ライフサイエンスコーパス: CEL

1 CEL and MG-H(1) significantly reduced final body weight

2 CEL I can detect 100% of the sequence variants present,

3 CEL I, isolated from celery, is the first eukaryotic nuc

4 CEL I-like nucleases are found in many plants.

5 CEL is also a major lipase in the breast milk of many ma

6 CEL is extremely polymorphic due to a variable number ta

7 CEL transgenic mice bred to an atherosclerosis susceptib

8 CEL-1 has a C-terminal domain containing motifs found in

9 CEL-1 shows a strong preference for RNA substrates of at

10 CEL-1 uses a mechanism similar to protein-tyrosine phosp

11 CEL-INS proteins may therefore be constantly produced fr

12 CEL-Seq2, in contrast, makes use of poly-dT primers to r

13 CEL-transfected cells secreted active enzyme into the me

14 We use data from >28 000 CEL files relating to 10 different Affymetrix GeneChip p

15 ewT2w: OR 1.69, 95% CI 1.10-2.59, p = 0.017; CEL: OR 1.54, 95% CI 1.01-2.34, p = 0.046).

16 oxyl ester lipase (CEL) gene, resulting in a CEL protein with increased tendency to aggregate.

17 Moreover, by using a CEL-INS-specific antibody, we observed patchy signals in

18 f raw microarray data files (e.g. Affymetrix CEL files) can be time consuming, complex, and requires

19 All CEL-HYB1 positive carriers from Hungary had the Thr488-T

20 Although CEL is synthesized predominantly in the pancreas, a low

21 gut microbiota composition, with MG-H(1) and CEL notably increasing Verrucomicrobiaceae and Erysipelo

22 t was high for detection of newT2w (97%) and CEL (96.8%).

23 embrane is attributed to the bipolar AEL and CEL that eliminate ion crossover.

24 o the duodenum of lymph fistula CEL(+/+) and CEL(-/-) mice at a rate of 0.3 ml/h.

25 ts showed no difference between CEL(+/+) and CEL(-/-) mice in the rate of cholesterol and triglycerid

26 ine residue in alphaBC increased the CML and CEL accumulation.

27 In addition, CML and CEL are ligands for RAGE, a receptor for AGEs, which has

28 understanding of the biosynthesis of CML and CEL could lead to the development of new therapies again

29 of GSH or N-acetylcysteine enhanced CML and CEL formation in alphaBC.

30 on with GO or MGO resulted in higher CML and CEL formation in the two cysteine residues containing al

31 Our data showed that CML and CEL formation occurs through a hemithioacetal intermedia

32 ues in alphaAC significantly reduced CML and CEL formation.

33 and K166 to be heavily modified with CML and CEL in GO- and MGO-modified alphaAC.

34 es of 82+/-3% and 91+/-10% (n=6) for CML and CEL respectively and, calibration curves (R(2)>0.9985) w

35 However, both control and CEL-transfected cells accumulated exogenously added CM-R

36 es of about zero, demonstrating that CUR and CEL could synergistically prevent peritendinous adhesion

37 itive multicomponent EPM loaded with CUR and CEL was tested for anti-adhesion capacity in vitro and i

38 methyltransferase identification (DamID) and CEL-Seq2.

39 es the current state of knowledge of HES and CEL and the implications of the FIP1L1-PDGFRA discovery

40 Recent reports indicate that HES and CEL are imatinib-responsive malignancies, with rapid and

41 However, not all HES and CEL patients respond to imatinib, suggesting disease het

42 MGH1 and CEL intake were not significantly associated with SAF.

43 PNLIP, PNLIPRP2, and CEL were increased in fat necrosis.

44 d lipid absorption efficiency due to PTL and CEL inactivation also resulted in protection against die

45 Thus, this study documents that PTL and CEL serve complementary functions, working together to m

46 o 61.1 +/- 3.8% in mice lacking both PTL and CEL.

