRs) mediated by foldback inversions combined with whol

177 Gross Chromosomal Rearrangements (GCRs) play an important role in human diseases, includin

178 Gross chromosomal rearrangements (GCRs) play an important role in human diseases, includin

179 pontaneous gross chromosomal rearrangements (GCRs) seem to result from DNA-replication errors.

180 arise from gross chromosomal rearrangements (GCRs) such as translocations, which involve genetic exch

181 increased gross chromosomal rearrangements (GCRs) that are frequently observed in many cancers.

182 accumulate gross-chromosomal rearrangements (GCRs) that are suppressed by the DNA damage checkpoint a

183 acterizing gross chromosomal rearrangements (GCRs) to analyze genome instability in post-senescent te

184 ression of gross chromosomal rearrangements (GCRs), DNA repair, modification of chromatin, and proper

185 cumulating gross chromosomal rearrangements (GCRs), including translocations and deletions containing

186 t types of gross chromosomal rearrangements (GCRs), including translocations, interstitial deletions,

187 Gross chromosomal rearrangements (GCRs), including translocations, inversions amplificatio

188 ression of gross chromosomal rearrangements (GCRs), indicating that Cdc28 is required for formation o

189 ulation of gross chromosomal rearrangements (GCRs), such as translocations, deletion of a chromosome

190 rmation of gross chromosomal rearrangements (GCRs).

191 ncrease in gross chromosomal rearrangements (GCRs).

192 ed to form gross chromosomal rearrangements (GCRs).

193 y cause of gross chromosomal rearrangements (GCRs).

194 preventing gross chromosomal rearrangements (GCRs); however, relatively little is known about the rol

195 letions and gross chromosome rearrangements (GCRs) than interstitial DSBs, but found no difference in

196 Gross chromosome rearrangements (GCRs), such as translocations, deletion of a chromosome

197 ive rise to gross chromosome rearrangements (GCRs), which can result in disease/death.

198 e changes (gross chromosomal rearrangements [GCRs]) are common in genomes, and are often associated w

199 (KSHV) encodes a G-protein-coupled receptor (GCR) homolog.

200 of the rhodopsin G-protein coupled receptor (GCR) superfamily.

201 Alternative splicing of the GC receptor (GCR) pre-mRNA generates a second GCR, termed GCRbeta, wh

202 The expression of glucocorticoid receptor (GCR) beta, but not GCR-alpha, was significantly increase

203 cts of allergens on glucocorticoid receptor (GCR) binding affinity and glucocorticoid (GC) responsive

204 ated with IL-2, the glucocorticoid receptor (GCR) does not translocate to the cell nucleus after dexa

205 so showed a loss of glucocorticoid receptor (GCR) in pro-inflammatory lymphocytes following transplan

206 so showed a loss of glucocorticoid receptor (GCR) in proinflammatory lymphocytes after transplant.

207 was blocked by the glucocorticoid receptor (GCR) inhibitor RU486 and a monoclonal anti-GCR, suggesti

208 n the inhibition of glucocorticoid receptor (GCR) nuclear translocation in response to dexamethasone

209 Glucocorticoid receptor (GCR) number and the effective concentration of dexametha

210 Glucocorticoid receptor (GCR) signaling is commonly associated with anti-inflamma

211 tion of the nuclear glucocorticoid receptor (GCR).

212 functional role of glucocorticoid receptor (GCR)beta (a splicing variant, and dominant negative inhi

213 has homology to G protein-coupled receptors (GCR).

214 ed transcriptional effects via GC receptors (GCR), there is increasing evidence that GCs also initiat

215 of either the RAD1 or the RAD10 gene reduced GCR rates in many GCR mutator strains.

216 n (HR) proteins or the helicase Srs2 reduces GCR rates elevated by the rad5 or rad18 mutation.

217 ontribute to poor asthma control by reducing GCR binding affinity in mononuclear cells.

218 Bis-gamma-glutamylcystine reductase (GCR) is an orphan protein that was purified in 1988.

219 ver, we show that the global control region (GCR) long-range enhancer spatially colocalises with the

220 tory DNA element, the global control region (GCR), which regulates gene expression over distances of

221 Glucocorticoid resistance (GCR) is defined as an unresponsiveness to the therapeuti

222 sults in glucocorticoid receptor resistance (GCR) that, in turn, results in failure to down-regulate

223 The genetic compensation response (GCR) has recently been proposed as a possible explanatio

224 ment of eosinophils with lipoxin A4 restored GCR phosphorylation and the proaptoptotic function of GC

225 Resulting GCRs and CNVs are proposed to contribute to cancer devel

226 io of gametocyte to asexual-committed rings (GCR) varies widely (0-78%).

227 The enzyme had robust GCR activity but no mercuric reductase activity.

228 ons (GCR) in Peyer's patches and more robust GCR in mesenteric lymph nodes.

229 tor (R) pre-messenger RNA generates a second GCR, termed GCR-beta, which does not bind GCs but antago

230 C receptor (GCR) pre-mRNA generates a second GCR, termed GCRbeta, which does not bind GC but antagoni

231 that approximates the primary and secondary GCR field experienced at human organ locations within a

232 lower glycemic response, because of a slower GCR.

233 RE half-sites or point mutations at specific GCR binding sites eliminates dexamethasone inducibility,

234 Spontaneous GCRs are rare in Saccharomyces cerevisiae; however, the

235 This "SSA-GCR" pathway is likely to be important in the repair of

236 ese findings demonstrate that clonal, stable GCRs can be produced by a single engineered DNA DSB in H

237 had ablated H2ax did produce clonal, stable GCRs, including balanced translocations and megabase-pai

238 ation with M. morganii was able to stimulate GCRs anew, leading to a specific IgA antibody response.

