ライフサイエンスコーパス: LET

1 LET is neither sensitive nor specific as a predictor of

2 LET-23 EGFR accumulates in cytoplasmic foci in dhc-1 mut

3 LET-23 is also localized to the cell junctions, and both

4 LET-23 overexpression rescues the lin-2 or lin-7 vulvale

5 LET-23/EGFR and SOS-1, an exchange factor for Ras, are r

6 LET-381/FoxF directly activates the CC specification fac

7 LET-99 acts in a pathway parallel to anillin and is requ

8 LET-99 functions antagonistically to the Galpha/GPR-1/2

9 LET-99 is a DEP domain protein that is asymmetrically en

10 LET-99 is well characterized for generating the asymmetr

11 in the specification of P12 fate: the LIN-3/LET-23 epidermal growth factor signaling pathway, a Wnt

12 in genes encoding HPL-2/HP1, LIN-13, LIN-61, LET-418/Mi-2, and H3K9me2 histone methyltransferase MET-

13 inated by RGEF-1b in AWC neurons activated a LET-60 (Ras)-MPK-1 (ERK) signaling cascade.

14 or cells (VPCs) are spatially patterned by a LET-23/EGF receptor-mediated inductive signal and a LIN-

15 sop-1, that promote the ability of activated LET-23 to induce ectopic vulval fates.

16 es that antagonize the activity of activated LET-23, a member of the EGFR family of RTKs.

17 Surprisingly, expression of activated LET-60/Ras in the neighboring duct cell, but not in the

18 MEP-1 and LET-418 interact in vivo with the germline-protein PIE-1

19 f germ cells, while at later times MEP-1 and LET-418 remodel chromatin to establish new stage- or cel

20 In animals lacking MEP-1 and LET-418, germline-specific genes become derepressed in s

21 Here, we describe two proteins, MEP-1 and LET-418/Mi-2, required for maintenance of somatic differ

22 s can integrate the input from the BAR-1 and LET-60 Ras signaling pathways by coordinately regulating

23 pendent pathway requires anillin, NOP-1, and LET-99.

24 Other RGEF-1b and LET-60 effectors were dispensable for chemotaxis.

25 In this cell, both GPR-1/2 and LET-99 are asymmetrically localized in response to the M

26 The distribution of EMB-9 and LET-2 chains has been characterized using chain-specific

27 Simultaneous reduction of both ZYG-9 and LET-711 can rescue the centration and rotation defects o

28 ion framework as a rapid method for dose and LET estimation, capable of accounting for heterogeneity

29 helial cells via the LIN-3 growth factor and LET-23 transmembrane tyrosine kinase.

30 In addition, Galpha and LET-99 are required for spindle orientation during the e

31 rol levels but independent of the number and LET of the particles.

32 their roles in Ras signaling, SUR-6/PR55 and LET-92/PP2A-C cooperate to control mitotic progression d

33 Therefore SUR-6/PR55 and LET-92/PP2A-C probably act together to dephosphorylate a

34 Specifically, MIG-5/Dsh, RHO-1/RhoA and LET-502/ROCK appear to play major roles, while other PCP

35 se results suggest that Galpha signaling and LET-99 control centration by regulating polarized actomy

36 uitin conjugation enzyme UBC5 (also known as LET-70) are all required in vivo for CCCH finger protein

37 r more signal transduction proteins (such as LET-23) to either the basal membrane domain or the cell

38 nd to impaired downregulation of basolateral LET-23 in VPCs in which LIN-12 is active.

39 es through regulated activity of basolateral LET-23/EGF receptor and apical LIN-12/Notch.

40 ion codes were internally validated for both LET and acute limb ischemia.

41 ere have been significant reductions in both LET incidence and in-hospital mortality.

42 ation of endocytosis and trafficking of both LET-23 and LIN-12.

43 rowth factor receptor EGL-15 is activated by LET-756, a fibroblast growth factor, and attenuated by C

44 We conclude that IP(3) generated by LET-23 mediated activation of PLC-gamma induces repetiti

45 irmed chlamydial infections were negative by LET.