47 ficant clinical implications, as both PV and CEL patients are at high risk for thrombosis, and concom

48 Smart-seq, DP-seq and CEL-seq, and demonstrated significant technical variatio

49 red with commercial sample, while in TDB and CEL, phenolics remain almost unchanged.

50 s showed no difference between wild type and CEL knockout mice in the total amount of cholesterol abs

51 mulation than that observed in wild type and CEL(-/-) mice.

52 ter were not different between wild-type and CEL-deficient mice.

53 gh fat/high cholesterol diet, wild type, and CEL(-/-) mice gained approximately 24 g of body weight.

54 We found that both CEL-WT and CEL-MUT were secreted via the endoplasmic reticulum and

55 Both CEL and anti-CEL-producing plasmablasts could be isolated directly fr

56 Titers of anti-CEL IgG and IgA antibodies were highly elevated in HS co

57 Strikingly, the majority of anti-CEL IgG was of the IgG2 subclass and correlated independ

58 in pancreatic tissue from humans without any CEL-INS variant in the germline.

59 e it, suggesting that another enzyme besides CEL can hydrolyze dietary CE in mice.

60 ate that in the mouse, other enzymes besides CEL participate in the hydrolysis of dietary cholesteryl

61 een batches within an experiment and between CEL files within a batch.

62 Results showed no difference between CEL(+/+) and CEL(-/-) mice in the rate of cholesterol an

63 Both CEL and anti-CEL-producing plasmablasts could be isolate

64 using transfected cells indicated that both CEL-HYB1 haplotypes induced significant ER stress and th

65 We found that both CEL-WT and CEL-MUT were secreted via the endoplasmic ret

66 nt have suggested that MODY8 is initiated by CEL protein misfolding and aggregation.

67 strates indicated that those manufactured by CEL Associates, Inc. yield the highest oligo coverage.

68 induced specific DNA cleavage as measured by CEL-1 assays.

69 4 repeats in the VNTR (CEL14R) or C563fsX673 CEL (CEL maturity onset diabetes of youth with a deletio

70 1 (MG-H(1)), N(epsilon)-carboxyethyllysine (CEL), and a heated diet on metabolic health and gut micr

71 ine (CML) and N(epsilon)-carboxyethyllysine (CEL), formed by glycation from GO and MGO, are among the

72 compounds and N-epsilon-carboxyethyllysine (CEL) were reduced to 50%, after 13 min at 180 degrees C;

73 Twenty-eight samples (14.0%) carried CEL-INS alleles.

74 7) and controls (n = 9) from France carrying CEL-HYB1 contained the Thr488-Thr548 haplotype.

75 eats in the VNTR (CEL14R) or C563fsX673 CEL (CEL maturity onset diabetes of youth with a deletion mut

76 eukemia, chronic eosinophilic leukemia (CEL)/CEL, not otherwise specified (CEL-NOS), myeloid/lymphoid

77 er 2000 and April 2001 releases) and Celera (CEL; February 2001 release) databases.

78 that purified nucleases derived from celery (CEL I), mung bean sprouts and Aspergillus (S1) were able

79 ble polymers of chitosan (CS) and cellulose (CEL) to synthesize green chitosan-cellulose (CS-CEL) nan

80 ion of protein bound Amadori compounds, CML, CEL and dicarbonyls.

81 Participants consumed less CML, CEL, and MG-H1 during the low-AGE dietary period than du

82 owed to simultaneously quantify lysine, CML, CEL and the Nepsilon-(2-Furoylmethyl)-L-lysine (furosine

83 Overall, intakes of CML, CEL, and MG-H1 were not associated with the microvascula

84 Free forms of CML, CEL, and Ndelta-(5-hydro-5-methyl-4-imidazolon-2-yl)-orn

85 rmal inactivation in comparison with control CEL.

86 ) to synthesize green chitosan-cellulose (CS-CEL) nanocomposite as a new clarifying agent.

