ライフサイエンスコーパス: donor site

1 with inversion observed at the cyclopropane donor site.

2 the large intron utilizes a nonconsensus 5' donor site.

3 r L-dA), with either UDP or ADP bound to the donor site.

4 the identified M2 splice acceptor or splice donor site.

5 ce site D2 was changed to a consensus splice donor site.

6 ture, which lacks a ligand at the phosphoryl donor site.

7 er 6 weeks with no apparent morbidity at the donor site.

8 sites that could facilitate use of a cryptic donor site.

9 han any intrinsic limitation of a particular donor site.

10 tion sites unbiased by selection against the donor site.

11 e sites as the acceptor and the other as the donor site.

12 the splicing efficiency of the mutant splice donor site.

13 mutants specifically lacking the I mu splice donor site.

14 nonical AG splice-acceptor site or GT splice-donor site.

15 meshift, and one affected a canonical splice donor site.

16 missense, and one affects a canonical splice-donor site.

17 d by the sequence of the flanking DNA of the donor site.

18 epsilon subunit, and one occurs at a splice donor site.

19 as a G-T substitution at the IVS2 + 1 splice donor site.

20 roject carrying a point mutation in a splice donor site.

21 tcomes and morbidity at the costal cartilage donor site.

22 ly using free-tissue transfer from a distant donor site.

23 ectus abdominis muscle renders an acceptable donor site.

24 ng enhancer that lies adjacent to the second donor site.

25 oryl acceptor site and UDP at the phosphoryl donor site.

26 ibutes to recognition of nonconsensus splice donor sites.

27 ion with SCNM1 in recognition of weak splice donor sites.

28 olved in recognition of non-consensus splice donor sites.

29 with weak splice acceptor sites but not weak donor sites.

30 7, Lys503, Lys620, and Lys762 serve as amine donor sites.

31 between substrates bound to the acceptor and donor sites.

32 sposon lines, derived from four different Ds donor sites.

33 G islands, promoter regions and first splice-donor sites.

34 ns possess weak consensus sequences at their donor sites.

35 ilized, but with associated morbidity at the donor sites.

36 r with substrates bearing readily accessible donor sites.

37 nce flanked by consensus splice acceptor and donor sites.

38 version between the tprK expression site and donor sites.

39 ons, were found in the regions harboring the donor sites.

40 utation 3849 + 10 kb C --> T creates a novel donor site 10 kilobases (kb) into intron 19 of the gene

41 The mutation creates a false GT splice donor site 105 bases 5' of exon 3 and has been demonstra

42 on content of the exon 7 splice acceptor and donor sites (12.3 and 10.4 bits).

43 G introns do possess strong signals at their donor sites, a large subset of alternative GC-AG introns

44 The sites are categorised as: (i) donor sites, a set of 619 EST-confirmed donor sites, for

45 11E1dm and p11Rc-E1dm, mutated at the splice donor site, abolished these splices and increased GFP-E1

46 es can differ appreciably from the geometric donor-site/acceptor-site separation distances.

47 urther advantage is taken of the approximate donor-site/acceptor-site symmetry, in the context of a N

48 mutation abolished intron 6 splicing at the donor site, activated a cryptic splice site, generated p

49 trate loading step to generate the aminoacyl donor site) adjacent to an aminoacyl acceptor site provi

50 lters an invariable nucleotide in the splice donor site after exon 16 of the Trf gene.

51 e due to the nature of the nucleotide at the donor site, allowing us to rationalize the different kin

52 ment achieved with treatment, recipient- and donor-site anatomic characteristics, smoking-related out

53 ent achieved after treatment, recipient- and donor-site anatomic characteristics, smoking-related out

54 proceeds with inversion at the cyclopropane donor site and allows absolute stereochemical informatio

55 of the alternative intron between the splice donor site and alternative acceptor sites resulted in ab

56 lete glycosyltransferases, each containing a donor site and an acceptor site, in one polypeptide.

57 oth are predicted to create a cryptic splice donor site and an out-of-frame pseudoexon.

58 e 3' neighboring nucleotide of the GT splice-donor site and disrupts a predicted stem-loop structure.

