ライフサイエンスコーパス: donor site

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

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

3 with inversion observed at the cyclopropane donor site.

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

5 same splicing variant affecting a consensus donor site.

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

7 the identified M2 splice acceptor or splice donor site.

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

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

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

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

12 tion sites unbiased by selection against the donor site.

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

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

15 the splicing efficiency of the mutant splice donor site.

16 mutants specifically lacking the I mu splice donor site.

17 ectus abdominis muscle renders an acceptable donor site.

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

19 han any intrinsic limitation of a particular donor site.

20 tcomes and morbidity at the costal cartilage donor site.

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

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

23 ibutes to recognition of nonconsensus splice donor sites.

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

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

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

27 7, Lys503, Lys620, and Lys762 serve as amine donor sites.

28 between substrates bound to the acceptor and donor sites.

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

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

31 ns possess weak consensus sequences at their donor sites.

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

33 r with substrates bearing readily accessible donor sites.

34 version between the tprK expression site and donor sites.

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

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

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

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

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

40 11E1dm and p11Rc-E1dm, mutated at the splice donor site, abolished these splices and increased GFP-E1

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

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

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

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

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

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

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

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

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

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

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

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

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

54 5' end of the 5-kb RNA to a consensus splice donor site and localized the 3' end in the vicinity of a

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

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

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

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

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

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

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

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

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

64 letions in the packaging signal/major splice donor site, and 7 (1.0%) were sequence intact.

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

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

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

68 0.15) did not differ significantly among the donor sites (anterior, posterior, marginal, apical).

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

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

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

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

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

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

75 ding, and swelling at both the recipient and donor sites at 1 week, 2 weeks, 1 month, and 3 months.

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

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

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

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

80 PC did not accelerate donor site clinical healing.

81 Donor-site complications can be significant but are usua

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

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

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

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

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

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

88 70 polymorphism, which resides in the splice donor site controlling transcript-b production.

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

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

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

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

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

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

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

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

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

98 discomfort (eating, speaking, etc.) from the donor site during the first postoperative week; this was

99 31 genomes which had mutations in the splice donor site (E6SD) or the splice acceptor site (E6SA), a

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

101 ponge with or without sutures in the palatal donor sites following connective tissue grafting via the

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

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

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

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

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

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

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

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

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

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

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

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

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

115 e)/bis(amidinate) platforms with up to six N-donor sites has now been established.

116 Both palatal donor sites healed with spontaneous pigmentation.

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

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

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

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

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

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

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

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

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

126 +3delTG, which disrupts the invariant splice donor site in intron 42, in both affected individuals.

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

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

129 upported by its coevolution with the cryptic donor site in primate species.

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

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

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

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

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

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

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

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

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

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

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

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

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

143 At the same time, they tolerate many donor sites, including basic nitrogen and numerous heter

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

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

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

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

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

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

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

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

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

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

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

155 e defects resulting from trauma or diseases, donor site morbidity and limited availability restrict t

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

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

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

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

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

161 Limiting factors for this treatment include donor site morbidity, potential disease transmission, an

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

163 th high infection rates, implant erosion and donor site morbidity.

164 abundant, can be harvested and cause minimal donor site morbidity.

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

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

167 togenous soft tissue grafts are countered by donor site morbidity.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 res and can be used for wound closure of the donor site of CTG.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 We identified mutations in splice donor sites of genes coding melanophilin (MLPH) and micr

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

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

219 ct of suturing on the early wound healing of donor sites of subepithelial connective tissue grafts (S

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

243 1 + 1655A > G) that creates a cryptic splice donor site resulting in the insertion of a pseudoexon (e

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

259 ential clinical difficulties associated with donor site surgery.

260 al clinical difficulties associated with the donor site surgery.

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

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

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

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

265 7.2-kb transcript maps to a consensus splice-donor site that is conserved among all cytomegaloviruses

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

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

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

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

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

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

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

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

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

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

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

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

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

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

280 features, we identified a homozygous splice donor site variant (GenBank: NM_001378.2:c.607+1G>A).

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

282 nfluence of two harvesting approaches on the donor site vascular injury.

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

284 Healing of the gingival unit donor site was uneventful.

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

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

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

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

289 All donor sites were closed primarily.

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

291 The donor sites were treated with PC and placebo.

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

293 Nonetheless, the location of the donor site (whether anterior-, lateral-, superficial-, d

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

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

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

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

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

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

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

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