87 It was also observed that CS-CEL has high mechanical stability.

88 Overall, we can conclude that CS-CEL nanocomposite has considerable efficiency in sugarca

89 The CS-CEL nanocomposite showed outstanding results in zeta pot

90 Also, Turbidity decreased using CS-CEL nanocomposite compared to the traditional phosphotat

91 ier and reservoir of curcumin/celecoxib (CUR/CEL) to prevent peritendinous adhesion.

92 e and fibrous adhesion number in the EPM+CUR/CEL group were close to extremely low values of about ze

93 mputational analyses, M3D provides raw data (CEL file) and normalized data downloads of each compendi

94 his issue by chemically synthesizing defined CEL modifications on Abeta1-42 at Lys-16 (Abeta-CEL16),

95 ng two of the six ORF that had been deleted: CEL ORF3 (HopPtoM) and ORF4 (ShcM).

96 We found that the loss of virulence in Delta CEL and dspA/E mutants was linked to their inability to

97 The Delta CEL mutant activated SA-dependent callose deposition in

98 nt pathogens Pseudomonas syringae (the Delta CEL mutation), Erwinia amylovora (the dspA/E mutation),

99 e also compare with Smart-Seq to demonstrate CEL-Seq2's increased sensitivity relative to other avail

100 refore investigated nondiabetic and diabetic CEL-mutation carriers by pancreatic imaging studies and

101 Mice with different CEL genotypes [wild type (WT), knockout (CELKO), heteroz

102 We demonstrated that double-CEL glycations at Lys-16 and Lys-28 of Abeta1-42 had the

103 ncreatic enzyme activities related to either CEL or PTL were separated using DEAE-chromatography.

104 The Caenorhabditis elegans CEL-1 capping enzyme consists of an N-terminal region wi

105 on due to mutations in the CEL gene encoding CEL.

106 operty of the mismatch-specific endonuclease CEL I to cleave heteroduplex DNA with a very high specif

107 gene with the mismatch specific endonuclease CEL I.

108 cked at mismatched sites by the endonuclease CEL I and cut strands are visualized using Li-cor gel an

109 were transfected with constructs expressing CEL with 14 repeats in the VNTR (CEL14R) or C563fsX673 C

110 terials for converting the raw data files (*.CEL) for comparative analysis.

111 s infused into the duodenum of lymph fistula CEL(+/+) and CEL(-/-) mice at a rate of 0.3 ml/h.

112 .87 mg/d for MGH1, and 3.11 +/-0.89 mg/d for CEL.

113 assessed the highest antioxidant effect for CEL with starters (21.7mg Trolox eq/g FW; 8.5mumol hydro

114 vel and physiologically significant role for CEL, namely the promotion of large chylomicron productio

115 Other suggested roles for CEL include the direct facilitation of the intestinal ab

116 total CML were three times higher than free CEL levels.

117 PMaP (SNP microarrays and pooling) data from CEL files to Relative Allele Scores in the rich R statis

118 the presence of bile salt and distinct from CEL, is present, compatible with the results from our ac

119 Peritoneal macrophages from CEL transgenic mice displayed a 4-fold increase in [(3)H

120 Here we characterize a gene (CEL-1) believed to encode the C. elegans capping enzyme.

121 t that F/P is not sufficient to induce a HES/CEL-like disease but requires a second event associated

122 gel electrophoresis band for the homogeneous CEL I, with and without the removal of its carbohydrate

123 r of wild-type, heterozygous, and homozygous CEL-deficient mice, the levels of bile salt-dependent re

124 However, CEL(-/-) mice produced predominantly smaller lipoprotein

125 However, CEL-1 has no detectable PTP activity.

126 However, CEL-INS variants with insertions occurring in the most p

127 region that resembles known GTases, However, CEL-1 has not previously been shown to have GTase activi

128 hydrolytic activity inhibited by anti-human CEL IgG.

129 ock-in mice expressing the most common human CEL VNTR with 16 repeats.

130 We implemented CEL-Seq2 on Fluidigm's C1 system, providing its first si

131 ted that amino acid positions 488 and 548 in CEL-HYB1 determined pathogenicity.

