ライフサイエンスコーパス: LAD

1 LAD coronary blood flow velocity and free-breathing myoc

2 LAD group had modest but significant slowing in conducti

3 LAD stenosis and additional diagonal graft remained pred

4 LAD wall-thickening (27+/-3 to 46+/-6%, P<0.05) and EF (

5 LAD-2 may thus function in the semaphorin complex by com

6 LAD-III, which presents with bleeding similar to that in

7 LADs are constructed using either a single lignocellulos

8 LADs are redistributed in LMNA-associated DCM in associa

9 LADs are simple, low-cost, easy to use, provide rapid re

10 LADs encompass ~20% of the genome in human cardiac myocy

11 LADs encompassed ~20% of the genome and were predominant

12 LADs were associated with increased CpG methylation and

13 LADs were identified using enriched domain detector prog

14 LADs were redistributed in DCM as evidenced by a gain of

15 bjects with leukocyte adhesion deficiency-1 (LAD-I) do not express beta2 integrins because of mutatio

16 s with leukocyte adhesion deficiency type 1 (LAD-1) had reduced C3 transcripts and diminished effecto

17 from a leukocyte adhesion deficiency type 1 (LAD-I) patient identified CD18 as a putative cell surfac

18 ata that shows that L1-like adhesion gene 2 (LAD-2), a Caenorhabditis elegans L1CAM, functions in axo

19 Genome-wide 331+/-77 LADs with an average size of 2.1+/-1.5 Mbp were identifi

20 s of Skap2 function is sufficient to cause a LAD-like phenotype in mice.

21 thly depot LHRH agonist leuprorelin acetate (LAD-3M; n = 299) and chemotherapy with cyclophosphamide,

22 unction, SCM is indistinguishable from acute LAD-territory MI.

23 Several lung adenocarcinoma (LAD) cell lines were screened to characterize epidermal

24 d anoikis resistance in lung adenocarcinoma (LAD).

25 oncogenic addiction in lung adenocarcinoma (LAD).

26 (b) Coronary angiography projection after LAD stent placement.

27 Although LAD syndromes are rare maladies, their investigation is

28 packed with Juniperus chinensis branches: An LAD that was uniformly distributed, linearly increasing

29 plaque distribution in coronary arteries and LAD predisposition to plaque formation.

30 ocardial PBS injections (control group), and LAD ligation followed by NP12 administration (NP12 group

31 s in their expression levels between IMA and LAD, which included the TES gene encoding Testin.

32 nes differentially expressed between IMA and LAD.

33 on at 1 and 8 weeks post-MI than the LCx and LAD groups, along with early and severe impairment of LA

34 In the LCx and LAD groups, LA dysfunction was less pronounced and not c

35 ic extent in transmural ischemia for LCX and LAD occlusion but not in subendocardial ischemia (associ

36 pe of the relationship between flow rate and LAD, SAD, and volume was significantly different accordi

37 tolic stiffness were elevated in the SCM and LAD MI groups compared with the control group.

38 d diastolic stiffness were higher in SCM and LAD MI patients than in control subjects but no differen

39 SCM and LAD MI show severe diastolic dysfunction.

40 eft ventricular ejection fraction in SCM and LAD MI were 40.8+/-12.3% and 49.6+/-5.6%, respectively,

41 coupling were similarly abnormal in SCM and LAD MI.

42 ic dysfunction is equally reduced in SCM and LAD MI.

43 Moreover, attempts to reconcile TADs and LADs to replication-timing data have not revealed a comm

44 First, considerable overlap between TADs and LADs was observed with the TAD repositioning as a unit.

45 e, 63+/-12 years), those with left anterior (LAD) ST-segment-elevation MI (n=36; mean age, 63+/-10 ye

46 represents the first structural data on any LAD and provides a molecular basis for understanding the

47 in left anterior descending coronary artery (LAD) expands the risk stratification potential of stress

48 he left anterior descending coronary artery (LAD) perfusion territory before microembolization and is

49 he left anterior descending coronary artery (LAD).

50 he left anterior descending coronary artery (LAD).

51 %, with mid left anterior descending artery (LAD) being the most common segment involved.

