ライフサイエンスコーパス: SCE

1 SCE cells and TM cells exposed to isoproterenol or epine

2 SCE cells produce mucilage, a specialized secondary wall

3 SCE frequencies were measured after cells were exposed t

4 A low working potential (0V (SCE)), fast amperometric response (<5s), and high sensit

5 At negative potentials (-0.2V(SCE)), however, the molecules are highly mobile and can

6 At intermediate potentials (-0.2 to +0.2V(SCE)), the TPyP formed a highly ordered adlayer.

7 At positive potentials (>0.5V(SCE)), a disordered layer of TPyP is formed on the Au(11

8 To characterize factors affecting SCE frequency, we analyzed dimer resolution at the dif s

9 rmine with great ease in which cell cycle an SCE occurred.

10 s important for both checkpoint function and SCE.

11 We analyzed the association between LCD and SCE for the population as a whole, and for subsets.

12 IOP-related LCD and SCE result from a complex combination of factors, includ

13 ent analysis was used to predict the LCD and SCE resulting from an increase in IOP.

14 and to determine the sensitivity of LCD and SCE to the eight factors, independently and in interacti

15 The association between LCD and SCE varied greatly depending on the properties of the la

16 tiff lamina, the association between LCD and SCE was strong and consistent with the concept of "the s

17 ctors (35% and 7% of the variance in LCD and SCE, respectively).

18 a robust structure, particularly for LCD and SCE, which is tolerant to variations in tissue geometry

19 on when interpreting measurements of LCD and SCE.

20 IOP, some cases had peculiarly large LCD and SCE.

21 analysis of the relationship between LCD and SCE.

22 suggest that simple slipped misalignment and SCE-associated misalignment intermediates are similarly

23 ore profound defect in RAD51 recruitment and SCE induced by replication fork collapse when ATR is dep

24 nd that BRCA1 promotes RAD51 recruitment and SCE induced by replication fork stalling independent of

25 t of the nascent strand and its template and SCE-associated misalignment involving both nascent stran

26 th cellulosic rays and show that Arabidopsis SCE cells represent an excellent model in which to study

27 AD54, are required for DNA damage-associated SCE but not for spontaneous SCE.

28 hether spontaneous and DNA damage-associated SCE requires specific genes within the RAD52 and RAD3 ep

29 utant was defective in DNA damage-associated SCE when cells were exposed to either radiation or chemi

30 d for BIR, are required for X-ray-associated SCE but not for SCE stimulated by HO-induced DSBs.

31 Secondary structure-associated SCE events occur via double-strand break repair.

32 The defect in DNA damage-associated SCEs in rad51 mutants correlated with an eightfold highe

33 e that many TNR expansion mutations occur by SCE.

34 In contrast, SCE frequencies were significantly elevated in BLM-defic

35 After mild DNA damage, SCE was threefold higher in the knockout cells, while no

36 This newly delineated SCE-->DMP-->mMAN-->HVC/pHVC pathway is the first report

37 study, we have adapted Strand-seq to detect SCE in the yeast Saccharomyces cerevisiae.

38 gives significantly improved power to detect SCEs after in silico correction of normal tissue contami

39 lysis of CNAs and affect the power to detect SCEs in clinical samples.

40 o T-SCE, other genomic rearrangements (i.e., SCE) were also significantly increased in mTert-/- ES ce

41 of -1.70 V vs. saturated calomel electrode (SCE) for the couple involving the neutral organic donor

42 -0.4 V vs. the saturated calomel electrode (SCE) in acetonitrile solutions.

43 -0.35 V versus saturated calomel electrode (SCE), specific to ds-ON and highly sensitive to base pai

44 mum of 15 mV vs saturated calomel electrode (SCE).

45 - 14) mV versus saturated calomel electrode (SCE).

46 l of +1.2V (vs. saturated calomel electrode [SCE]), no added nitrogen source except the lysozyme itse

47 isually guided) single-cell electroporation (SCE) and extracellular electrophysiology, and can be use

48 tes the ability of RMI2 to suppress elevated SCE.

49 d BLM protein level and rescued the elevated SCE phenotype in TopBP1-depleted cells.