46 This process is regulated by LET-23-mediated epidermal growth factor signaling and LI

47 Signals transduced by LET-23 control ovulation through changes in spermathecal

48 s are mediated by neuronal EGFR (also called LET-23) and phospholipase C-gamma (PLC-gamma), diacylgly

49 tion is necessary and sufficient for certain LET-23 functions.

50 llular accumulation of the alpha2(IV) chain, LET-2, indicating that LET-2 assembly and/or secretion r

51 Efficacy outcomes of women who chose LET (PLAC-LET group) were compared with those who did no

52 zing transgenic nematodes for three distinct LET-23 functions, we show that six of eight potential si

53 T-23 epidermal growth factor receptor (EGFR)/LET-60 Ras/MPK-1 MAP kinase signaling pathway in the vul

54 repeat only (eLRRon) proteins in C. elegans (LET-4 and EGG-6) that are expressed on the apical surfac

55 In par-1 and par-4 embryos, LET-99 accumulates at the entire posterior cortex, but r

56 In Caenorhabditis elegans embryos, LET-99 and G protein signaling act downstream of the PAR

57 s elegans has identified the polarity factor LET-99 and its heterotrimeric G-protein regulators as co

58 s, the single FoxF/FoxC transcription factor LET-381 functions in a feed-forward mechanism in the spe

59 a putative guanine nucleotide exchanger for LET-60 RAS.

60 The in-hospital mortality for LET decreased significantly from 8.28% between 1988 and

61 tyrosine kinase and subsequently the GTPase LET-60/ras is required within epidermal cells, the subst

62 High LET IR produces structurally different forms of DNA dama

63 icated than these same relationships at high LET or high doses of low LET radiation.

64 than low LET radiation, mainly because high LET radiation-induced DNA damage is more difficult to re

65 s the ratio of the effects generated by high LET radiation to low LET radiation.

66 agments (</=40 bp) directly produced by high LET radiation, the size of which prevents Ku protein fro

67 sical characteristics (short half-life, high LET alpha-particle emissions).

68 RBE is involved in the interference of high LET radiation with non-homologous end joining but not ho

69 mall DNA fragments during the repair of high LET radiation-induced base damage, which contributes to

70 which contributes to the higher RBE of high LET radiation-induced cell killing.

71 ET) X-rays to generate simple breaks or high LET HZE particles (Fe ions) to generate complex breaks,

72 xic effect on isolated cells due to the high LET (linear energy transfer) of alpha-particles.

73 patients by sensitizing tumor cells to high LET radiotherapy.

74 Irradiation with high LET particles induced pSmad2 and Smad7 foci tracks indic

75 levels of these proteins correlate with high LET-99 accumulation.

76 reveal a smooth transition from low to high LETs which is an advantage of the current method over me

77 er response was investigated by using a high-LET heavy particle microbeam, which allows selected cell

78 al tissue injury in the lungs following high-LET radiation exposure is unknown.

79 Clonal expansion following high-LET radiation exposure was correlated with elevated prog

80 fragments in vitro and to the DNA from high-LET irradiated cells in vivo.

81 Importantly, high-LET radiation induces greater long-term damage to normal

82 We discovered that the effects of high-LET radiation exposure on progenitor cells occur in a p5

83 efficiencies of HRR and NHEJ to repair high-LET radiation induced DSBs.

84 These data show that high-LET radiation depletes the distal airway progenitor pool

85 , CRC risk prediction after exposure to high-LET cosmic heavy ion radiation exposure is hindered due

86 ice or DT40 cells are more sensitive to high-LET IR than to low-LET IR, NHEJ deficient mice or DT40 c

87 Furthermore, exposure to high-LET radiation induced clonal expansion of a subset of pr

88 Here we show that exposure to high-LET radiation led to a prolonged loss of in vitro colony

89 Following exposure to high-LET radiation, immortalized human bronchial (BEP2D) and

90 due to its high linear energy transfer (high-LET) characteristics deposits higher energy per unit vol

91 animal level and the mechanism by which high-LET IR does not affect the efficiency of HRR remains unc

92 idermal growth factor (EGF)-receptor homolog LET-23.