59 resulted in extensive end degradation at the donor site and greatly increased the frequency of recomb

60 The excision of transposon Tn7 from a donor site and its insertion into its preferred target s

61 5' end of the 5-kb RNA to a consensus splice donor site and localized the 3' end in the vicinity of a

62 -derived distance between the flavin hydride donor site and quinone hydride acceptor site in the QPAs

63 splice acceptor site, a suboptimal 5' splice donor site and the small size of the exon.

64 transposition, transposons are excised from donor sites and inserted at new locations.

65 rmed between zinc porphyrins equipped H-bond donor sites and pyridine ligands equipped with H-bond ac

66 ses both hard catecholate and soft phosphine donor sites and serves such a role, using soft (C(2)-sym

67 To identify the splice donor sites and splice acceptor sites accurately and qui

68 Biopsies were taken from donor sites and submitted for histology and immunohistoc

69 and gelatin sponge on the healing of palatal donor sites and the patient's morbidity.

70 Five 5' splice sites (donor sites) and six 3' splice sites (acceptor sites) th

71 , a de novo substitution disrupting a splice donor site, and a 3 bp duplication that cosegregated in

72 or site, g(+ 1)-->a transition of the exon 6 donor site, and t(+ 2)-->a substitution at the exon 9 do

73 skipping, use of cryptic splice-acceptor or -donor sites, and intron inclusion.

74 from alternative acceptor sites, alternative donor sites, and retained introns in the transcripts.

75 0.15) did not differ significantly among the donor sites (anterior, posterior, marginal, apical).

76 Although the alcohol H-bond donor sites are involved in H-bond interactions with oth

77 Limbal epithelial stem cells repopulate the donor site as early as 1 year after limbus removal for L

78 rformed comparative sequence analysis of the donor sites, as well as the tprK expression sites, among

79 was abolished by cis mutations in the splice donor site at nucleotide (nt) 226, the splice acceptor s

80 sequence originated via the loss of a splice donor site at the 3' end of exon 14, leading to the subs

81 duced via a run-on event in which the splice donor site at the end of the last constant domain exon (

82 ely involved in guiding acceptors toward the donor site because its disruption kinetically compromise

83 ite, located nine nt 5' to the normal splice donor site, begins with the dinucleotide GC.

84 tation in USP9Y: a 4-bp deletion in a splice-donor site, causing an exon to be skipped and protein tr

85 In family M456, we detected a splice-donor site change in a novel MKS gene, B9D1.

86 PC did not accelerate donor site clinical healing.

87 Donor-site complications can be significant but are usua

88 Donor-site complications in 25 patients (18.5%) included

89 Factors associated with increased donor-site complications included the use of pedicled fl

90 This low rate of donor-site complications strongly supports the use of th

91 Patients with donor-site complications were compared with patients who

92 term results, and no reports have focused on donor-site complications.

93 our Tns proteins and the DNA substrates, the donor site containing Tn7, and the preferred target site

94 70 polymorphism, which resides in the splice donor site controlling transcript-b production.

95 The high percentage of open N-donor sites, coupled with the low framework density resu

96 site mutations led to use of cryptic splice donor sites, creation of a downstream premature terminat

97 Independent of the donor site, DE-harvested CTG contained a significantly h

98 ncing the osteogenic potential of mandibular donor-site defects.

99 that is located 23 bp from the SS#5 exon 23 donor site displays association with P = 0.0007 (odds ra

100 rom DNA via double-strand breaks between the donor-site DNA and the transposon ends, and the newly ex

101 elevated expression and lacking the exon 1B donor site do not confer risk of SLE.

102 steps that liberate the transposon from its donor site, does not involve a site-specific DNA-binding

103 a significant reduction in splicing at this donor site during B19V infection of permissive CD36(+) e

104 31 genomes which had mutations in the splice donor site (E6SD) or the splice acceptor site (E6SA), a

105 d during piggyBac transposition, both at the donor site following transposon excision and at the inse

106 group of methanol is the main hydrogen atom donor site for both 3- and 4-dehydropyridinium cations (

107 e STAT3 genes revealed a highly conserved 5' donor site for generation of both alpha and beta mRNA an

108 thus confirming the necessity for the splice donor site for Sag function.