50 To elucidate SCE recombination mechanisms, we determined whether spon

51 btle CT findings of centrilobular emphysema (SCE).

52 eshwork (TM) or Schlemm's canal endothelial (SCE) cells were grown on porous filter supports.

53 computing the sequence correlation entropy (SCE) using the quenched probability P(sk)(i,j) of findin

54 A SUMO-conjugating enzyme (SCE) (E2, Ubc9) in C. reinhardtii was shown to be functi

55 (Arabidopsis thaliana) seed coat epidermis (SCE) to study cell wall synthesis.

56 ons (CNAs) and significant consensus events (SCEs) in cancer genomes is a main task in discovering po

57 tion related to the skin cancer examination (SCE) for melanoma, a relevant competency gap that influe

58 osed normal human cells, can cause excessive SCEs to an extent equivalent to that observed when the c

59 by high levels of sister-chromatid exchange (SCE) and cancer predisposition.

60 Sister chromatid exchange (SCE) can occur by several recombination mechanisms, incl

61 an be used to map sister chromatid exchange (SCE) events genome-wide in single cells.

62 tentially harmful sister chromatid exchange (SCE) events in wild-type cells but not in cells derived

63 levated levels of sister chromatid exchange (SCE) found in BLM(-/-) cells.

64 Utilizing sister chromatid exchange (SCE) frequencies as a marker of the BSE, we performed ce

65 the dependence of sister chromatid exchange (SCE) frequencies on location [i.e., genomic (G-SCE) vs.

66 we report that a sister chromatid exchange (SCE) generated by crossover-associated HR efficiently oc

67 te of spontaneous sister chromatid exchange (SCE) in Bloom syndrome (BS) cells, but not in their BLM-

68 Sister chromatid exchange (SCE) in Escherichia coli results in the formation of cir

69 ontaneous unequal sister-chromatid exchange (SCE) in vegetatively growing yeast cells.

70 ontaneous unequal sister-chromatid exchange (SCE) in yeast.

71 ells, spontaneous sister chromatid exchange (SCE) occurred with twice the frequency observed in norma

72 by adjustments in sister chromatid exchange (SCE) rate, rather than by direct selection on the number

73 NA damage-induced sister chromatid exchange (SCE) was evident by a 10-fold reduction in HO endonuclea

74 ytogenetically as sister chromatid exchange (SCE), and that this rate is dependent on genotype.

75 Spontaneous sister chromatid exchange (SCE), as monitored between truncated his3 fragments, was

76 lution mapping of sister chromatid exchange (SCE), facilitating the study of this type of genomic rea

77 te of spontaneous sister chromatid exchange (SCE), heteroallelic recombination and translocations, re

78 n is disrupted by sister chromatid exchange (SCE), the dark chromatid is always in the center, so tha

79 the frequency of sister chromatid exchange (SCE), whereas deleting both Blm and Recql5 lead to an ev

80 ncreased level of sister chromatid exchange (SCE)--the hallmark feature of Bloom syndrome cells.

81 oint response and sister chromatid exchange (SCE).

82 ogenous levels of sister chromatid exchange (SCE).

83 vel and increased sister chromatid exchange (SCE).

84 associated with sister chromosome exchange (SCE).

85 sult in elevated sister chromatid exchanges (SCE).

86 ity and increased sister chomatid exchanges (SCEs).

87 by increases in sister chromatid exchanges (SCEs) and numbers of micronuclei.

88 evated levels of sister chromatid exchanges (SCEs) and patients with Bloom's syndrome develop a broad

89 nce of excessive sister chromatid exchanges (SCEs) as an index of DNA damage in human lung fibroblast

90 uced spontaneous sister chromatid exchanges (SCEs) but this was not due to a defect in HDR-mediated c

91 the induction of sister chromatid exchanges (SCEs) by UV irradiation are greatly enhanced.

92 ized by elevated sister chromatid exchanges (SCEs), as well as chromosomal breaks, deletions, and rea

93 sociated unequal sister chromatid exchanges (SCEs), translocations, and inversions.

94 induced DSBs and sister chromatid exchanges (SCEs), two RAD51-dependent processes, are 53BP1 independ

95 reased number of sister-chromatid exchanges (SCEs).