52 nfarct with left anterior descending artery (LAD) occlusion followed by reperfusion (group 4), or the

53 wine with a left anterior descending artery (LAD) stenosis to produce chronic hibernating myocardium

54 h a chronic left anterior descending artery (LAD) stenosis to produce hibernating myocardium underwen

55 osis of the left anterior descending artery (LAD) underwent vasodilator challenges with hypercapnia a

56 ated in the left anterior descending artery (LAD), and 20 contrast material-enhanced volume scans wer

57 erritories: left anterior descending artery (LAD), left circumflex artery (LCX), and right coronary a

58 stly in the left anterior descending artery (LAD), then in the right coronary artery (RCA), circumfle

59 ry (LCX) or left anterior descending artery (LAD).

60 y (LCA) and left anterior descending artery (LAD).

61 der of glycosylation, CDG-IIc (also known as LAD-II), which is also the result of a GFR deficiency.

62 GEDDs correlate with the lamina-associated (LADs) and replication domains of mammalian cells.

63 of 0.7 mg/kg intraperitoneally 30 min before LAD occlusion.

64 Canyons mostly form between LADs and are enriched in genes and enhancers.

65 ral versus subendocardial ischemia, for both LAD and LCX occlusion.

66 Subjects with LAD-III show symptoms of both LAD-I and Glanzmann's thrombasthenia.

67 C57BL/6 mice underwent 30 min of ischemia by LAD coronary artery ligation followed by various periods

68 gh cell-to-cell consistency, interspersed by LADs with more variable NL interactions.

69 ed genes whose expressions were regulated by LADs or CpG methylation, or by both, the latter pertaine

70 dings suggest that changes that characterize LAD extend beyond the social and communicative symptoms

71 ing was depressed under baseline conditions (LAD 3.7+/-0.3 versus 6.6+/-0.3 in remote regions, P<0.01

72 umber of site-directed variants of N. crassa LAD that are capable of utilizing NADP(+) as cofactor, y

73 similar correlation with previously curated LADs and repressive histone modifications.

74 and observed overlap with previously curated LADs.

75 To establish a last appearance date (LAD) for M. americanum regionally, we obtained 53 new (1

76 es, including leukocyte adhesion deficiency (LAD) patient-derived immortalized B lymphocytes, where n

77 egrin lead to leukocyte adhesion deficiency (LAD) syndrome and mutations in beta(3) integrin cause th

78 e hallmark of leukocyte adhesion deficiency (LAD) syndrome in humans, characterized by impaired leuko

79 F REVIEW: The leukocyte adhesion deficiency (LAD) syndromes are rare genetically determined condition

80 L-arabinitol 4-dehydrogenase (LAD) catalyzes the conversion of l-arabinitol into l-xyl

81 terogeneity in horizontal leaf area density (LAD) within the canopy impacts the ultrafine particle (U

82 ng myocardium were confirmed, with depressed LAD wall thickening and no significant infarction.

83 angiography of the left anterior descending (LAD) and left circumflex (LCX) arteries (30 degrees righ

84 angiography of the left anterior descending (LAD) and left circumflex (LCX) arteries (30 degrees righ

85 angiography of the left anterior descending (LAD) and left circumflex (LCX) arteries (30 degrees righ

86 angiography of the left anterior descending (LAD) and left circumflex (LCX) arteries (30 degrees righ

87 fect of a dominant left anterior descending (LAD) artery and important non-LAD targets on outcomes af

88 for bypassing the left anterior descending (LAD) artery in patients undergoing coronary artery bypas

89 A) grafting of the left anterior descending (LAD) at reoperative coronary artery bypass grafting (CAB

90 sclerosis, whereas left anterior descending (LAD) coronary arteries are athero-prone.

91 (n = 9) underwent left anterior descending (LAD) coronary artery ligation to mimic vulnerable athero

92 ting branch of the left anterior descending (LAD) coronary artery most commonly perfuses the right bu

93 to catheterize the left anterior descending (LAD) coronary artery with x-ray guidance and to delineat

94 nt ligation of the left anterior descending (LAD) coronary artery, and 100 microL of saline, hydrogel

95 e evolution in the left anterior descending (LAD) coronary artery.

96 gery (sham group), left anterior descending (LAD) ligation of the coronary artery followed by intramy

97 LCx group); and 3) left anterior descending (LAD) occlusion (LAD group).

98 of stenosis of the left anterior descending (LAD) or circumflex (LCx) coronary arteries during adenos

99 ularization of the left anterior descending (LAD) territory.