132 Thr488-Ile548 haplotype, which was absent in CEL-HYB1 positive controls from Germany (n = 13) and Pol

133 could find structural pancreatic changes in CEL-MODY subjects during the course of diabetes developm

134 nd accumulation of neoplastic eosinophils in CEL.

135 s of ceramide and lysophosphatidylcholine in CEL-expressing cells than in CEL-negative cells.

136 ide hydrolytic activity than that present in CEL(+/+) mice.

137 C and cyanidine-3-glucoside and quercetin in CEL.

138 We also studied tissue uptake of CM-RE in CEL-deficient mice generated by targeted disruption of t

139 show the involvement of arginine residues in CEL-bile salt interaction.

140 tidylcholine in CEL-expressing cells than in CEL-negative cells.

141 ' linkages in SRELs were higher than that in CEL.

142 sing and absorption of RE were unimpaired in CEL-deficient mice.

143 om Hungary and found significantly increased CEL-HYB1 carrier frequency in CP cases (9/319, 2.8%) ver

144 in inducing lipolysis and lipotoxic injury, CEL required bile acid concentrations higher than in hum

145 se polyamide layer, a cation exchange layer (CEL), and an anion exchange layer (AEL).

146 Full-length CEL-1 has RTPase and GTase activities, and the cDNA can

147 ons (newT2w) and contrast-enhancing lesions (CEL).

148 ome (HES) and chronic eosinophilic leukemia (CEL) comprise a spectrum of indolent to aggressive disea

149 F/P-positive chronic eosinophilic leukemia (CEL) in humans.

150 Chronic eosinophilic leukemia (CEL) is a myeloproliferative neoplasm characterized by e

151 GFRA-positive chronic eosinophilic leukemia (CEL), little is known about optimal dosing, duration of

152 f both PV and chronic eosinophilic leukemia (CEL).

153 lic leukemia, chronic eosinophilic leukemia (CEL)/CEL, not otherwise specified (CEL-NOS), myeloid/lym

154 osis (SM) and chronic eosinophilic leukemia (CEL)/hypereosinophilic syndrome (HES).

155 A cellulolytic enzyme lignin (CEL) was also prepared as a comparison.

156 SP, like CEL I, does not turn over after incision at a mismatched

157 le salt activation of carboxyl ester lipase (CEL) activity.

158 the contributions of carboxyl ester lipase (CEL) and pancreatic triglyceride lipase (PTL) in lipid n

159 hybrid allele of the carboxyl ester lipase (CEL) gene and its pseudogene (CELP) has been associated

160 the last exon of the carboxyl ester lipase (CEL) gene, resulting in a CEL protein with increased ten

161 Pancreatic carboxyl ester lipase (CEL) hydrolyzes cholesteryl esters (CE), triglycerides (

162 To study the role of carboxyl ester lipase (CEL) in hepatic retinoid (vitamin A) metabolism, we inve

163 Carboxyl-ester lipase (CEL) maturity-onset diabetes of the young (MODY) is a mo

164 peat (VNTR) domain of carboxyl ester lipase (CEL) presents an opportunity to study the pathogenesis o

165 patocytes showed that carboxyl ester lipase (CEL), a broad-spectrum lipase secreted by pancreas and l

166 tion of R-9-PAHSA and carboxyl ester lipase (CEL), a PAHSA degradative enzyme, selectively hydrolyzin

167 Bile salt-stimulated carboxyl ester lipase (CEL), also called cholesterol esterase, is one of the ma

168 ein 2 (PNLIPRP2), and carboxyl ester lipase (CEL), which may leak into the visceral fat or systemic c

169 iously we showed that carboxyl ester lipase (CEL)-deficient (CELKO) mice have normal levels of pancre

170 Carboxyl ester lipase (CEL, also called cholesterol esterase or bile salt-depen

171 Carboxyl ester lipase (CEL; EC 3.1.1.13) hydrolyzes cholesteryl esters and reti

172 n that mutations in conserved effector loci (CEL) in the plant pathogens Pseudomonas syringae (the De

173 n of one ipx gene, conserved effector locus (CEL) orf1, encoding a putative lytic murein transglycosy

174 ORF) in the DC3000 conserved effector locus (CEL) reduces parasitic growth and abolishes disease symp

175 locus (EEL) and a conserved effector locus (CEL).

