ライフサイエンスコーパス: ICL

1 ICL confers an increased risk of opportunistic infection

2 ICL formation quenches the fluorescence of coumarin, whi

3 ICL predisposes patients to severe opportunistic infecti

4 ICL-1 utilizes a bioinspired endoperoxide trigger to rel

5 ICLs are produced upon irradiation under anoxic conditio

6 ICLs are thought to be processed by proteins from a vari

7 ICLs can be repaired by the Fanconi anemia (FA) pathway

8 characterization of iron-caged luciferin-1 (ICL-1), a bioluminescent probe that enables longitudinal

9 causes genetic instability without affecting ICL repair.

10 e angle narrowing was detected 1 month after ICL V4c implant, this narrowing remained stable at 3 mon

11 It localizes to telomeres in S phase after ICL damage where it has enhanced association with TRF1 a

12 1 month, 3 months, 1 year, and 2 years after ICL implant.

13 95% CI, 10.1%-25.8%) at 5 and 10 years after ICL implantation, respectively.

14 pment and refractive outcomes 10 years after ICL implantation.

15 PolH contributions to the protection against ICL-inducing agents were evaluated by its siRNA-mediated

16 niscent of a replication fork arrested at an ICL.

17 tivation of a reporter plasmid containing an ICL.

18 onuclease mechanism allows FAN1 to excise an ICL from one strand through flanking incisions.

19 mutants display towards mechlorethamine, an ICL-inducing compound.

20 sing the leading strand at the 3' side of an ICL lesion.

21 lisions, either from one or both sides of an ICL, initiate repair processes required for resumption o

22 the structure and extent of processing of an ICL, its bypass may not absolutely require TLS polymeras

23 e consistent with replication traverse of an ICL, without lesion repair.

24 vivo from DNA replication fork bypass of an ICL.

25 When a replication fork collides with an ICL, it triggers a damage response that promotes multipl

26 After replication forks collide with an ICL, the leading strand approaches to within one nucleot

27 atin after replication forks collide with an ICL.

28 erent lengths into complementary strands and ICL formation using a double reductive amination with a

29 pathways (BER, MMR, NER, NHEJ, HR, TLS, and ICL repair) are specifically discussed for inhibitor dis

30 umulation of CSB at sites of monoadducts and ICLs, but it did not affect recruitment to (although sli

31 nd resection and homologous recombination at ICL damage.

32 ith monoubiquitinated FANCD2 (FANCD2(Ub)) at ICLs.

33 ay in Rh30 rhabdomyosarcoma cells attenuated ICL-induced activation of ATM, accompanied with the decr

34 te can unhook either or both sides of an AZB ICL, providing a basis for understanding the mechanisms

35 of the available patient information before ICL implantation.

36 rosslinks (ICLs), although MMR proteins bind ICLs and other DNA structures that form at stalled repli

37 recognition and the Fanconi anemia (FA)-BRCA ICL repair network.

38 ent on Polbeta misincorporation at cisplatin ICL sites, which results in persistent cisplatin ICLs an

39 MR participation in non-productive cisplatin ICL processing is downstream of BER processing and depen

40 Cisplatin ICLs inhibit transcription as effectively as 1,2-d(GpG)

41 revealed the unique properties of cisplatin ICLs on nucleosome mobility and on transcription, and th

42 plays a key role in the removal of cisplatin ICLs, acting in a replication-independent fashion.

43 sites, which results in persistent cisplatin ICLs and sensitivity to cisplatin.

44 e decline in multiple organs, yet it confers ICL-induced anti-cancer drug resistance in several cance

45 FANCD2 proteins that subsequently coordinate ICL removal and repair of the ensuing DNA double-strande

46 We hypothesized that MMR proteins corrupt ICL repair in cells that lack crosstalk between BRCA-FA

47 acts, we describe here a replication-coupled ICL repair pathway that does not require incisions or FA

48 extracts, which support replication-coupled ICL repair, we show that the 3' flap endonuclease XPF-ER

49 promotes a key event in replication-coupled ICL repair.

50 plication-coupled DNA interstrand crosslink (ICL) repair, the XPF-ERCC1 endonuclease is required for

51 tion primarily in DNA interstrand crosslink (ICL) repair.

52 genes regulating DNA interstrand crosslink (ICL) repair.

53 ecombination (HR) and interstrand crosslink (ICL) repair.

54 s one defense against interstrand crosslink (ICL)-inducing agents.