93 s epidermal growth factor receptor homologue LET-23 has multiple functions during development and has

94 lidity of the codes was good for identifying LET cases but poor for identifying acute limb ischemia c

95 lin-10 acts in LET-23 receptor tyrosine kinase basolateral localization

96 A gain-of-function mutation in LET-23 EGF receptor and ectopic expression of LIN-3 EGF

97 With increasing LET, less DNA strand breaks are formed per unit dose, bu

98 ling localizes GPR-1/2 by locally inhibiting LET-99, a GPR-1/2 antagonist.

99 ARK-1 inhibits LET-23-mediated ovulation, a RAS-independent function.

100 nds on PAR-3 and its downstream intermediate LET-99.

101 n, RHGF-1 acted through Rho-dependent kinase LET-502/ROCK and activated a conserved, retrograde DLK-1

102 he actions of RHO-1, and its effector kinase LET-502, during establishment phase and CDC-42, and its

103 desmosomes or the activity of the Rho kinase LET-502/ROCK were partially compromised.

104 or signaling by the receptor tyrosine kinase LET-23.

105 17 trial examined the efficacy of letrozole (LET) started within 3 months of 5 years of adjuvant tamo

106 omplete estrogen blockade) versus letrozole (LET) in receptor-positive advanced breast cancer (ABC).

107 n proteasome system, including the E2 ligase LET-70/UBE2D2 functioning with E3 components CUL-3, RBX-

108 trate an in vivo role for dynein in limiting LET-23 EGFR signaling via endosomal trafficking.

109 PAR-3 and PAR-2 localize LET-99 to a posterior cortical band through an unknown m

110 One function of LIN-2 is to localize LET-23 to the basal membrane domain of vulval precursor

111 ow bystander responses, especially after low LET radiation such as X- or gamma-rays and whether the s

112 wever, recent studies using low doses of low LET radiation suggest that the relationship between gene

113 ity of this relationship at low doses of low LET radiation suggests that more of the population may b

114 ansfer (LET) radiation, or high doses of low LET radiation.

115 lationships at high LET or high doses of low LET radiation.

116 ot been fully determined at low doses of low LET radiation.

117 diotherapy machine kills more cells than low LET radiation, mainly because high LET radiation-induced

118 These data provide evidence that low LET radiation can induce bystander mutagenesis in a thre

119 fects generated by high LET radiation to low LET radiation.

120 radiation and compared the response with low LET gamma-radiation ((137)Cs; 0.5 Gy/min; 2 Gy).

121 observation of bystander responses with low LET radiation suggests that these may be important in un

122 cells are equally sensitive to high- and low-LET IR.

123 02 to 190 millirads, yielding an average low-LET dose rate of 11.2 millirads per day inside the modul

124 sue than the relative equivalent dose of low-LET gamma-rays, which has implications in therapeutic de

125 energy transfer (LET) alpha-particles or low-LET gamma-rays leads to stimulation of intercellular ind

126 Measurements of the low-LET (linear energy transfer) component obtained from the

127 r day inside the module, about twice the low-LET dose rate measured on previous flights of the space

128 re more sensitive to high-LET IR than to low-LET IR, NHEJ deficient mice or DT40 cells are equally se

129 thus more damaging to cells relative to low-LET radiation such as gamma rays.

130 exposure to low linear energy transfer (low-LET) radiation such as gamma-ray is highlighted by the s

131 cells at the same dose as compared with low-LET IR (such as X or gamma rays) is due to inefficient N

132 TOR 60 mg (ATA + TOR), or letrozole 2.5 mg (LET).

133 Despite a modest LET (~19 keV/mum), antiproton spread out Bragg peak (SOB

134 9.24 months (ATA + TOR) versus 10.44 months (LET).

