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-363/TOR and DAF-15/Raptor are required for developme

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

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

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

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

11 LET-99 is well characterized for generating the asymmetr

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

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

14 Genotyping was successful for 50 of 79 LET subjects with CS-CMVi.

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

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

17 Activated LET-60/Ras and LIN-12/Notch repress expression of the 3

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

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

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

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

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

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

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

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

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

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

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

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

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

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

32 DNA damage and repair with absorbed dose and LET have been published as the Manchester mechanistic (M

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

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

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

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

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

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

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

40 function in mesoderm fate specification and LET-381 function in elongation.

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

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

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

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

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

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

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

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

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

50 irmed chlamydial infections were negative by LET.

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

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

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

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

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

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

57 wed us to identify the UBE2D2/3 E2 conjugase LET-70 working with UBR-5 to exit stem fate.

58 was 64%, 75%, and 80% for attention control, LET, and NLET, respectively.

59 ects 2 and 3, respectively, had discontinued LET prophylaxis and received preemptive therapy with gan

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

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

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

63 a novel beam delivery strategy with elevated LET.

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

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

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

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

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

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

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

71 At 1 year post-HCT, LET was associated with closing the mortality disparity

72 High LET IR produces structurally different forms of DNA dama

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

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

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

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

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

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

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

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

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

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

83 patients by sensitizing tumor cells to high LET radiotherapy.

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

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

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

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

88 A double-strand breaks (DSB) induced by high-LET radiation.

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

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

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

92 In contrast, Auger radiation has high-LET properties with nanometer ranges in tissue, efficien

93 In contrast, Auger radiation has high-LET properties with nanometer ranges in tissue, efficien

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

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

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

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

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

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

100 development frequency after exposure to high-LET particle radiation was significantly higher compared

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

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

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

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

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

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

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

108 lovirus genotyping was performed to identify LET-resistance-associated variants (RAVs) among subjects

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

110 0.8+/-1.8 mL O(2).kg(-1).min(-1) (P=0.07) in LET and NLET, respectively, compared with attention cont

111 d from -3.6 to 5.1 mL O(2).kg(-1).min(-1) in LET and NLET, respectively.

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

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

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

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

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

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

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

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

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

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

122 Letermovir (LET), a cytomegalovirus (CMV) deoxyribonucleic acid (DNA

123 17 trial examined the efficacy of letrozole (LET) started within 3 months of 5 years of adjuvant tamo

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

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

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

127 erventions delivered with a standard linear (LET) (fixed dose intensity per session for 160 min/wk) o

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

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

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

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

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

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

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

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

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

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

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

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

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

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

142 02 to 190 millirads, yielding an average low-LET dose rate of 11.2 millirads per day inside the modul

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

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

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

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

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

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

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

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

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

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

153 9.24 months (ATA + TOR) versus 10.44 months (LET).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

174 dose equivalent from secondary particles of LET(infinity)H(2)O >=15 keV/mum deposited within the pla

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

194 propriately activated 1 and 2 fate-promoting LET-60/Ras and LIN-12/Notch, respectively.

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

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

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

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

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

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

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

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

203 Among all R+, LET was associated with decreased mortality, driven by 7

204 Among R+, LET was associated with decreased risk of death (aHR, 0.

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

206 f CMV resistance among subjects who received LET as prophylaxis in this Phase 3 trial was low.

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

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

209 nd 3 who experienced CS-CMVi while receiving LET prophylaxis, and 2 other variants (encoding pUL56 E2

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

232 The LET RAVs that were detected mapped to the CMV UL56 gene

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

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

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

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

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

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

239 e weights of low-energy beams to elevate the LET therein.

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

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

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

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

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

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

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

247 -1, functions as a negative regulator of the LET-23 receptor tyrosine kinase and our demonstration th

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

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

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

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

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

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

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

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

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

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

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

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

260 sess their potential to confer resistance to LET.

261 ns associated with reduced susceptibility to LET based on resistance selections in cell culture.

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

263 otective role of HLH-30 and DAF-16/FOXO, TOR/LET-363 and the IIS-regulated Zn-finger transcription fa

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

265 on (600 MeV/nucleon, Linear Energy Transfer (LET) = 175 keV/mum).

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

267 e on factors such as linear energy transfer (LET) and dose.

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

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

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

271 tases due to the low linear energy transfer (LET) properties of high-energy beta particles.

272 low-energy and high-linear energy transfer (LET) protons present within the Bragg peak.

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

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

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

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

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

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

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

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

281 The linear energy transfer (LET) spectrum, absorbed dose and dose equivalent from se

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

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

284 ng atomic number and linear energy transfer (LET).

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

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

287 s because of the low-linear-energy-transfer (LET) properties of high-energy beta-particles.

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

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

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

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

292 Unfortunately, LET admissions extracted from an administrative database

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

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

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

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

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

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

299 plicities per cluster steadily increase with LET.

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