55 ancer cell line to interstrand-crosslinking (ICL) agents.

56 or the repair of DNA interstrand crosslinks (ICL).

57 on and repair of DNA interstrand crosslinks (ICL).

58 in the repair of DNA interstrand crosslinks (ICLs) and regulates cellular responses to replication st

59 in the repair of DNA interstrand crosslinks (ICLs) are associated with the genome instability syndrom

60 DNA interstrand crosslinks (ICLs) are extremely cytotoxic lesions that block essenti

61 DNA interstrand crosslinks (ICLs) are generated by endogenous sources and chemothera

62 Interstrand crosslinks (ICLs) are toxic DNA lesions that cause severe genomic da

63 to survive toxic DNA interstrand crosslinks (ICLs), although MMR proteins bind ICLs and other DNA str

64 umor agents form DNA interstrand crosslinks (ICLs), but their clinical efficiency is counteracted by

65 DNA interstrand crosslinks (ICLs), highly toxic lesions that covalently link the Wat

66 emotherapy cause DNA interstrand crosslinks (ICLs), which covalently link both strands of the double

67 calizing SLX4 to DNA interstrand crosslinks (ICLs), yet how SLX4 is targeted to other functional cont

68 he processing of DNA interstrand crosslinks (ICLs).

69 ng the repair of DNA interstrand crosslinks (ICLs).

70 of resistance to DNA interstrand crosslinks (ICLs).

71 ersensitivity to DNA interstrand crosslinks (ICLs).

72 damage, specifically interstrand crosslinks (ICLs).

73 ducts and trioxsalen interstrand crosslinks (ICLs).

74 optical cavity operating with a 3.29 mum cw ICL is detailed, and a quantitative characterization of

75 gher accumulation of the extremely cytotoxic ICLs and DSBs lesions, which in turn triggers the induct

76 pon ICL induction, suggesting that defective ICL repair causes karyomegaly.

77 s (KIN), but it is unclear whether defective ICL repair is responsible or whether Fan1 nuclease activ

78 ng, differentiated state, as well as delayed ICL processing as revealed by a modified Comet assay and

79 D2, and Merit40-null cells exhibited delayed ICL unhooking coupled with reduced end resection and hom

80 i and NEIL1 excise unhooked psoralen-derived ICLs in three-stranded DNA via hydrolysis of the glycosi

81 ike DNA glycosylases unhook psoralen-derived ICLs in various DNA structures via a genuine repair mech

82 ductive amination and yield a set of diverse ICLs that will be invaluable for exploring structure-act

83 py and form an array of structurally diverse ICLs.

84 critical for telomere maintenance after DNA ICL damage.

85 tment of FAN1 to ICLs or for its role in DNA ICL resistance.

86 that alphaIISp is critical for repair of DNA ICLs at telomeres, likely by facilitating the recruitmen

87 tical, to its proposed role in repair of DNA ICLs in genomic DNA and that this function in turn is cr

88 of LC-MS/MS for assessing the repair of DNA ICLs.

89 transfer between coumarin and dG slows down ICL formation.

90 Interestingly, Merit40 mutation exacerbated ICL-induced chromosome instability in the context of con

91 ycosylase that protects its host by excising ICLs derived from azinomycin B (AZB), a potent antimicro

92 Following ICL implant, corresponding values fell to 31.2 +/- 11.5,

93 roteins act in a linear hierarchy: following ICL detection on chromatin, the FA core complex monoubiq

94 age and is most rapid and robust as follows: ICLs>DSBs>monoadducts>oxidative lesions.

95 ential use as an immunotherapeutic agent for ICL.

96 al of 107 eyes from 56 patients assessed for ICL implantation at our institution were included in the

97 ld serve to identify suitable candidates for ICL placement.

98 The SIMs of SLX4 are dispensable for ICL repair but important for processing CPT-induced repl

99 ment of Fan1 by Ub-Fancd2 is dispensable for ICL repair.

100 of a favorable architectural environment for ICL repair processing.

101 rug Administration's accepted guidelines for ICL sizing, clinicians should be aware of and account fo

102 o stalled replication forks is important for ICL repair.

103 The Fan1 nuclease, also required for ICL repair, is recruited to ICLs by ubiquitinated (Ub) F

104 mice, we show that Trp53 is responsible for ICL-induced bone marrow failure and that loss of Trp53 i

105 myopic subjects consecutively scheduled for ICL implant, FDOCT (RTVue; Optovue Inc) iridocorneal ang

106 nthesis of structurally diverse major groove ICLs that induce severe, little or no distortion in the

107 f XPF-ERCC1, RPA and SNM1A might explain how ICL unhooking is achieved in vivo.