109 It acts as the donor site for the first template switch, called primer

110 Their enzymatic cavity is composed of a donor site for the growing glycan chain (where the inhib

111 In extensive third-degree burns, donor sites for conventional split thickness skin grafts

112 s of tprK and the identification of putative donor sites for new V region sequences, and we propose a

113 (i) donor sites, a set of 619 EST-confirmed donor sites, for which 138 are either the sites or the r

114 ation and the activation of a cryptic splice donor site from the insertion mutation.

115 iefly, the inflammation status of individual donor sites from 101 patients was visually assessed at t

116 hyria: g(+ 1)-->t transversion of the exon 4 donor site, g(+ 1)-->a transition of the exon 6 donor si

117 cted, the loss of these two NH hydrogen bond donor sites greatly reduces the anion affinity for the d

118 hat contained the acceptor site, whereas the donor site had to be provided by the other subunit.

119 tograft (AG) was performed to assess whether donor-site harvesting can be reduced quantitatively and

120 Both palatal donor sites healed with spontaneous pigmentation.

121 lied on DGGs placed in the recipient bed and donor site immediately after surgery and at days 1 and 3

122 and a G(- 1)-->A substitution at the exon 9 donor site in an additional family.

123 The use of this splice donor site in conjunction with the splice acceptor site

124 The first ATG and splice donor site in exon -1 is predicted to transcribe a cDNA

125 emonstrates a 94 bp deletion using a cryptic donor site in exon 10.

126 increase utilization of an alternate splice donor site in exon 11 of LMNA (the gene encoding lamin C

127 This mutation activates a cryptic splice donor site in exon 11, and leads to an in-frame deletion

128 n 8 was skipped, and one that used a cryptic donor site in exon 8.

129 entified the usage of a non-consensus splice donor site in four families with an intron 4 splice dono

130 tified a g(+ 5)-->a transition of the exon 1 donor site in four unrelated families with erythropoieti

131 +3delTG, which disrupts the invariant splice donor site in intron 42, in both affected individuals.

132 A third mutation affecting the splice donor site in intron 7 was found in one (1.5%) family.

133 ne mutations at the p14ARF exon 1beta splice donor site in melanoma pedigrees.

134 le nucleotide change that abolishes a splice donor site in the ARV1 gene (c.294 + 1G > A homozygous).

135 ve indicated that a polymorphism in a splice donor site in the cyclin D1 gene is associated with alte

136 mbryos have a G-->T transversion at a splice donor site in the ferrochelatase gene, creating a premat

137 mere sequences and were not deleted from the donor site in the genome, leading to the hypothesis that

138 , which is defective in splicing the mutated donor site in the Scn8a(medJ) transcript.

139 fficient in vivo splicing of a mutant splice donor site in the sodium channel Scn8a.

140 s, and creation of splice-acceptor or splice-donor sites in either introns or exons.

141 Paucity of donor sites in massive burns makes the use of expanded s

142 The ASO (ISIS 337846) binds to exon II donor sites in the MyD88 pre-mRNA.

143 rved when improving several potential splice donor sites in the presence of 3' CAG.

144 onsensus region was determined by offering 4 donor sites in the same intron.

145 mutation (IVS3+5G-->A at the intron 3 splice-donor site) in two unrelated families with SEDL.

146 erved that the intrinsically weak variant GC donor sites, in order to be recognized by the U2-type sp

147 -donor substituents and the hydrogen-bonding donor sites increases beta by approximately 50%.

148 cally, we proposed that K140 and R148 in the donor site, instead of the previously proposed E156, are

149 tested so far have left the I mu exon splice donor site intact.

150 Consequently, the normal splice donor site is disrupted and an internal cryptic splice s

151 The carboxylic acid H-bond donor site is inaccessible in the dimer and is not avail

152 t self-association, because the amide H-bond donor site is not accessible in the middle of a polymeri

153 side of the intron, encompassing the splice donor site, is prominently protected by nuclear proteins

154 led the G to A mutation in the exon 1 splice donor site (IVS1+1G-->A) which is predicted to destroy t

155 wo splicing enhancers surrounding the second donor site led to a significant reduction in splicing at

156 One activated donor site, located nine nt 5' to the normal splice dono

157 In addition, two splice donor sites may be utilized to generate Cbfa1/Osf2 cDNAs

158 However, in large burns, sufficient donor sites may not be available to achieve total covera

159 afting material; however, limited supply and donor site morbidity are problematic.

