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 expression by CD8+ T cells from small airways correl

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

5 GCR methylation was not associated with particulate air

6 GCR suppression by Rad5 and Rad18 appears to be exerted

7 GCR types in helicase double mutants include telomere ad

8 GCRs and CNVs underlie human genomic disorders and are a

9 GCRs are therefore likely to be produced through the res

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

11 ould induce diminished GCR binding-affinity (GCR Kd = 34.4 +/- 2.3 nM with IL-13 vs Kd = 8.8 +/- 0.7

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

29 Both GCR and ultraviolet mechanisms may occur more rapidly th

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

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

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

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

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

35 the transactivating activity of the classic GCR.

36 oth muscle fibre types expressed a cytosolic GCR.

37 ity; and no additive effect to the decreased GCR-binding affinity was noted when IL-13 was cocultured

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

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

40 lar actions as IL-4, could induce diminished GCR binding-affinity (GCR Kd = 34.4 +/- 2.3 nM with IL-1

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

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

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

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

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

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

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

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

49 nealing, and are therefore prone to generate GCRs.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

64 t REV1 deficiency causes a major increase in GCRs.

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

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

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

68 tants with small but significantly increased GCR rates.

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

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

71 f mutants to identify progeny with increased GCR rates.

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

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

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

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

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

77 f an expression vector containing the intact GCR, yet 3) cotransfection with a plasmid that contains

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

79 30546; a 149-nt intron is present in the K14/GCR intergenic region.

80 on and similar genetic interactions as known GCR suppressors.

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

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

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

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

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

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

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

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

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

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

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

92 No GCRs were detected despite dramatic decreases in spore v

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

118 reases the de novo telomere addition type of GCR.

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

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

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

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

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

124 DNA damage while promoting the formation of GCRs.

125 0 heterodimer and monitored the formation of GCRs.

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

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

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

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

130 c28 is required for formation or recovery of GCRs.

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

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

133 e proteins functioning in the suppression of GCRs.

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

135 granulocyte-macrophage-CSF had no effect on GCR-binding affinity; and no additive effect to the decr

136 eptune's brightness suggests nucleation onto GCR ions.

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

138 rearranges to form a translocation and other GCRs.

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

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

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

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

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

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

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

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

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

148 We report the molecular cloning of two rat GCR genes (rat CXCR1-like and rat CXCR2) whose conceptua

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

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

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

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

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

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

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

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

157 s leads to gross chromosomal rearrangements (GCR).

158 and induces gross chromosome rearrangements (GCR).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

177 rmation of gross chromosomal rearrangements (GCRs).

178 ncrease in gross chromosomal rearrangements (GCRs).

179 ed to form gross chromosomal rearrangements (GCRs).

180 y cause of gross chromosomal rearrangements (GCRs).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

197 The glucocorticoid receptor (GCR) seems to be indispensable to this process because 1

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

199 asthma by reducing glucocorticoid receptor (GCR)-binding affinity.

200 tion of the nuclear glucocorticoid receptor (GCR).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

217 lower glycemic response, because of a slower GCR.

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

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

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

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

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

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

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

225 ast, multiple pathways cooperate to suppress GCR.

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

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

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

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

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

231 wo GIS genes were identified that suppressed GCR formation.

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

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

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

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

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

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

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

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

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

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

242 The GCR provides an explanation for the colinear genetic lin

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

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

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

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

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

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

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

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

251 strains containing defects that increase the GCR rate.

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

253 mutation in the ligand binding domain of the GCR does not activate the CYP3A5 enhancer in the presenc

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

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

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

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

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

259 related with impaired phosphorylation of the GCR.

260 alities in the DNA binding capability of the GCR.

261 ylation and the proapoptotic function of the GCR.

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

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

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

265 The GCRs were translocations and chromosome fusions formed b

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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