108 nd the immunomodulatory effects of rhIL-7 in ICL patients.

109 fic siRNA improved CD4(+) T-cell activity in ICL, as this restored TCR-induced extracellular signal-r

110 at PTEN and FANCD2 function cooperatively in ICL repair.

111 on protein A (RPA), show profound defects in ICL repair.

112 prevalent hypothetical role of MUS81-EME1 in ICL repair is to unhook the damage by incising the leadi

113 The earliest DNA processing event in ICL repair is the incision of parental DNA on either sid

114 case unloading as a critical, early event in ICL repair.

115 rovide insight into the mechanism of FAN1 in ICL repair and demonstrate that the Fan1 mouse model eff

116 We also establish that PTEN function in ICL repair is dependent on its protein phosphatase activ

117 nucleases, and the DOG-1 (FANCJ) helicase in ICL resolution, influenced by the replicative-status of

118 sent a promising therapeutic intervention in ICL.

119 y or the Slx4-Slx1 nuclease also involved in ICL repair.

120 -1) and transcription-coupled (CSB-1) NER in ICL sensing were exposed.

121 grates with the FA complex to participate in ICL repair.

122 ANCI-FANCD2 (ID) complex and participates in ICL repair.

123 en together, our findings implicated PolH in ICL repair as a mechanism of cancer drug resistance and

124 xploring structure-activity relationships in ICL repair.

125 ceptor (TCR) signaling have been reported in ICL, but the mechanistic and causative links remain uncl

126 Cdc48/VCP segregase plays a critical role in ICL repair by unloading the CMG complex from chromatin.

127 No obvious or critical role in ICL repair was seen for non-homologous end-joining (cku-

128 BRCA1 and BRCA2 also play important roles in ICL repair.

129 gs identify a premature T-cell senescence in ICL that might be caused by chronic T-cell activation an

130 ecifically introduces negative supercoils in ICL-containing plasmids in HeLa cell extracts.

131 The increased ICL sensitivity of PTEN-deficient cells is caused, in pa

132 in human cells, and its depletion increases ICL-induced mutagenesis in human cells without altering

133 cover replication-dependent and -independent ICL repair networks, and establish nematodes as a model

134 be recruited to localized trioxsalen-induced ICL damage in human cells, with accumulation being suppr

135 laser-induced DSBs but not psoralen-induced ICLs is dependent on nuclease-active MRE11.

136 to cleave psoralen- and abasic site-induced ICLs in Xenopus egg extracts.

137 abolish interaction with RFWD3 also inhibit ICL repair, demonstrating that RPA-mediated RFWD3 recrui

138 he formation of intrastrand and interstrand (ICL) crosslinks, but the precise downstream effects of t

139 Intriguingly, ICL repair protein, Fanconi anemia complementation group

140 using mid-infrared interband cascade lasers (ICLs) is a sensitive technique for trace gas sensing.

141 after 2 years of implantable collamer lens (ICL) V4c (STAAR Surgical AG, Nidau, Switzerland) placeme

142 Importance: Intraocular collamer lenses (ICLs) are posterior chamber phakic lenses that provide a

143 substrate containing a nitrogen mustard-like ICL two nucleotides in the duplex region because FAN1, u

144 ed with chromosomal DNA replication to limit ICL repair-associated mutagenesis.

145 show that FAN1 was able to degrade a linear ICL substrate.

146 Quantitative DNA interstrand cross-link (ICL) formation was observed with the coumarin moieties c

147 Interstrand cross-link (ICL) hypersensitivity is a characteristic trait of Fanco

148 uring eukaryotic DNA interstrand cross-link (ICL) repair, cross-links are resolved ("unhooked") by nu

149 N1's function in DNA interstrand cross-link (ICL) repair.

150 AN1 nuclease and DNA interstrand cross-link (ICL) unhooking.

151 y lethal lesion are interstrand cross-links (ICL), a property exploited by several anti-cancer chemot

152 ooking highly toxic interstrand cross-links (ICLs) and bulky minor groove adducts normally recognized

153 Interstrand cross-links (ICLs) are extremely toxic DNA lesions that create an imp

154 Interstrand cross-links (ICLs) are highly cytotoxic DNA lesions that block DNA re

155 DNA interstrand cross-links (ICLs) are highly toxic lesions associated with cancer an

156 Interstrand DNA cross-links (ICLs) are repaired by mechanisms using translesion DNA s

157 DNA interstrand cross-links (ICLs) are repaired in S phase by a complex, multistep me

158 mong these adducts, interstrand cross-links (ICLs) are the most toxic, as they stall replication by g

159 DNA interstrand cross-links (ICLs) block replication fork progression by inhibiting D

160 rsensitivity to DNA interstrand cross-links (ICLs) but not whole-body irradiation.