100 evation, 15 min left anteriorior descending, LAD, occlusion in rabbits) with EC50 values of 190 and 8

101 usly in patients with the recently described LAD type III (LAD-III).

102 the model by the Least Absolute Deviations (LAD) approach and implement the computation by median po

103 of lignocellulose-based analytical devices (LADs) for rapid bioanalysis in low-resource settings.

104 ividuals who have lost the autism diagnosis (LAD); that is, they were diagnosed with ASD in early chi

105 ial fibrillation (AF), left atrial diameter (LAD) and low voltage area (LVA) are intermediate phenoty

106 Increased left atrial diameter (LAD) is associated with elevated risk of atrial fibrilla

107 s with AF had a larger left atrial diameter (LAD), waist circumference, and body mass index, and a lo

108 Long-axis diameter (LAD), short-axis diameter (SAD), and volume were measure

109 ations of left and right anterior digastric (LAD, RAD), masseter, buccinator, and genioglossus (GG) m

110 hnology called light-activated dimerization (LAD) to artificially induce protein hetero- and homodime

111 f HCC progression: locally advanced disease (LAD), extrahepatic disease (EHD), and macrovascular inva

112 mina (NL) and the lamina-associated domains (LAD).

113 n about how these lamina-associated domains (LADs) are directed to the nuclear lamina.

114 sm by which these lamina associated domains (LADs) are established remains to be elucidated.

115 Lamina-associated domains (LADs) are regions of repressive heterochromatin position

116 Such lamina-associated domains (LADs) are thought to help organize chromosomes inside th

117 e heterochromatin/lamina-associated domains (LADs) domains are difficult to profile and warrants a si

118 ermore, we mapped Lamina-associated domains (LADs) in mouse liver cells and found that boundaries of

119 " Mesas form at lamin B1-associated domains (LADs) in replicative senescence and oncogene-induced sen

120 , the coverage of lamina-associated domains (LADs) in the genome increases from 53.1% to 68.6%, and a

121 focused either on lamina-associated domains (LADs) or on topologically associated domains (TADs), def

122 Comparison to Lamin-associated domains (LADs) revealed that NPC binding sites can be found withi

123 A/C that tethers lamina-associated domains (LADs) to the nuclear periphery.

124 omains (NADs) and lamina-associated domains (LADs), respectively.

125 entral regions of lamina-associated domains (LADs), which are enriched for Lys9 trimethylation on his

126 hundreds of large lamina-associated domains (LADs).

127 n correlates with lamina-associated domains (LADs).

128 as part of large lamina-associated domains (LADs).

129 d with H3K9me2 and lamin-associated domains (LADs).

130 y mapped lamin-associated chromatin domains (LADs) into two HiLands, HiLands-B and HiLands-P, which a

131 A dominant LAD was defined as one that was wrapped around the left

132 A dominant LAD was present more frequently in patients with less im

133 chniques, we find that low alcohol drinking (LAD) mice have dramatically higher ventral tegmental are

134 dian survival according to cause of dropout (LAD, EHD, or MVI) was 1.0, 4.4, or 3.3 months, respectiv

135 ruitment of YY1 proteins facilitated ectopic LAD formation dependent on histone H3 lysine 27 trimethy

136 The engineered LAD mutants with altered cofactor specificity should be

137 xploratory overall survival analysis favored LAD-3M (HR, 1.50; 95% CI, 1.13 to 1.99; P = .005).

138 Sex-specific growth curves for LAD were estimated for individuals with low, intermediat

139 number of positive sites in the E group for LAD, RAD, and GG muscles in face-M1 and face-S1 at days

140 ay that reached statistical significance for LAD and LVA in both enrichment tools and was also signif

141 After increasing PaO2 to >300 mm Hg, LAD flow decreased in all animals.

142 ils to leukocyte adhesion deficiency type I (LAD-I), a complex inherited disorder in which reduced or

143 ed in the leukocyte adhesion deficiency III (LAD-III) disorder, leading to widespread infection due t

144 disorder leukocyte adhesion deficiency III (LAD-III), integrins on platelets and leukocytes are expr

145 ople with leukocyte adhesion deficiency III (LAD-III).

146 ts with the recently described LAD type III (LAD-III).