160 n socioeconomically challenged group because donor site morbidity can hinder manual labour and vigoro

161 reconstruct the craniofacial bone and avoid donor site morbidity for CSBDs.

162 Operation time, donor site morbidity, and postoperative recovery between

163 ar condyles suffer from deficiencies such as donor site morbidity, immunorejection, implant wear and

164 met with the challenges of cell scarcity and donor site morbidity, requiring expanded cells that poss

165 han one surgical procedure and can result in donor site morbidity.

166 rvested tissue and can result in significant donor site morbidity.

167 emand prolonged transfer surgery, and induce donor site morbidity.

168 nd located to the nucleus, except one splice-donor site mutant whose protein did not accumulate in th

169 athogenic mutations, such as a common splice donor site mutation (IVS1+2T-->C) and various missense m

170 nked LGMD1D/1E to be due to an intron splice donor site mutation (IVS3+3A>G) of the desmin gene locat

171 ssing a missense mutation (R92Q) or a splice donor site mutation (trunc) in the cardiac troponin T (c

172 A disease-segregating splice donor site mutation in MYH11 (c.4599+1delG) was identifi

173 gs and identifies a highly associated splice donor site mutation in SNX14, with an autosomal recessiv

174 he white recessive allele is due to a splice donor site mutation in the scavenger receptor B1 (SCARB1

175 An intron 1 splice donor site mutation of the Waxy gene is responsible for

176 The intron 9 alternative splice donor site mutation seen in Frasier syndrome leads to lo

177 ties in Northeast Asia also carry the splice donor site mutation, suggesting that partial suppression

178 ed to genotype individual dogs at the splice donor site mutation.

179 y, we identified a NFKB1 heterozygous splice-donor-site mutation (c.730+4A>G), causing in-frame skipp

180 ith a nonsense mutation (R315X) and a splice-donor-site mutation at position +3 of intron 16 (IVS16+3

181 equencing ADAMTS17 revealed a GT-->AT splice-donor-site mutation at the 5' end of intron 10.

182 h Marshall syndrome, we demonstrate a splice-donor-site mutation in the COL11A1 gene that cosegregate

183 r), or an experimentally demonstrated splice-donor-site mutation, c.270+4A>G.

184 udy, we identified novel splice acceptor and donor sites, namely, A1' and D1', in the large nonstruct

185 ary function of U1 snRNA is to define the 5' donor site of an intron, it can also block the accumulat

186 a homozygous splicing mutation in the splice donor site of exon 2 (c.504+1G>A) of RMND1 (required for

187 hat GC instead of GT was found in the splice donor site of exon 4.

188 The mutant splice-donor site of intron 16 harbors five discordant nucleoti

189 ause of a base substitution at the 5' splice donor site of intron 2 of the HLA-A2 gene.

190 leotide substitution in the conserved splice donor site of intron 2.

191 ular, the 8127 g-->a mutation present at the donor site of intron 28 may cause an RNA splice defect.

192 daries conform to the GT/AG rule; the splice donor site of intron 3 is GC/AG.

193 ared to function redundantly with the splice donor site of intron 36.

194 sition at the first nucleotide in the splice donor site of intron 37 completely disables this splice

195 A mutation in the splice donor site of intron 4 of PSEN-1 has been described rece

196 orm to the GT-AG rule, except for the splice donor site of intron 4 that is GC instead of GT.

197 uncovered a mutation in the canonical splice-donor site of intron 5 of JAM3.

198 , and heterozygous point mutations in the 5' donor site of intron 52 and in the middle of exon 73 in

199 shown that a splicing mutation in the splice donor site of intron 7 of the gene encoding the enamel-s

200 iously reported splice variant in the splice donor site of intron IV in the hKLK2 gene.

201 report a novel mutation in the exon 6 splice donor site of keratin 1 (G4134A) that segregates with a

202 s from a point deletion (G) in the 5' splice donor site of MICA intron 4 leading to exon 3 and exon 4

203 In CEF, electrons flow back from the donor site of photosystem I to the plastoquinone pool vi

204 At the intron 8 splice-donor site of the COL1A1 gene, we identified a G+1-->A t

205 The palatal donor site of the epithelialized connective tissue (CT)

206 ore, site-directed mutagenesis of the splice donor site of the first intron affects both correct spli

207 ryotic genes, which overlaps with the splice donor site of the first intron.