161 hat BrdU yields DNA interstrand cross-links (ICLs) in non-base-paired regions motivated us to develop

162 d breaks (DSBs) and interstrand cross-links (ICLs), but its mechanism of action is not well understoo

163 l for repairing DNA interstrand cross-links (ICLs), but the underlying mechanisms are unclear.

164 ity to generate DNA interstrand cross-links (ICLs), which effectively block the progression of transc

165 rsensitivity to DNA interstrand cross-links (ICLs).

166 upled repair of DNA interstrand cross-links (ICLs).

167 for processing DNA interstrand cross-links (ICLs).

168 d for repair of DNA interstrand cross-links (ICLs).

169 epducin for the beta2AR, intracellular loop (ICL)1-9, was used to decouple beta-arrestin-biased signa

170 In contrast, intracellular loops (ICLs) and C-terminalresidues exited the ribosome into a

171 a tetrahelix bundle of intracellular loops (ICLs) during channel opening.

172 ace involving a pair of intracellular loops (ICLs) that form ball-and-socket joints.

173 e of the glyoxylate shunt, isocitrate lyase (ICL), may mediate survival of Mtb during the acute and c

174 Isocitrate lyase (ICL, types 1 and 2) is the first enzyme of the glyoxylat

175 igger activation of Mtb's isocitrate lyases (ICLs), metabolic enzymes commonly assumed to be involved

176 ndly than deletion of its isocitrate lyases (ICLs).

177 Idiopathic CD4 lymphopenia (ICL) is a rare heterogeneous immunological syndrome of u

178 Idiopathic CD4 lymphopenia (ICL) is a rare syndrome defined by low CD4 T-cell counts

179 Idiopathic CD4(+) lymphopenia (ICL) is a rare syndrome characterized by low peripheral

180 FANCA), greatly enhances MUS81-EME1-mediated ICL incision.

181 78 patients undergoing consecutive V4 model ICL implantations, which took place from January 1, 1998

182 enses implanted were as follows: 53 V4 model ICLs of -15.5 D or greater, 73 V4 model ICLs of less tha

183 odel ICLs of -15.5 D or greater, 73 V4 model ICLs of less than -15.5 diopter (D), and 7 V4 model tori

184 d a panel of model unhooked nitrogen mustard ICLs to systematically investigate how the state of an u

185 where alphaIISp levels are 35-40% of normal, ICL damage results in failure of XPF to localize to telo

186 We observed ICL-induced chromosomal breakage in 9 of 17 (53%) HNSCC

187 Application of ICL-1 in a model of systemic bacterial infection reveals

188 to be an important long-term complication of ICL implantation.

189 d in the defective hematopoietic function of ICL-repair deficient myeloid progenitors.

190 ically restored survival, but not growth, of ICL-deficient Mtb metabolizing acetate or propionate.

191 oxylate levels using a chemical inhibitor of ICL restored growth of MS-deficient Mtb, despite inhibit

192 FAN1's mechanism of ICL excision is well suited for processing other localiz

193 ase, or "unhook", ICLs, but the mechanism of ICL unhooking remains largely unknown.

194 o the structure and reactivity parameters of ICL formation by double reductive amination and yield a

195 The pathogenesis of ICL remains unclear, and whether effector sites are also

196 tion and represents the preferred pathway of ICL repair in a vertebrate cell-free system.

197 of NER and DSB/R (P <0022), similar rates of ICL/R, and more condensed chromatin structure compared w

198 rates of NER and DSB/R, comparable rates of ICL/R, more condensed chromatin structure, and higher se

199 PolH attenuation reduced repair of ICL lesions as measured by host cell reactivation assays

200 Deep sequencing of ICL repair products showed that the approach and extensi

201 o report that unloading of RPA from sites of ICL induction is perturbed in RFWD3-deficient cells.

202 eby preventing RFWD3 recruitment to sites of ICL-induced replication fork stalling.