239 We found that SFB stimulated GCRs in PP from day 6 after monoassociation, that GCRs o

240 ast, multiple pathways cooperate to suppress GCR.

241 nt and the mitotic exit network can suppress GCRs in strains containing defects that increase the GCR

242 t least three distinct pathways can suppress GCRs: two that suppress microhomology-mediated GCRs (RFA

243 , indicating that the pathways that suppress GCRs all compete for the same DNA substrates.

244 ling, and telomere maintenance that suppress GCRs have been identified.

245 knowledge of other pathway(s) that suppress GCRs, we developed a generally applicable genome-wide sc

246 wo GIS genes were identified that suppressed GCR formation.

247 ng the number of origins on a YAC suppresses GCR formation in our dpb11 mutant but enhances it in our

248 ca2 has an essential function in suppressing GCR formation after chromosome breakage.

249 th DNA mismatch repair (MMR) for suppressing GCRs and for suppressing recombination between divergent

250 tivating activity of the classic GCR, termed GCR-alpha.

251 messenger RNA generates a second GCR, termed GCR-beta, which does not bind GCs but antagonizes the tr

252 We conclude that GCR signaling directly inhibits the formation of MGPCs,

253 rch, we present new geological evidence that GCR flux change had a greater impact on continental clim

254 In the chick retina, we find that GCR is expressed by progenitors in the circumferential m

255 in PP from day 6 after monoassociation, that GCRs only gradually waned over the entire length of colo

256 h increased genome instability suggests that GCRs are actively suppressed.

257 The GCR provides an explanation for the colinear genetic lin

258 The GCR simulator exposes state-of-the art cellular and anim

259 The GCR-promoting activity of Mph1p appears to depend on its

260 additional nongenomic effects of DM and the GCR on resting human T cells, inducing Lck and downstrea

261 of a chromatin loop between 5' HoxD and the GCR regulatory module at the time and place of distal li

262 e family contains an enhancer that binds the GCR and that this binding is critical to transcriptional

263 ls was dependent on the presence of both the GCR and the CD45 molecule.

264 In contrast, the GCR in IL-4-stimulated HT-2 cells does translocate into

265 that there is an alternative pathway for the GCR formation that is independent of Rad1-Rad10.

266 rovide a potential mechanistic basis for the GCR, and may help lead to the development of therapeutic

267 A significant reduction (p < 0.001) in the GCR binding affinity (Kd) was observed in ragweed-allerg

268 strains containing defects that increase the GCR rate.

269 in telomerase-deficient cells increased the GCR rate, even though telomeres were maintained.

270 ibitor restored nuclear translocation of the GCR even in the presence of IL-2.

271 mplications for the potential role(s) of the GCR in KS pathogenesis.

272 ects of IL-2 on nuclear translocation of the GCR occurred within 30 min even in the presence of cyclo

273 is necessary for alternative splicing of the GCR pre-mRNA to create mRNA encoding GCRbeta.

274 r, the underlying molecular mechanism of the GCR remains uncharacterized.

275 purified GCR, 2) can displace binding of the GCR to a consensus GRE, and 3) shifts a protein in HepG2

276 alities in the DNA binding capability of the GCR.

277 related with impaired phosphorylation of the GCR.

278 ylation and the proapoptotic function of the GCR.

279 ccordance with the low insulin response, the GCR was lower after pasta consumption, which explained t

280 Furthermore, we demonstrate that the GCR is accompanied by an enhancement of histone H3 Lys4

281 designed transgenes, we demonstrate that the GCR is dependent on both the presence of a PTC and the n

282 Ultimately, the GCR simulator will require validation across multiple ra

283 lace of distal limb bud development when the GCR participates in initiating Hoxd gene quantitative co

284 duced by transfection of cell lines with the GCR-beta gene resulting in significant reduction of thei

285 The GCRs were translocations and chromosome fusions formed b

286 Although the GCRs induced by treatment with DNA-damaging agents were

287 NASA has developed the "GCR Simulator" to generate a spectrum of ion beams that

288 resulting in significant reduction of their GCR-alpha DNA binding capacity.

289 the breakpoint junctions of GCRs from these GCR mutator mutants were determined with modified breakp

290 kout cells, and that the production of these GCRs is ameliorated by H2ax expression.

291 , were highly specific for suppressing these GCRs compared to GCRs mediated by single-copy sequences.

292 We find that signaling through GCR has a significant impact upon the ability of Muller

293 cific for suppressing these GCRs compared to GCRs mediated by single-copy sequences.

294 ponse to steroids, but failed to translocate GCR when they were grown in the presence of CD19(-) cell

295 y replaced by de novo telomere-addition-type GCR.

296 , srs2, and srs2 rrm3 mutants have wild-type GCR rates.

297 ations, the translocation- and deletion-type GCRs created by a single double-strand break are mostly

298 d significantly less with the receptor under GCR conditions is p300.

299 The mechanism underlying GCR formation appears to involve interactions between DN

300 regions of the viral genome (v-bcl-2 gene, v-GCR gene, and gene 73) are transcribed during latency wi

301 ding a G-protein coupled receptor homolog, v-GCR).

302 experience demonstrated GCR; and those with GCR were at higher risk of subsequently developing a col