96 displacement (LCD), scleral canal expansion (SCE), and the stresses (forces) and deformations (strain

97 al hypothalamus (stratum cellulare externum [SCE]), which may also relay information to the same dors

98 equired for X-ray-associated SCE but not for SCE stimulated by HO-induced DSBs.

99 E) frequencies on location [i.e., genomic (G-SCE) vs. telomeric (T-SCE) DNA] in primary human fibrobl

100 ERCC1-XPF-deficient cells, neither T- nor G-SCE frequencies differed from controls.

101 egative WRN-deficient cells, T-SCE-but not G-SCE-frequencies were significantly increased compared wi

102 s 1-1417) in BS cells can correct their high SCEs to normal levels, whereas expression of a BLM fragm

103 in both MMR- and rad1-mutant cells; however, SCE events for both IR- and non-IR-containing substrates

104 ellular stratum of the lateral hypothalamus (SCE).

105 rating the rearrangements that arise after I-SCE:I-induced double-strand breaks.

106 eatment with the rare-cutting endonuclease I-SCE:I.

107 n unexpected effect of ERCC1 deficiency on I-SCE:I-stimulated rearrangements, which are not dependent

108 We suggest that if SCEs represent homologous recombination between sister c

109 iated repair of endogenous DNA damage and in SCE formation during normal DNA replication.

110 onstrate globally increased heterogeneity in SCE subjects compared with NS and SNI subjects but demon

111 ecA mutation, reflecting the role of RecA in SCE and virtually all homologous recombination in E. col

112 nd thickness (46% and 36% of the variance in SCE, respectively).

113 that ectopic expression of FANCD2 increased SCE.

114 he complex in solution and lead to increased SCE levels in cells that are similar to those observed i

115 10-fold reduction in HO endonuclease-induced SCE and no detectable X-ray stimulation of SCE in a rad9

116 not enhanced in dun1 mutants, but UV-induced SCE and heteroallelic recombination were enhanced.

117 In contrast, UV-induced SCE is largely a product of the trimethylated state, whi

118 Interestingly, SCE produced by replication fork collapse following DNA

119 mino acids 133-1417) results in intermediate SCE levels.

120 ling the repair of double-strand breaks into SCE.

121 A short-lived, SCE-inducing factor(s) was generated in alpha-irradiated

122 In both UM and PD20 cells, low SCE was reversed by inhibiting DNA-PKcs (DNA-dependent p

123 For the class of proteins with low SCE values, there are significant numbers of mixed charg

124 Since IR-mediated SCE events are reduced in msh2 cells, we propose that TN

125 Our results also show that TNR-mediated SCE events are independent of RAD50, MRE11 and RAD51, wh

126 We use a combination of SCE and clustering based on the principle component anal

127 hibit a significantly increased frequency of SCE compared with the corresponding wild-type control.

128 d Recql5 lead to an even higher frequency of SCE.

129 ase flow through the paracellular pathway of SCE and TM cells through a beta-receptor mediated respon

130 An increase in the rate of SCE is an indicator of elevated recombination activity a

131 d SCE and no detectable X-ray stimulation of SCE in a rad9 mutant.

132 Our findings suggest that the low values of SCE and the presence of (CH) and/or (CP) may be indicati

133 that proteins with relatively low values of SCE are predominantly associated with various diseases.

134 MUS81 or SLX4 reduces the high frequency of SCEs in Bloom's syndrome cells, indicating that MUS81 an

135 Strikingly, in PML-/- cells the frequency of SCEs is increased relative to PML+/+ cells.

136 eral vexing questions about the induction of SCEs (genetic damage and its repair) after exposure to v

137 nd that are responsible for the induction of SCEs, persist before being repaired and thus lose their

138 se in UV sensitivity and in the induction of SCEs.

139 cation, and by demonstrating high numbers of SCEs in cultured murine Blm-/- fibroblasts.