208 U group, a localized pannus formation at the donor site of the limbal graft was noted in 5 eyes (12.8

209 that the U1 RNA that binds to the 5' splice donor site of the second intron is fully responsible for

210 The primary mutation (medJ) changes a splice donor site of the sodium channel gene Scn8a (Nav1.6).

211 A mutation in an intron 1 splice donor site of the Waxy gene is responsible for the chang

212 Splice acceptor and donor sites of all introns conformed to the GT/AG rule.

213 r that precisely orients the Cys-rich copper donor sites of CCS and the His-rich acceptor sites of SO

214 ly targeting both the 3' and 5' acceptor and donor sites of exon 4 of COX-2's pre-mRNA sequence.

215 ified reactive glutamine acceptor and lysine donor sites of FnbA may participate in transglutaminase-

216 KA derivative binds to both the acceptor and donor sites of HIV-1 integrase, whereas the monofunction

217 ffected the consensus sequence at the splice donor sites of introns 1 and 9, and produced unstable va

218 in EPSPS was biased towards providing splice donor sites of the inserted Ds sequence.

219 gene yields >90% single cell sectors; empty donor sites often have deletions and insertions, includi

220 upstream and downstream of the major splice donor site on the formation of HIV-2 RNA dimers in vitro

221 ave been identified around three of the four donor sites on chromosomes 1 and 5, as well as near the

222 ll by strongly coordinating to hydrogen bond donor sites on the cellulose surface.

223 ive tissue grafts (CTGs) varies depending on donor site or harvesting technique in terms of relative

224 ngly, mutant genomes in either the E6 splice-donor site or splice-acceptor site were reduced in repli

225 mal or alternative GT-AG introns having weak donor sites or weak polypyrimidine tracts.

226 face disease, conjunctival overgrowth of the donor site, or decrease in vision throughout the follow-

227 the previously identified acceptor site, the donor site, or the catalytic site were inactive, selecti

228 By virtue of containing two splice donor sites, ORF0 can also form fusion proteins with pro

229 GG is associated with a greater incidence of donor site pain compared to CTG at the early postoperati

230 nt, bis-monodentate bridges having their two donor sites pointing in the same direction.

231 was used to discover a mutation in a splice donor site predicted to cause exon skipping.

232 the entire 7.2-kb coding domain, the splice-donor site predicted to function in the generation of th

233 on, or identified splice acceptor and splice donor sites present in the previously characterized M2 g

234 ain root coverage may alleviate the need for donor site procurement of connective tissue.

235 gene (LMNA) that activates a cryptic splice donor site, producing a truncated mutant protein termed

236 The very low-abundance cryptic exon 8 donor site product could have arisen from either pathway

237 sequences downstream from the exon 11 splice donor site promote alternate splicing in both wild-type

238 nized and the higher number of hydrogen bond donor sites provides a remarkable enhancement of its bin

239 ransferase in complex with moenomycin in the donor site, provides a direction for antibacterial drugs

240 (snRNA), the molecule responsible for splice-donor-site recognition.

241 1 + 1655A > G) that creates a cryptic splice donor site resulting in the insertion of a pseudoexon (e

242 on constitutively activates a cryptic splice donor site, resulting in a mutant lamin A protein known

243 the MCM9 c.1732+2T>C variant alters a splice donor site, resulting in abnormal alternative splicing a

244 mutations in LMNA activate a cryptic splice donor site, resulting in expression of a truncated, pren

245 e mutation, a change in the intron 15 splice donor site, results in two truncated forms of troponin T

246 Analysis of 1,801 native splice-donor sites reveals that presence of a G nucleotide at +

247 occurs with insertions closely linked to the donor site roughly one-third of the time.

248 at least one-but sometimes both-chromosomal donor site(s).

249 l genome, and also contains the major splice-donor site (SD) for mRNA splicing.