135 osed of the carboxyl-terminal amino acids of LET-23 fused to truncated nerve growth factor receptor/P

136 Activity of LET-23, the C. elegans homolog of the epidermal growth f

137 nctions to inhibit the signaling activity of LET-60 Ras.

138 they are required for most, but not all, of LET-23 activity.

139 -year span, there were 1.76 million cases of LET.

140 Antisense-mediated depletion of LET-858 activity in early embryos causes a lethal phenot

141 However, we found different distributions of LET-23 EGFR foci in rab-7 versus dhc-1 mutants, suggesti

142 RAS-dependent signaling events downstream of LET-23 EGFR, EGL-15 FGFR and an unknown RTK.

143 data positions PTP-2 activity downstream of LET-23 in the vulval induction signaling pathway.

144 endent, tissue-specific positive effector of LET-23.

145 Molecular identification of LET-711 shows it to be an ortholog of NOT1, the core com

146 The incidence of LET decreased significantly from 42.4 per 100 000 person

147 cting either upstream of or independently of LET-60 RAS.

148 e activity is required for the inhibition of LET-99 localization, and PAR-1 associates with LET-99.

149 results suggest that proper localization of LET-23 receptor to the Pn.p cell junctions is required f

150 a mechanism for basolateral localization of LET-23 receptor tyrosine kinase by direct binding to the

151 are required for basolateral localization of LET-23, since LET-23 is mislocalized to the apical membr

152 PAR-3 and PAR-1 inhibit the localization of LET-99 to generate a band pattern.

153 in-10 mutations result in mislocalization of LET-23 to the apical membrane domain and cause a signali

154 h the incidence and in-hospital mortality of LET.

155 embryos suggests that the banded pattern of LET-99 is critical for normal posterior spindle displace

156 The corresponding performance of LET versus LCR was 53.1, 67.3, 10.1, and 95.8%.

157 ) that suppresses the negative regulation of LET-23 by the Cbl homolog Sli-1 in C. elegans prevented

158 ne product c-Cbl, is a negative regulator of LET-23-mediated vulval differentiation.

159 Our results indicate that the role of LET-502 in junctional remodeling is likely to be indepen

160 However, whether the role of LET-99 in cytokinesis is specific to asymmetric division

161 LIN-10 may function in secretion of LET-23 to the basolateral membrane domain, or it may be

162 that dynein functions at an earlier step of LET-23 EGFR trafficking to the lysosome than RAB-7.

163 rther, we identify an inhibitory tyrosine of LET-23 requiring sli-1(+) for its effects: removal of th

164 which in turn inhibits signaling upstream of LET-60 RAS in a manner not wholly dependent on the ubiqu

165 nts who received placebo (PLAC) were offered LET.

166 Lateral inhibition depends on LET-99, which inhibits GPR-1/2 localization to produce a

167 Glycine substitutions in either EMB-9 or LET-2 cause intracellular accumulation of both chains.

168 t the Caenorhabditis elegans EGFR orthologue LET-23 is constitutively dimeric, yet responds to its li

169 In particular, LET-99 is uniformly localized in one-cell par-3 embryos

170 ficacy outcomes of women who chose LET (PLAC-LET group) were compared with those who did not (PLAC-PL

171 There were 1,579 women in the PLAC-LET group (median time from tamoxifen, 2.8 years) and 80

172 Patients in the PLAC-LET group were younger; had a better performance status;

173 to 0.74; P = .004) were superior in the PLAC-LET group.

174 of tau(decay) and peak amplitude after PURE-LET de-noising compared to raw signals.

175 t a wavelet-based de-noising algorithm (PURE-LET) to enhance signal/noise ratio for Ca(2+) fluorescen

176 The higher pSNR provided by PURE-LET de-noising increased discrimination accuracy between

177 to binomial filter, no optimization of PURE-LET de-noising was required for reducing arbitrary bias.