140 High numbers of SCEs were uniformly seen in members of the panel, and se

141 his method, which permits the observation of SCEs in endoreduplicated cells, makes it possible to det

142 of amino acids 133-1417 in the reduction of SCEs was not explained by a defect in DNA helicase activ

143 A more persistent SCE-inducing factor(s), which can survive freeze-thawing

144 ells, indicating that MUS81 and SLX4 promote SCE formation, in events that may ultimately drive the c

145 esis that functions of proteins with similar SCE values may be linked.

146 amage-associated SCE but not for spontaneous SCE.

147 e switch pathway, play a role in spontaneous SCE.

148 quantifiable evidence that most spontaneous SCE events in wild-type cells are not due to the repair

149 parison with wild type, rates of spontaneous SCE are 10-fold lower in rad51 rad1 but not in either ra

150 e reductase in mec1-21, rates of spontaneous SCE increased 15-fold above wild-type.

151 data suggest FANCD2 may promote spontaneous SCE by influencing which double-strand break repair path

152 Therefore, reduced spontaneous SCE could be a manifestation of the same defect that cau

153 aemia patients displayed reduced spontaneous SCE formation relative to their FANCD2-complemented coun

154 involvement of p53 in regulating spontaneous SCE is BLM dependent.

155 ith the Blm helicase to suppress spontaneous SCE events.

156 Our results suggest that spontaneous SCE occurs by a template switching mechanism.

157 wed no difference in the rate of spontaneous SCEs; however, the rate of spontaneous inversions was de

158 is consistent with a model where spontaneous SCEs are the end product of endogenous recombination eve

159 AD50, MRE11 and RAD51, whereas IR-stimulated SCEs are dependent on the RAD52 epistasis-group genes.

160 analysis revealed that RMI2 and BLM suppress SCE within the same pathway.

161 TopBP1 in S phase cells in order to suppress SCE and thereby prevent genomic instability.

162 -deficient cells with mutations that cause T-SCE levels to rise.

163 n telomerase-negative WRN-deficient cells, T-SCE-but not G-SCE-frequencies were significantly increas

164 her studies, we found evidence of elevated T-SCE in telomerase-negative but not telomerase-positive b

165 Elevated T-SCE was associated with greater immortalization potentia

166 hrough telomere sister chromatid exchange (T-SCE) in murine telomere reverse transcriptase-deficient

167 lished telomere sister chromatid exchange (T-SCE), indicating that WRN normally represses T-SCEs.

168 Furthermore, T-SCE-driven premature cellular senescence may be a factor

169 elomere length but no SFEs, no increase in T-SCE was observed.

170 nto the cellular consequences of increased T-SCE frequency.

171 odel predicts that in cells with increased T-SCE, the onset of replicative senescence is dramatically

172 omologous recombination between telomeres (T-SCE).

173 tion [i.e., genomic (G-SCE) vs. telomeric (T-SCE) DNA] in primary human fibroblasts deficient in WRN,

174 In addition to T-SCE, other genomic rearrangements (i.e., SCE) were also

175 Furthermore, T-SCEs were more often detected in ES cells than in spleno

176 at telomeres, and observed an increase in T-SCEs only in a subset of mTert-/- splenocytes or ES cell

177 E), indicating that WRN normally represses T-SCEs.

178 a therapy by promoting fluid flow across the SCE and TM cells lining tissues of the major aqueous out

179 s of instruction related to melanoma and the SCE, a description of the integrated skin examination as

180 ), and at least 1 opportunity to observe the SCE (OR, 1.95).

181 ), and at least 1 opportunity to observe the SCE (OR, 2.70).

182 and at least 4 opportunities to observe the SCE were most predictive of intent to perform an integra

183 n, and at least 1 opportunity to observe the SCE were most predictive of performance of the SCE (ORs,

184 a, and at least 1 opportunity to observe the SCE.

185 edictive of confidence in performance of the SCE (odds ratios [ORs], 15.35 and 11.48, respectively).

186 E were most predictive of performance of the SCE (ORs, 21.67, 15.48, and 9.92, respectively).

187 To augment the practice of the SCE among medical students, course directors may design

188 n examination, and actual performance of the SCE.

189 on skin cancer (OR, 2.42) and lecture on the SCE (OR, 5.04).