176 l)lysine (CML), N(euro)-(carboxyethyl)lysin (CEL), and methylglyoxal-derived hydroimadazolidine (MG-H

177 rected against Nepsilon-carboxyethyl lysine (CEL), a methylglyoxal-induced advanced glycation end-pro

178 e (CML) and N-epsilon-(carboxyethyl) lysine (CEL)) in the crust and crumb of gluten-free bread enrich

179 ne (CML), N(epsilon)-(1-carboxyethyl)lysine (CEL) and N(delta)-(5-hydro-5-methyl-4-imidazolon-2-yl)-o

180 N (e)-(Carboxyethyl)lysine (CEL) is a common AGE associated with AD patients and occ

181 sine (CML), Nepsilon-(1-carboxyethyl)lysine (CEL), and Ndelta-(5-hydro-5-methyl-4-imidazolon-2-yl)-or

182 sine (CML), Nepsilon-(1-carboxyethyl)lysine (CEL), and pentosidine were measured in plasma.

183 )-ornithine (MGH1), and carboxyethyl-lysine (CEL)] was estimated using FFQs and the content of AGEs m

184 ine (CML), Nepsilon-(Carboxyethyl)-L-lysine (CEL).

185 and free Nepsilon-(1-Carboxyethyl)-L-Lysine (CEL).

186 and physiological significance of macrophage CEL expression.

187 s study used transgenic mice with macrophage CEL expression at levels comparable with that observed i

188 Collectively, the improvements make CEL-Seq2 uniquely suited to single-cell RNA-Seq analysis

189 id requirements for effective lipolysis make CEL an unlikely mediator of lipotoxic injury in AP.

190 K), MODY3 (HNF1A), MODY5 (HNF1B), and MODY8 (CEL) with a polycistronic lentiviral vector expressing a

191 SM development and pathogenesis in a murine CEL model induced by F/P in hematopoietic stem cells and

192 ution of the wild type (WT) and mutant (MUT) CEL proteins in cellular models.

193 studies revealed less R63A and R423G mutant CEL were bound to 1,2-diolein monolayer at saturation co

194 system, and after its secretion, the mutant CEL protein was re-internalized, transported to the lyso

195 rmite di Bitetto (TDB) and Cellina di Nardo (CEL) were studied, highlighting also the cultivars influ

196 al therapeutic approaches against neurotoxic CEL-glycated Abeta1-42.

197 lication to identifying predictors of newT2w/CEL after BCDT start.

198 sent study, we further investigated this non-CEL REH activity in pancreas homogenates of CELKO and wi

199 atic activity comparable with that of normal CEL.

200 ent for mutation detection, a novel nuclease CEL I from celery.

201 re, we investigated four naturally occurring CEL variants, arising from single-base deletions in diff

202 ignificantly increased RCT in the absence of CEL and suggest a novel mechanism by which to manipulate

203 In contrast, the addition of CEL to the apical medium increased the amount of large l

204 Colocalization of CEL in the vicinity of OxLDL formation was supported by

205 We measured the concentration of CEL in human plasma as 1.2+/-0.5 ng/ml (in the range rep

206 ed that Thr488 is the primary determinant of CEL-HYB1 misfolding and associated endoplasmic reticulum

207 The N-terminal domain of CEL-1 has RNA triphosphatase activity.

208 The effect of CEL on RCT of HDL cholesterol was assessed by measuring

209 Expression of CEL MODY increased endoplasmic reticulum stress, activat

210 along with the high population frequency of CEL-INS alleles strongly suggests that these variants ar

211 te] were generated to study the functions of CEL in a physiological system.