178 levels, we analyzed the ability of the PURE-LET algorithm to retrieve the underlying signal.

179 The PURE-LET de-noising algorithm also provided a approximately 3

180 of fluorescent Ca(2+) transients using PURE-LET enhances detection and characterization of Ca(2+) re

181 estigation into different radiation quality, LET and dose/dose rate effect in healthy organs.

182 The hazard ratios (LET/ATA + TOR) were 1.00 (95% CI, 0.92 to 1.08) for TTP,

183 g ATA + TOR and in 36% of patients receiving LET (P < .1).

184 was identical to that for patients receiving LET, representing the first endocrine therapy comparable

185 LC-4, as well as of its upstream regulators, LET-502 (Rho-associated coiled-coil forming kinase) and

186 K-1, and a RhoA-like pathway, involving ROCK/LET-502, control the remodeling of apical junctions and

187 DNA damage than heavier ions do at the same LET.

188 or basolateral localization of LET-23, since LET-23 is mislocalized to the apical membrane in lin-2,

189 o patterns known from cell survival studies, LET-dependencies with pronounced maxima around 100-200 k

190 We find that the PP2A catalytic subunit LET-92, the scaffolding subunit PAA-1, and the B55 regul

191 Is, MCF-7aro cells resistant to letrozole (T+LET R), anastrozole (T+ANA R), and exemestane (T+EXE R),

192 these resistant lines showed that LTEDaro, T+LET R, and T+ANA R cells contained a constitutively acti

193 ated the use of the leukocyte esterase test (LET) on first-catch urine specimens from women as a scre

194 e domain, or it may be involved in tethering LET-23 at the basolateral plasma membrane once it is sec

195 We provide evidence that LET-99 is a link between polarity cues and the downstrea

196 Together, the data indicate that LET-99 acts downstream of PAR-3 and PAR-2 to determine s

197 the alpha2(IV) chain, LET-2, indicating that LET-2 assembly and/or secretion requires EMB-9.

198 We therefore propose that LET-711 inhibits the expression of ZYG-9 and potentially

199 Here we report that LET-99 asymmetry depends on cortically localized PAR-1 a

200 Here we show that LET-99 contributes to furrowing in both asymmetrically a

201 Genetic experiments suggest that LET-60 (L19F) interacts with GAP and GNEF, since mutatio

202 ssociated with ptp-2(op194), suggesting that LET-60 Ras acts downstream of, or in parallel to, PTP-2

203 boundary are complementary, suggesting that LET-99 and Galpha/GPR-1/2 signaling function in opposite

204 tation of this cohort analysis suggests that LET improves DFS and distant DFS even when there has bee

205 This result suggests that LET-23 in proximal vulval precursor cells might bind and

206 This suggests that LET-99 determines the direction of a force on the NCC th

207 The LET-99 localization pattern is dependent on PAR polarity

208 a signal from the anchor cell activates the LET-23 epidermal growth factor receptor (EGFR)/LET-60 Ra

209 ) to behavior (chemotaxis) by activating the LET-60-MPK-1 pathway in specific neurons.

210 rmal growth factor-like ligand LIN-3 and the LET-23 tyrosine kinase receptor induces ovulatory contra

211 hway is activated in hypodermal cells by the LET-23 epidermal growth factor receptor homologue, but a

212 In C. elegans, the LET-23 receptor tyrosine kinase is localized to the baso

213 e in TTP assuming a TTP of 9.4 months in the LET population.

214 only minor structural rearrangements in the LET-23 dimer to promote signalling.

215 , mutations in the lin-2 gene inactivate the LET-23 receptor tyrosine kinase/Ras/MAP kinase pathway r

216 we found that gap-1 may directly inhibit the LET-60 Ras signaling pathway.