190 es on skin cancer (OR, 6.35), lecture on the SCE (OR, 7.54), knowledge of melanoma risk (OR, 3.71), a

191 y outcomes were confidence in performing the SCE, intent to perform an integrated skin examination, a

192 classify protein families in terms of their SCE.

193 Non-IR-associated unequal SCE events are increased in both MMR- and rad1-mutant ce

194 he rate of spontaneous IR-stimulated unequal SCE events in yeast is significantly reduced in strains

195 ntial is stepped to higher values (0.5-0.8 V(SCE)).

196 are -25(+/- 14) mV and -433(+/- 8) mV versus SCE whereas protein B' had no effect though it did alter

197 queous solution with E(1/2) = +0.41 V versus SCE at pH 4 and involves the transfer of one electron an

198 in 0.075 M Me4NBF4/CH3CN were -1.04 V versus SCE for the n-doping of P(C) and 0.40 and 0.30 V versus

199 n-doping of P(C) and 0.40 and 0.30 V versus SCE for the p-doping of P(C) and P(A), respectively.

200 based on steady-state currents at 0 V versus SCE in the presence of H2O2 were in the order horseradis

201 giving SWV peaks at approximately 1 V versus SCE that grow larger with reaction time.

202 ential in the range -1.39 to -1.58 V (versus SCE) and estimated electron affinities (LUMO levels) of

203 s can be varied from -0.05 to 0.15 V (versus SCE) by modification of the substituents on phosphorus (

204 s buffer are in the range 0.15-0.35 V versus SCE, and the rate constants for the oxidation GO(red) (w

205 le one-electron transfer waves at E(1/2) (vs SCE in MeCN) = -1.121, 0.007, and 0.329 V, and a fourth

206 nging in potential from -0.77 to +2.5 eV (vs SCE) and including thermal reductants, indirect electrol

207 wing results: FeIII/II E(1/2) at -260 mV (vs SCE), approximately 300 mV positive of the value measure

208 ave the same redox potential (ca. -180 mV vs SCE).

209 ersible one-electron reduction at -0.09 V vs SCE (MeCN), and reduced forms of DCNT have yet to be iso

210 e oxidation peaks in the region 0.6-1.1 V vs SCE after incubations with styrene oxide, DNA/AQ films g

211 (o)(1,red) = -2.02, E(o)(2,red) = -2.07 V vs SCE and E(o)(1,ox) = 1.14, E(o)(2,ox) = 1.20 V vs SCE.

212 e of DPA, which shows E(o)(red) = -2.06 V vs SCE and E(o)(ox) = 1.15 V vs SCE.

213 tion of TPrA began at approximately 0.6 V vs SCE and exhibited a broad irreversible anodic peak.

214 potential region more negative than 1.0 V vs SCE and one at more positive potentials.

215 lic voltammetric wave observed at -0.58 V vs SCE at a Pt electrode was originally proposed to corresp

216 s conductive between about 0.1 and -0.4 V vs SCE at pH 4.5.

217 p-GaP system (E(CBM) approximately -1.5 V vs SCE at pH 5) and the photochemical [Ru(phen)3](2+)/ascor

218 oxidation potentials greater than >1.7 V vs SCE do not react.

219 t 0.47 V vs SCE for (PCA)Co(2) and 0.39 V vs SCE for (BCA)Co(2).

220 ity of E(1/2) which was located at 0.47 V vs SCE for (PCA)Co(2) and 0.39 V vs SCE for (BCA)Co(2).

221 duction potential E(Br(*)/Br(-)) = 1.22 V vs SCE in acetone, which is about 460 mV less positive than

222 at potentials between -0.55 V and -0.20 V vs SCE in CH3CN.

223 ved except for some broad ones at ~-3.2 V vs SCE in THF, which is consitent with the wide highest occ

224 talytic SWV peaks at approximately 0.75 V vs SCE to increase nearly linearly over the first 10-20 min

225 rsors with oxidation potentials <or=1.7 V vs SCE undergo ready oxidative C-C bond formation with DDQ/

226 he HER or for CO(2) conversion at -1.25 V vs SCE using a glassy carbon electrode.