147 ENT) IV trial participants who underwent IMA-LAD revascularization and had 12- to 18-month angiograph

148 integrins, which are deficient or absent in LAD-I, and new beta(2) integrin-dependent functions of n

149 Interestingly, similar to activated AKT in LAD cells, although unable to induce epithelial-mesenchy

150 associated positively with 4-year change in LAD (P<0.001).

151 AD flow reserve, with no immediate change in LAD wall thickening.

152 We also related risk factors to changes in LAD during a 4-year period in 3365 participants.

153 Fluorescence signals were detected in LAD coronary, thymus, and liver.

154 ty in subendocardial ischemia, especially in LAD occlusion, as reentries were favoured by the ischemi

155 R signaling maintained aerobic glycolysis in LAD cells.

156 A (VTA-NAc) neurons is selectively higher in LAD mice.

157 sting for age and sex, each unit increase in LAD (mm) was significantly associated with increment of

158 treatment experienced a greater increase in LAD with age (0.95 versus 0.63 mm per 10-year age increm

159 Men had a greater increase in LAD with BMI than women (2.02 versus 1.77 mm in women, p

160 cally more severe bleeding manifestations in LAD-III patients, in which all platelet integrins are fu

161 scovery of 3 cases of reversion mutations in LAD-1 at one center suggests that this may be a relative

162 ence and distribution of coronary plaques in LAD were similar in patients with and without myocardial

163 ough the bleeding disorder is more severe in LAD-III patients, classic aggregometry or perfusion of G

164 defective selectin binding and signaling in LAD-II are now apparent.

165 showed higher TES expression in IMA than in LAD.

166 nternal nuclear organization, and changes in LADs during T-cell activation may provide an important a

167 Third, genes and a putative enhancer in LADs that were released from the periphery during T-cell

168 As a result, pravastatin increased LAD myocyte nuclear density from 830+/-41 to 1027+/-55 n

169 hanism for active AKT-driven EMT-independent LAD metastasis and indicates the great potential of targ

170 Contact of individual LADs with the NL are dependent upon H3K9me2 introduced b

171 d through cell division such that individual LADs are re-established at the nuclear periphery in daug

172 Gene activation inside LADs typically causes NL detachment of the entire transc

173 imarily governed by the spatially integrated LAD when differences in aerodynamic attributes (e.g., fo

174 onary artery bypass grafting in intermediate LAD stenosis without functional evidence of ischemia.

175 cularization, and patients with intermediate LAD stenosis or with an additional bypass graft to the d

176 r baseline HSP27S was associated with larger LAD, whereas baseline HSP27S was not correlated with LAD

177 rox or HDAC3 results in dissociation of LASs/LADs from the nuclear lamina.

178 l arrhythmias, equal groups of animals (LCX; LAD; and sham-operated) underwent sequential electrophys

179 ells and increased myocardial tissue levels (LAD CD133(+) cells from 140+/-33 to 884+/-167 cells/10(6

180 hemic region properties, including location (LAD/LCX occlusion), transmural/subendocardial ischemia,

181 To address this, we mapped LADs using Lamin B1-DamID during Jurkat T-cell activatio

182 For RF ablation lesions, the mean LAD, SAD, and volume demonstrated a significant inverse

183 elegans divergent L1 cell adhesion molecule LAD-2 acting as a non-canonical ephrin receptor to EFN-4

184 t role in aerobic glycolysis in EGFR-mutated LAD cells.

185 the global metabolic pathway in EGFR-mutated LAD cells.

186 herapies to treat patients with EGFR-mutated LAD.

187 primary CABG and whose anterior myocardium (LAD) was at risk at reoperation: 2,389 had LITA grafting

188 In the SDQL neuron, LAD-2 mediates dorsal axon guidance via the secreted MAB

189 G9a-induced H3K9me2 of histones, and for NL-LAD interaction.

190 Non-LAD targets were graded based on their terminal reach to

191 or descending (LAD) artery and important non-LAD targets on outcomes after BITA grafting.

192 lusions, incomplete revascularization of non-LAD territories, and >=70% lesions in nonrevascularized

193 In patients with a nondominant LAD, a second ITA grafted to a less important artery was

194 In patients with a nondominant LAD, selecting an important target for the second ITA lo

195 Revascularization normalized LAD flow reserve, with no immediate change in LAD wall t

196 h a subset of putative active enhancers, not LADs, at locations co-bound by the transcriptional activ

197 3) left anterior descending (LAD) occlusion (LAD group).