217 tor receptor, the SEM-5 adaptor, but not the LET-60 RAS, suggesting that SLI-1 acts before RAS activa

218 can compensate for decreased function of the LET-23 epidermal growth factor receptor, the SEM-5 adapt

219 rther reveal that the preformed dimer of the LET-23 extracellular region is mediated by its domain II

220 -1, functions as a negative regulator of the LET-23 receptor tyrosine kinase and our demonstration th

221 pe is dependent upon the upregulation of the LET-607/CREBH transcription factor and its candidate tar

222 This recruitment requires the LET-711/Not1 subunit of the CCR4-NOT deadenylase and cor

223 g and are consistent with the model that the LET-99 band is important for rotation in wild-type embry

224 unction-associated protein that binds to the LET-23 receptor tyrosine kinase.

225 of the uterine pi lineage respond via their LET-23 epidermal growth factor-like receptors to a vulva

226 Once positioned there, LET-99 enhances myosin accumulation to promote furrowing

227 ite is promiscuous and can mediate all three LET-23 functions.

228 or lower-extremity arterial thromboembolism (LET) are limited and may result from either acute limb i

229 ndomly assigned (434 to ATA + TOR and 431 to LET) in 60 centers in the United States, Canada, Russia,

230 ng the first endocrine therapy comparable to LET in ABC.

231 tically functions upstream or in parallel to LET-23 EGFR.

232 elopment, and acts downstream or parallel to LET-60 (RAS).

233 cal fractures occurred in the women who took LET (5.2% v 3.1%, P = .02).

234 toxicity (AET) and late esophageal toxicity (LET) of four DEs were compared.

235 doses of either high linear energy transfer (LET) alpha-particles or low-LET gamma-rays leads to stim

236 Linear energy transfer (LET) has been scored from energy deposits in a cell nucl

237 Low linear energy transfer (LET) ionizing radiation (IR) is an important form of the

238 High-linear energy transfer (LET) IR (such as high energy charged particles) killing

239 High linear energy transfer (LET) radiation from space heavy charged particles or a h

240 llowing low and high linear energy transfer (LET) radiation in human fibroblasts and epithelial cells

241 ical effects of high-linear energy transfer (LET) radiation is essential for radiation protection and

242 Exposure to high-linear energy transfer (LET) radiation occurs in a variety of situations, includ

243 or low doses of high linear energy transfer (LET) radiation, leading to deviation from the linear dos

244 ominantly using high linear energy transfer (LET) radiation, or high doses of low LET radiation.

245 performed using high linear energy transfer (LET) radiation, such as alpha-particles.

246 d to investigate low linear energy transfer (LET) radiation-induced bystander genotoxicity.

247 Using low linear energy transfer (LET) X-rays to generate simple breaks or high LET HZE pa

248 after 2 or 6 Gy low linear energy transfer (LET), high dose-rate irradiation (Cs-137 irradiator).

249 le range, energy and linear energy transfer (LET).

250 dose and the proton linear energy transfer (LET).

251 s for low dose, high linear-energy-transfer (LET) radiation exposure.

252 al half-life and low linear-energy-transfer [LET] radiative emissions).

253 mLin-7 bound to the chimera with a wild-type LET-23 carboxyl-terminal tail (P75t-Let23WT), but not a

254 complex with E2-Ub conjugating enzyme, Ubc5(LET-70), leading to the formation of an active E3-Ub lig

255 Unfortunately, LET admissions extracted from an administrative database

256 ilar for patients receiving ATA + TOR versus LET, and serious AEs were 10% v 11%, respectively.

257 When LET was compared to TC, the sensitivity, specificity, po

258 ulation of apical LIN-12 in the VPC in which LET-23 is active is not affected.

259 ased accumulation of LIN-12 in VPCs in which LET-23 is not active, and to impaired downregulation of

260 s suggest a positive feedback model in which LET-99 localizes to the presumptive cleavage furrow in r

261 T-99 localization, and PAR-1 associates with LET-99.

262 plicities per cluster steadily increase with LET.

263 All admissions for patients with LET were extracted, and the respective International Cla