203 implicate MERIT40 in the earliest stages of ICL repair and define specific functional interactions b

204 Our data demonstrate that CIN in terms of ICL-induced chromosomal breakage and defective chromatid

205 pathways; however, a clear understanding of ICL recognition and repair processing in human cells is

206 lication forks stall, even in the absence of ICLs.

207 roduce metabolites that promote formation of ICLs leading to inhibition of trypanosomal growth.

208 h structures might prevent the generation of ICLs, while favoring intrastrand cross-links.

209 ors that protect against the genotoxicity of ICLs generated by trioxsalen/ultraviolet A (TMP/UVA) dur

210 chemosensitize cells by inhibiting repair of ICLs and DSBs.

211 Repair of ICLs requires sequential incisions, translesion DNA synt

212 ng the mechanisms of base excision repair of ICLs.

213 icate that CSB coordinates the resolution of ICLs, possibly in a transcription-associated repair mech

214 ecruitment, CSA itself localized at sites of ICLs, DSBs and monoadducts but not at oxidative lesions.

215 onitored protein assembly and disassembly on ICL-containing chromatin.

216 es the incision specificity of MUS81-EME1 on ICL damage and establishes that FANCA regulates the inci

217 , HMGB1 functions in association with XPA on ICLs and facilitates the formation of a favorable archit

218 vault height (distance between the posterior ICL surface and anterior lens surface) measured a mean (

219 Thus, Fan1 nuclease activity promotes ICL repair in a manner that controls ploidy, a role that

220 estores cell cycle progression, and promotes ICL resistance through a Rad18-dependent mechanism.

221 in principle explain how Ub-Fancd2 promotes ICL repair, but we show that recruitment of Fan1 by Ub-F

222 onse to ICL and that mTOR signaling promotes ICL-induced ATM-Chk2 checkpoint activation by sustaining

223 ME1 incises DNA at the 5' side of a psoralen ICL residing in fork structures.

224 Using laser-induced psoralen ICL formation in cells, we find that FANCA interacts wit

225 ) protein bound to triplex-directed psoralen ICLs (TFO-ICLs) in vitro, cooperatively with NER damage

226 We report the synthesis of a putative ICL repair intermediate that mimics the complete process

227 epair (NER), interstrand cross-links repair (ICL/R), double-strand breaks repair (DSB/R), and chromat

228 TbSNM1, a nuclease that specifically repairs ICLs, are hypersensitive to most ABQ prodrugs, a phenoty

229 biochemical basis of essentiality for Mtb's ICLs and survival on fatty acids.

230 Mtb's ICLs are catalytically bifunctional isocitrate and methy

231 Here, we report that Mtb's ICLs are essential for survival on both acetate and prop

232 tify a previously undescribed role for Mtb's ICLs in antioxidant defense as a mechanism of antibiotic

233 that while purified XPF-ERCC1 incises simple ICL-containing model replication fork structures, the pr

234 oking mechanism for psoralen and abasic site ICLs.

235 Here, we use repair of a site-specific ICL in Xenopus egg extracts to study the mechanism of le

236 usly reported the synthesis of site-specific ICLs mimicking those formed by nitrogen mustards to faci

237 fore, NBD2 might be critical for stabilizing ICLs 2 and 3 that form a tetrahelix bundle at the NBD2 i

238 MSH2 depletion also suppresses ICL sensitivity in cells deficient for BRCA1 or FANCD2,

239 bound to triplex-directed psoralen ICLs (TFO-ICLs) in vitro, cooperatively with NER damage recognitio

240 ons and facilitated error-free repair of TFO-ICLs in mouse fibroblasts.

241 re, we demonstrate that HMGB1 recognizes TFO-ICLs in human cells, and its depletion increases ICL-ind

242 ospective single center study indicates that ICL implantation provides good long-term safety and stab

243 Our results show that ICL repair and replication termination both utilize a si

244 Here, we show that ICL sensitivity of cells lacking the interaction between

245 We further show that ICL-deficient Mtb strains are significantly more suscept

246 icient human cells significantly altered the ICL-induced mutation spectrum from predominantly T-->A t

247 cised the substrate predominantly beyond the ICL and, therefore, failed to release the 5' flap.

248 ivity and chromosome radial formation by the ICL-inducing agent mitomycin C (MMC).

249 How DNA polymerases bypass the ICL is incompletely understood.

250 nick, NEIL3 targets both DNA strands in the ICL without generating single-strand breaks.