212 Homologies of CEL I with S1 and P1 nucleases are much lower.

213 Although higher intake of CEL was associated with higher flicker light-induced ven

214 Internalization of CEL-MUT also led to reduced viability of pancreatic acin

215 The proximal intestine of CEL(-/-) mice was also found to possess significantly le

216 These data indicate that the lack of CEL expression does not affect the uptake of dietary CM-

217 nce in C. elegans embryos shows that lack of CEL-1 causes development to arrest with a phenotype simi

218 redominantly in the pancreas, a low level of CEL expression was reported in human macrophages.

219 ticipate in micellar bile salt modulation of CEL enzymatic activity through intramolecular hydrogen b

220 /P-dependent proteins in the pathogenesis of CEL.

221 The physiological role of CEL was originally thought to be its mediation of dietar

222 Secretion of CEL MODY was decreased compared with that of CEL14R.

223 irst (DEL1) or fourth (DEL4) VNTR segment of CEL cause maturity-onset diabetes of the young, type 8 (

224 However, the x-ray crystal structure of CEL failed to show the involvement of arginine residues

225 subcellular distributions differed, as only CEL-MUT was observed as an aggregate at the cell surface

226 The CUR- or CEL-loaded EPM possessed a better anti-adhesion ability

227 in 4.13 hours ($28); 79% showed no newT2w or CEL.

228 processes data generated from the CEL-Seq or CEL-Seq2 protocols and reports comprehensive data qualit

229 present CEL-Seq2, a modified version of our CEL-Seq method, with threefold higher sensitivity, lower

230 In vivo, pancreatic CEL is thought to liberate cholesterol and retinol from

231 lipids were incubated with purified porcine CEL without or with cholate (10 or 100 microM, concentra

232 T-cell overexpression of IL-5 (F/P-positive CEL mice).

233 clonal population in FIP1L1/PDGFRA-positive CEL and suggest that molecular monitoring may be the mos

234 ions, 5 patients with FIP1L1/PDGFRA-positive CEL with documented clinical, hematologic, and molecular

235 Here, we present CEL-Seq2, a modified version of our CEL-Seq method, with

236 0% in PTL(-/-) mice (p < 0.05) and PTL(-/-), CEL(-/-) mice (p < 0.01), respectively.

237 e body weight gain in PTL(-/-) and PTL(-/-), CEL(-/-) mice was attributed to their absorption of fewe

238 g less (p < 0.01) in PTL(-/-) and PTL(-/-), CEL(-/-) mice, respectively, despite their consumption o

239 difference was not exaggerated in PTL(-/-), CEL(-/-) mice.

240 We have purified CEL I 33 000-fold to apparent homogeneity.

241 Recognizing this new PV/CEL-overlap MPN has significant clinical implications, a

242 -RH7777) cells stably transfected with a rat CEL cDNA.

243 alt-independent hydrolytic activities of rat CEL.

244 lyzed the haplotype distribution of reported CEL-HYB1 carriers from three European cohorts and found

245 Since CEL is expressed mainly in pancreatic acinar cells, we a

246 Single-CEL glycations at Lys-28 of Abeta1-42 had the least impa

247 paediatric AIDs (pAIDs), including JIA, SLE, CEL, T1D, UC, CD, PS, SPA and CVID, attributable to comm

248 the understanding of how the acinar-specific CEL-MUT protein causes both exocrine and endocrine pancr

249 Meanwhile, a mismatch-specific CEL II enzyme (Surveyor((R)) nuclease) cleaved the imper

250 inophilic leukemia, not otherwise specified (CEL, NOS) is assigned to patients with MPN with eosinoph

251 leukemia (CEL)/CEL, not otherwise specified (CEL-NOS), myeloid/lymphoid neoplasm with eosinophilia an

252 be confined to the gastrointestinal system, CEL has been reported in the plasma of humans and other

253 We conclude that CEL has the capability to modify normal human LDL and HD

254 These studies documented that CEL expression in macrophages is pro-atherogenic and tha

255 The current study tests the hypothesis that CEL in the intestinal lumen may influence the type of li

256 , was required for absorption, implying that CEL was not the responsible enzyme.