250 Mutations in the major splice donor site (SD) markedly reduced viral RNA expression bu

251 of a rigid weak anion-exchange site and a H-donor site separated from each other in a defined distan

252 Manipulation of the splice donor site sequence enables control of the relative amou

253 inity of U1 snRNP binding to the intervening donor site, significantly augmented inhibition of (pA)p,

254 leotide mutations affecting consensus splice donor sites, some of which are recurrent, that lead to s

255 ear RNAs (snRNA) complementary to the splice donor sites strongly improved or completely rescued spli

256 ingle nucleotide at the 3' end of the splice-donor site suggests a model whereby the yeast RNA-repair

257 branes offers the advantages of preventing a donor site surgery and a second surgical procedure for b

258 ential clinical difficulties associated with donor site surgery.

259 al clinical difficulties associated with the donor site surgery.

260 ation of the C(3)-fac-isomer with all PPh(2) donor sites syn to each other or facile fac/mer isomeriz

261 utation generates a more accessible splicing donor site than does WT and produces an alternatively sp

262 inant containing a mutation in the 5' splice donor site that defines the 5' end of the RNA and found

263 mmediately downstream of the nonconsensus 5' donor site that functions as an intronic splicing enhanc

264 7.2-kb transcript maps to a consensus splice-donor site that is conserved among all cytomegaloviruses

265 s missense mutation creates a cryptic splice donor site that produces a mutant lamin A protein, terme

266 ) globin allele has a mutation in the splice donor site that produces the same aberrant transcripts i

267 itfa(vc7)ts allele is a mutation in a splice donor site that reduces the level of correctly-spliced t

268 e, and t(+ 2)-->a substitution at the exon 9 donor site; these mutations are predicted to cause splic

269 apy (ESWT) can enhance healing of skin graft donor sites, this study focused on shock wave effects in

270 sue graft (CTG) wound healing and maintained donor site tissue thickness.

271 s ability to excise precisely, restoring the donor site to its pretransposon state.

272 slation start site and the intron 7-8 splice donor site to knock down spastin function in the develop

273 LMNA) gene, which activates a cryptic splice donor site to produce abnormal lamin A; this disrupts th

274 c transposon 5' end, which provided a splice donor site to yield abundant novel transcripts.

275 IV), Sn(IV)) metallaligands via their soft P donor sites to C(2)-symmetric PdBr(2) units gives exclus

276 d, via exon skipping and alternate 5'-splice donor sites, to yield five splice variants (canine mda-7

277 borne MMTV transmission, we mutated a splice donor site unique to a spliced sag RNA from the 5' envel

278 framework with a large percentage (67%) of N-donor sites unused for bonding with metals.

279 region; the fourth mutation affects a splice donor site upstream of this region.

280 ssfully identify a disease-associated splice donor site variant in the sorting nexin 14 gene (SNX14)

281 The GABRG2 intron 6 splice donor site was found to be mutated from GT to GG.

282 Healing of the gingival unit donor site was uneventful.

283 n of recognized and potential cryptic splice donor sites was able to abrogate these splicing events a

284 The right palate, which served as the donor site, was deepithelialized, and a large connective

285 sus nucleotides at the +3 position of splice-donor sites, we constructed a minigene that spans exons

286 both the nucleoside acceptor and nucleotide donor sites, we solved the crystal structures of the enz

287 PC-treated palatal donor sites were 1.10 mm thicker than control sites.

288 All donor sites were closed primarily.

289 Furthermore, the splice acceptor and splice donor sites were conserved, and the size of the introns

290 The donor sites were treated with PC and placebo.

291 ally deleted Ds elements can arise at the Ac donor site when Ac transposes to another site in the gen

292 terpene cyclases have ionization and alkene-donor sites which spatially overlap those found in CrtM.

293 ically used for such indications, requires a donor site, which may lead to various clinical complicat

294 und within the fragment two cryptic splicing donor sites whose products were present in transgenic mo

295 Hemostasis was achieved at the palatal donor sites with moistened gauze, and an acrylic stent w

296 only one quasi-equatorial conformer on both donor sites, with charge-transfer (CT) emission close to

297 arises from the use of an alternative splice donor site within intron 1, is conserved in the mouse ge

298 12, through the use of an alternative splice donor site within intron 1.

299 a potentially aberrant splice from a cryptic donor site within the first exon to the splice acceptor

300 dented dual utilization of a splice acceptor/donor site within the IRF-3 mRNA governs the production