251 Instead, the ICL is unhooked when one of the two N-glycosyl bonds for

252 d approaches to within one nucleotide of the ICL ("approach"), a nucleotide is inserted across from t

253 cision of parental DNA on either side of the ICL ("unhooking"), which allows lesion bypass.

254 n fatty acids accumulated high levels of the ICL aldehyde endproduct, glyoxylate, and increased level

255 l of these pathways require unhooking of the ICL from one strand of a DNA duplex by nucleases, follow

256 TRF2 and is required for recruitment of the ICL repair protein, XPF, to damage-induced foci at telom

257 e strand of the duplex on either side of the ICL.

258 ing strand of a replication fork strikes the ICL Here, we report that while purified XPF-ERCC1 incise

259 ent recruitment of XPF-ERCC1 and SLX4 to the ICL depends on FANCD2 and its ubiquitylation.

260 ws leading strands to be extended toward the ICL, followed by endonucleolytic processing of the cross

261 is study included 17 eyes implanted with the ICL V4b model and 18 eyes implanted with the ICL V4c mod

262 ICL V4b model and 18 eyes implanted with the ICL V4c model.

263 ver, the recruitment of XPA and HMGB1 to the ICLs is co-dependent.

264 Inefficient repair of these ICL can lead to leukemia and bone marrow failure.

265 -associated nuclease 1 (FAN1) contributes to ICL repair, FAN1 mutations predispose to karyomegalic in

266 e mutagenic DNA repair following exposure to ICL-inducing agents.

267 t FANCA interacts with and recruits MUS81 to ICL lesions.

268 MERIT40 was rapidly recruited to ICL lesions prior to FANCD2, and Merit40-null cells exhi

269 vation of ATM-Chk2 checkpoint in response to ICL and that mTOR signaling promotes ICL-induced ATM-Chk

270 In response to ICL V4c implant, considerable angle narrowing was detect

271 ilitate the studies of cellular responses to ICL formation.

272 for the initial rapid recruitment of FAN1 to ICLs or for its role in DNA ICL resistance.

273 is central to the pathway, and localizes to ICLs dependent on its monoubiquitination.

274 uitinates and recruits the FANCD2 protein to ICLs on chromatin.

275 lso required for ICL repair, is recruited to ICLs by ubiquitinated (Ub) Fancd2.

276 ed for cellular and organismal resistance to ICLs.

277 exhibited an impaired RAD51 foci response to ICLs, but not to DNA double-strand breaks.

278 than -15.5 diopter (D), and 7 V4 model toric ICLs for myopia.

279 This ability of FAN1 to traverse ICLs in DNA could help to elucidate its biological funct

280 for the incisions that release, or "unhook", ICLs, but the mechanism of ICL unhooking remains largely

281 lly investigate how the state of an unhooked ICL affects pol eta activity.

282 length of the duplex surrounding an unhooked ICL critically affects polymerase efficiency.

283 imics the complete processing of an unhooked ICL to a single crosslinked nucleotide, and find that it

284 ucleases, followed by bypass of the unhooked ICL by translesion synthesis (TLS) polymerases.

285 The structures of the unhooked ICLs remain unknown, yet the position of incisions and p

286 of incisions and processing of the unhooked ICLs significantly influence the efficiency and fidelity

287 from Fan1(nd/nd) mice become polyploid upon ICL induction, suggesting that defective ICL repair caus

288 In vertebrates, ICL repair is triggered when replication forks collide w

289 Visian ICL implantation improves visual function in special nee

290 achieved by sulcus implantation of a Visian ICL (STAAR Surgical, Monrovia, California, USA) under ge

291 unilateral intraocular collamer lens (Visian ICL) implantation for moderate to high myopia.

292 Treatment of Fan1-deficient mice with ICL-inducing agents results in pronounced thymic and bon

293 mucosal biopsy specimens from patients with ICL and healthy controls were evaluated.

294 erved in the mucosal tissue of patients with ICL by flow cytometry and immunohistochemistry, compared

295 e-differentiated T cells in 20 patients with ICL displayed defective TCR responses and aging markers

296 uman IL-7 (rhIL-7) per week in patients with ICL who were at risk of disease progression.

297 s factor, were not elevated in patients with ICL, compared with healthy controls, whereas soluble CD1

298 These data suggest that patients with ICL, despite gut mucosal lymphopenia and local tissue in

299 vated in the colonic mucosa of patients with ICL.

300 was preserved in the mucosa of patients with ICL.

301 alizing encounters of replication forks with ICLs as they occur in living cells.