227 trolysis experiments, conducted at -1.2 V vs SCE using Et3NHCl as a proton source, N2O is produced se

228 tials of E(4+/3+) approximately 1.6-1.7 V vs SCE were determined for four-electron oxidation to the c

229 lues of 2.48 +/- 0.03 and 2.26 +/- 0.02 V vs SCE were obtained for benzene and toluene, respectively.

230 lectrocatalyzes H(2) generation at -0.9 V vs SCE with i(cat)/i(p) approximately 4, corresponding to a

231 event, while ECL from luminol at +0.45 V (vs SCE) could be enhanced by the same Pt NPs, in the presen

232 ed on glassy carbon electrode at -1.25 V (vs SCE) could be quenched by closely contacted Pt nanoparti

233 s are also observed at +1.94 and +2.15 V (vs SCE) for 1 and 3.

234 between E(p) values of -1.75 and -1.93 V (vs SCE), corresponding to reductions of the alkyne units.

235 more positive than approximately -0.1 V (vs SCE).

236 reduction wave (E degrees (red) = -1.18 V vs SCE) and two nernstian one-electron oxidation waves (E d

237 ery negative reduction potential (-1.37 V vs SCE) for the formation of pyrH(*).

238 rst reduction of these compounds (-0.70 V vs SCE) occurs prior to TiO2 reduction.

239 )'s LUMO (E(0)(calc) approximately -1.3 V vs SCE) to form the solution phase PyH(0) via highly reduci

240 ly positive hole (Eox approximately 1.7 V vs SCE), which allows to drive demanding photo-oxidation re

241 1,ox) = 1.01 V, E degrees (2,ox) = 1.24 V vs SCE).

242 rogenase mimics reported to date (-0.74 V vs SCE).

243 by electrochemical methods (up to -1.3 V vs SCE).

244 cathodic onset potential (E(cat) = -1.2 V vs SCE).

245 eroxide at low applied potentials (-0.1 V vs SCE).

246 rometric response toward glucose at 0.6 V vs SCE, demonstrating the anchoring of this enzyme via two

247 obtained by using applied voltage -0.6 V vs SCE, O(2), and 100 mM H(2)O(2).

248 with formal potentials of 0.34 and 0.76 V vs SCE, respectively.

249 ion potentials more positive than -2.21 V vs SCE, which is much higher than the thermodynamic redox p

250 O)(TBP8Cz(*+)):Zn(II) gives Ered = 0.69 V vs SCE, which is nearly +700 mV above its valence tautomer

251 n behavior with E degrees (red) = -1.56 V vs SCE.

252 d) = -2.06 V vs SCE and E(o)(ox) = 1.15 V vs SCE.

253 nd E(o)(1,ox) = 1.14, E(o)(2,ox) = 1.20 V vs SCE.

254 the solution over the range 0.106-1.001 V vs SCE.

255 on potentials ranging from -1.6 to -3.4 V vs SCE.

256 /+1) = +0.99 V and E(1/2)(0/-1) = -0.45 V vs SCE.

257 IP(1-/0) processes, at -0.86 and -1.20 V vs SCE.

258 n of ADH heme proceeded at around -0.05V vs. SCE.

259 sity of 510microAcm(-2) at pH 7.0 and 0V vs. SCE.

260 ration source, a lower potential (+0.85V vs. SCE), and a platinum basket electrode.

261 gand complex of Al(3+) occurs at -1.16 V vs. SCE (500 mV overpotential).

262 ability to the reduction of FA at 0.3 V (vs. SCE) with the electron transfer rate constant (ks) of 1.

263 alytic activity towards the HER (-0.46 V vs. SCE) upon the 1000th cycle, such potential is the closes

264 he desired value of platinum at (-0.25 V vs. SCE).

265 pH 7.0, at low applied potentials (0.0 V vs. SCE).

266 ating with an applied potential of 0.3 V vs. SCE.

267 eriorly) and -12.9 mum (anteriorly), whereas SCE was between 0.5 and 15.2 mum (all expansions).

268 e to DNA polymerase III exonuclease, whereas SCE-associated events are sensitive to exonuclease I.

269 the variance in LCD, respectively), whereas SCE was most sensitive to scleral modulus and thickness