198 n 3-IPRR is unable to restore the ability of LAD-III B cells to adhere to and migrate on LFA-1 ligand

199 datasets are a resource for the analysis of LAD rewiring by transcription and reveal a remarkable fl

200 k flow velocity pulsed-Doppler assessment of LAD flow.

201 ifying the KINDLIN-3 protein as the cause of LAD-III in Maltese and Turkish subjects.

202 n the KINDLIN3 (FERMT3) gene is the cause of LAD-III in patients from the Middle East, Malta, and Tur

203 reperfusion (group 4), or the combination of LAD occlusion and 32-mm(3) microemboli followed by reper

204 e EMG responses in different combinations of LAD, RAD, and GG muscles.

205 We evaluated clinical correlates of LAD for a 16-year period in 4403 Framingham Study partic

206 greater BMI as key modifiable correlates of LAD, suggesting that maintaining optimal levels of these

207 arding the short- or long-term correlates of LAD.

208 s IgE- and calcium-mediated degranulation of LAD-2 cells, in a dose-dependent manner.

209 ) as cofactor, yielding the first example of LAD with an almost completely switched cofactor specific

210 Groups of LAD, current ASD, and typically developing (TD) particip

211 The proximal part of LAD was the most commonly affected coronary artery (14 c

212 Location was not a significant predictor of LAD, SAD, or volume (P >/= .4).

213 interaction is increased in the presence of LAD-2, which can interact independently with MAB-20 and

214 in repair of 8-OHG in vulnerable regions of LAD brain.

215 posed model needed in discerning the role of LAD heterogeneity on UFP collection.

216 Here we report the crystal structure of LAD from the filamentous fungus Neurospora crassa at 2.6

217 .7% of LV mass +/- 2.6 compared with that of LAD territory (P = .03).

218 te and platelet functions similar to that of LAD-III patients.

219 e significantly decreased after treatment of LAD cells with EGFRTKI.

220 use liver cells and found that boundaries of LADs are enriched for macroH2A.

221 Here, we demonstrate the implementation of LADs for food and water safety (i.e., nitrite assay in h

222 Fine-scale mapping of LADs reveals numerous lamina-associating sequences (LASs

223 The overall position of LADs was not altered in trisomic cells; however, the H3K

224 Here, we discuss the properties of LADs, the molecular mechanisms that determine their asso

225 The success rate for CFVR on LAD was 3,002 of 3,410 (feasibility = 88%).

226 location, ablation device, and flow rate on LAD, SAD, and volume.

227 ic aggregometry or perfusion of Glanzmann or LAD-III platelets over collagen-coated slides under phys

228 Adhesion Deficiency-III syndrome (LAD-III or LAD-1/variant) present with increased bleeding tendency

229 nary artery disease findings in 16 patients; LAD was affected in 16 (72.3%), RCA in 14 (63.3%), and L

230 a core architecture consisting of gene-poor LADs that contact the NL with high cell-to-cell consiste

231 e EFN-4 engineered to be soluble can promote LAD-2-mediated axon guidance.

232 whether controlled infarction in a proximal LAD septal perforator caused RBBB or LBBB.

233 ze than LBBB is, and occlusion of a proximal LAD septal perforator causes RBBB.

234 Thus, proximal LAD occlusions should cause RBBB, not LBBB.

235 Regional LAD wall thickening slowly improved but remained depress

236 Regional LAD wall thickening was depressed under baseline conditi

237 ontribution to electroanatomical remodeling (LAD, LVA) and AF type via the calcium signaling pathway.

238 was present as reflected by reduced resting LAD flow (0.75+/-0.14 versus 1.19+/-0.14 mL x min(-1) x

239 ated with angina was a poorly revascularized LAD territory.

240 3 (GLUT3) was downregulated in TKI-sensitive LAD cells.

241 Leukocyte Adhesion Deficiency-III syndrome (LAD-III or LAD-1/variant) present with increased bleedin

242 isruption of the gene regulatory rather than LAD tethering function of Lamin A/C may underlie the pat

243 These results suggest that LAD-2 functions as a MAB-20 coreceptor to secure MAB-20

244 g genomic repositioning assays, we show that LADs, spanning the developmentally regulated IgH and Cyp

245 The LAD perfusion territory was 35% of left ventricular (LV)

246 The LAD-III lesion has been attributed to a C --> A mutation

247 e difference in lesion frequency between the LAD and the LCx as these are both parts of the left coro

248 that this change is not responsible for the LAD-III disorder.