257 Our results indicate that CEL I mutation detection is a highly sensitive method fo

258 ious tissues did not differ, indicating that CEL deficiency does not affect hepatic retinoid metaboli

259 and 1.6+/-0.1, respectively, indicating that CEL interaction varied with lipoprotein class.

260 We propose that CEL I exemplifies a new family of neutral pH optimum, ma

261 These findings further support the view that CEL mutations cause pancreatic disease through protein m

262 The CEL carries at least seven ORFs that are conserved betwe

263 The CEL gene encodes carboxyl ester lipase, a pancreatic dig

264 The CEL-1 RTPase domain is related by sequence to protein-ty

265 The CEL-HYB1 hybrid allele of the carboxyl ester lipase (CEL

266 28% of the CEL I polypeptide, we cloned the CEL I cDNA.

267 .5-fold higher in macrophages expressing the CEL transgene.

268 This is the case for the CEL gene, which is specifically expressed in pancreatic

269 of A-T-rich regions distinguish SP from the CEL I family of neutral pH mismatch endonucleases recent

270 ge that preprocesses data generated from the CEL-Seq or CEL-Seq2 protocols and reports comprehensive

271 re found for 5% and 2% of the markers in the CEL and HGP-sc sequences, respectively.

272 exocrine dysfunction due to mutations in the CEL gene encoding CEL.

273 The hopPtoM and avrE genes in the CEL of P. syringae were found to encode suppressors of t

274 nic lysophosphatidylcholine was lower in the CEL transgenic mice, but plasma cholesterol level and li

275 and frameshift mutation (C563fsX673) in the CEL VNTR causes CP through proteotoxic gain-of-function

276 mice generated by targeted disruption of the CEL gene.

277 w and developed normally, independent of the CEL genotype of the pup or nursing mother.

278 SP nuclease may be a natural variant of the CEL I family of mismatch endonucleases is discussed.

279 ion of the amino acid sequence of 28% of the CEL I polypeptide, we cloned the CEL I cDNA.

280 results, along with computer modeling of the CEL protein, indicated that Arg(63) and Arg(423) are not

281 , whereas deletion of a large portion of the CEL strongly reduces growth and abolishes pathogenicity

282 dominantly smaller lipoproteins, whereas the CEL(+/+) mice produced primarily large chylomicrons and

283 position of single-base deletions within the CEL VNTR affects pathogenic properties of the protein.

284 lesion area than apoE(-/-) mice without the CEL transgene when both were fed a high fat/cholesterol

285 nd removal of various blob defects from the .CEL files of different types of Affymetrix microarrays.

286 id content were similar in mice of all three CEL genotypes.

287 The mechanism appears to be mediated through CEL hydrolysis of ceramide generated during the lipid ab

288 inly to PTL, and to a much smaller extent to CEL.

289 Similar to CEL I, the presence of a DNA polymerase or a DNA ligase

290 aled to form heteroduplexes and subjected to CEL I incision.

291 ases in k(cat), in comparison with wild type CEL, for bile salt-dependent cholesteryl ester hydrolysi

292 es, respectively, in comparison to wild type CEL.

293 olayer at saturation compared with wild type CEL.

294 In both cell types, CEL MODY formed intracellular aggregates.

295 le method of enzyme mutation detection using CEL I can efficiently identify mutations and polymorphis

296 he least impact on fibril formation, whereas CEL glycations at Lys-16 of Abeta1-42 delayed fibril for

297 into cholesteryl [(3)H]oleate compared with CEL-negative macrophages when the cells were incubated u

298 nd only in rats and WT mice, consistent with CEL-mediated cholesteryl ester hydrolysis.

299 After a 4-h incubation with CEL, the lysoPC content of OxLDL was depleted 57%.

300 These findings show that subjects with CEL-MODY develop multiple pancreatic cysts by the time t