249 In the LAD and LCx, plaques tend to cluster within the proximal

250 ptal branches generate disturbed flow in the LAD and PDA in a similar fashion to the myocardial bridg

251 associated with lower (absolute) Ecc in the LAD and RCA regions (regression coefficient 0.37 per uni

252 Similarly, individuals in the LAD group showed a contraction bias.

253 In the LAD group, LA remodeling was not observed by cardiac mag

254 bolic agent was selectively delivered in the LAD in six pigs.

255 number of side branches is lower than in the LAD or RCA and there are no septal perforators with intr

256 Perfusion measurements in the LAD, left circumflex artery (LCx), right coronary artery

257 tegrin-related adhesion and migration in the LAD-III patient's T and B lymphocytes.

258 that the left circumflex artery, and not the LAD, group had atrial infarction.

259 ar courses like in the proximal third of the LAD and the posterior descending artery (PDA).

260 At 20 years, LITA grafting of the LAD at reoperation resulted in an absolute mortality ris

261 MI was induced by permanent occlusion of the LAD coronary artery.

262 dothelium, which are impaired in each of the LAD syndromes, continues to be refined.

263 ance images of the midapical segments of the LAD territory.

264 Results: The LAD territory was 32.4% +/- 3.8(stadard error of the mea

265 , a LITA should be used to revascularize the LAD at coronary reoperations.

266 ary DNA but not CALDAGGEF1 cDNA reverses the LAD-III defect, restoring integrin-mediated adhesion and

267 We show that the LAD estimator is robust in the sense that it has bounded

268 rafting, 2,551 received 1 ITA grafted to the LAD and had an evaluable coronary angiogram.

269 LITA grafting to the LAD is the gold standard for primary CABG, but its value

270 nd 1,084 saphenous vein (SV) grafting to the LAD.

271 demonstrated the following compared with the LAD or control groups: greater slowing in atrial conduct

272 Thus, these LAD-III patient mutations have highlighted functionally

273 Thus, LADs through genomic alterations contribute to the patho

274 74 (43%), and 61 (35.5%) dropped out due to LAD, EHD, and MVI, respectively.

275 inct subcellular sites, into chromatin or to LAD, is not known.

276 h IL-18-neutralizing antibodies 1 h prior to LAD ligation.

277 diabetes, and antihypertensive treatment to LAD.

278 3D space through differences in proximity to LADs along chromosomes.

279 reduced correlation of replication timing to LADs and heterochromatin.

280 LITA-to-LAD grafting at reoperation is safe and confers a risk-a

281 cumulative effects on activity (eg, "total" LAD PDC activity was 21.9+/-3.1 versus 42.8+/-1.9 mU, P<

282 Female FVB mice (n=70) underwent LAD ligation and intramyocardially received one cell typ

283 from borders of fibroblast-specific variable LADs that are sufficient to target these ectopic sites t

284 Predictors of IMA graft failure were LAD stenosis <75% (odds ratio, 1.76; 95% confidence inte

285 ggregates upon collagen stimulation, whereas LAD-III platelets were not.

286 iolar geometric changes were associated with LAD dilatation in 11 children with new onset of KD.

287 .e. CACNA1C, RyR2) that were associated with LAD, LVA and AF type.

288 SNPs found significantly associated with LAD, LVA or AF type were used for gene-based association

289 factor burden was positively associated with LAD.

290 BOLD MR signal changes in canines with LAD stenosis during hypercapnia and adenosine infusion w

291 reas baseline HSP27S was not correlated with LAD in controls.

292 The HSP27S levels were correlated with LAD, left atrial voltage, and fractionated intervals, an

293 Swine were chronically instrumented with LAD and LCX stenoses to produce viable dysfunctional myo

294 nt (0.54 mm) were associated positively with LAD (P<0.001).

295 sweating were initially more pronounced with LAD-3M.

296 Subjects with LAD-III show symptoms of both LAD-I and Glanzmann's thro

297 demonstrated the utility of this system with LAD constructs that can recruit the small G-protein Rac1

298 ociate with nucleoli but do not overlap with LADs.

299 d that NPC binding sites can be found within LADs, demonstrating a linear binding of the genome along

300 cal time-matched surgical procedures without LAD ligation.