ライフサイエンスコーパス: splicing enhancer

1 the RNA level (such as selection for exonic splicing enhancers)?

2 dicating that CAGACAT is a functional exonic splicing enhancer.

3 itch through its interaction with the exonic splicing enhancer.

4 r mutations in exon 6 that disrupt an exonic splicing enhancer.

5 SE3 enhancer, and a potentially novel exonic splicing enhancer.

6 ciated with disruption of a consensus exonic splicing enhancer.

7 at epsilon553del7 does not disrupt an exonic splicing enhancer.

8 splicing by an A/C-rich enhancer-type exonic splicing enhancer.

9 convert the hnRNP H-U1 snRNP complex into a splicing enhancer.

10 ing is caused by the disruption of an exonic splicing enhancer.

11 ther of which appears in any other published splicing enhancer.

12 s in S. cerevisiae contain a Mer1p-dependent splicing enhancer.

13 ell-characterized Drosophila doublesex (dsx) splicing enhancer.

14 eneous nuclear ribonucleoprotein F, onto the splicing enhancer.

15 cific and depends on the presence of the dsx splicing enhancer.

16 an upstream 5' splice site functioning as a splicing enhancer.

17 that this sequence functions as an intronic splicing enhancer.

18 by countering the activity of a neighboring splicing enhancer.

19 e Delta280K mutation, which weakens the same splicing enhancer.

20 ed in silico as neutralizing a putative exon splicing enhancer.

21 only one of these motifs acts as an intronic splicing enhancer.

22 These could serve as intronic splicing enhancers.

23 ndidate sequences for assessment as intronic splicing enhancers.

24 ive RNA splicing mediated by multiple exonic splicing enhancers.

25 s been identified previously in a few intron splicing enhancers.

26 R proteins and/or functioning as SR-specific splicing enhancers.

27 sequences capable of functioning as pre-mRNA splicing enhancers.

28 a purine-rich sequence similar to known exon splicing enhancers.

29 clusion in regulated splicing through exonic splicing enhancers.

30 peated binding sites found in Tra2-dependent splicing enhancers.

31 s juxtaposed immediately downstream of BPV-1 splicing enhancer 1 and negatively modulates selection o

32 plicing regulatory element in exon 3 (exonic splicing enhancer 2 (ESE2)), but we had not determined t

33 d splicing enhancers and a class of A/C-rich splicing enhancers (ACEs).

34 that three copies of B1 function as a strong splicing enhancer, activating an intron with suboptimal

35 This sequence acted as a strong splicing enhancer, activating splicing of the test exon

36 taining G- to U-mutations) which had minimal splicing enhancer activity also had very weak binding ca

37 ate exons previously demonstrated to contain splicing enhancer activity as well as in the well-charac

38 The splicing enhancer activity of CA21 in vivo is abolished

39 r SE2 resulted in a significant reduction of splicing enhancer activity.

40 ere that the purine-rich region of H-ras has splicing-enhancer activity in the homologous as well as

41 ouse, pufferfish, and zebrafish), and exonic splicing enhancers also appear broadly conserved in vert

42 the 5' end of intron 10 that functions as a splicing enhancer and causes an increase in exon 11 incl

43 ions within exon 11, we detected both exonic splicing enhancer and exonic splicing silencer elements.

44 This work defines a yeast splicing enhancer and shows that constitutively expresse

45 ic activator sequence 1 (IAS1), a known IIIb splicing enhancer and vice versa.

46 h motif that resembles previously identified splicing enhancers and a class of A/C-rich splicing enha

47 defined by three GAA motif-containing exonic splicing enhancers and a G/GU-rich intronic splicing enh

48 demonstrate that Hu proteins can function as splicing enhancers and expand the functional role of Hu

49 uman disease genes have lower frequencies of splicing enhancers and higher frequencies of splicing si

50 ation was facilitated by higher densities of splicing enhancers and lower densities of silencers than

51 Bioinformatic searches for splicing enhancers and repressors mapped four physically

52 , we identified multiple exonic and intronic splicing enhancers and silencers that regulate exon 13 i

53 was able to override the complex network of splicing enhancers and silencers that regulates the rati

54 We previously identified several splicing enhancers and silencers within exon 10 and intr

55 rithm can identify different combinations of splicing enhancers and silencers without assuming a pred

56 as splice site sequence and strength, exonic splicing enhancers and silencers, conserved and non-cons

57 We identified two RNA splicing enhancers and their binding proteins (U2AF65 an

58 in constitutive exons tend to create exonic splicing enhancers and to disrupt exonic splicing silenc

59 -nucleotide repeat elements, by heterologous splicing enhancers, and by artificially tethering a spli

60 f splicing regulatory elements, the intronic splicing enhancers, appears to differ substantially betw

61 These component elements of the src splicing enhancer are also apparently involved in the sp

62 rst direct evidence that SR protein-specific splicing enhancers are located within the coding regions

63 Splicing enhancers are RNA sequences consisting of one o

64 Splicing enhancers are RNA sequences required for accura

65 an transformer 2 beta (hTra2 beta; an exonic splicing enhancer-binding protein), hLucA (a potential c

66 Consistent with this pattern, exonic splicing enhancer-binding SR proteins are highly conserv

67 ences in U1 binding or the density of exonic splicing enhancers but may be partially attributed to lo

68 hat engagement of the SR protein with exonic splicing enhancers can regulate phosphoryl content in th

69 We conclude that only one splicing enhancer complex at a time is capable of intera

70 one or more proteins in the female-specific splicing enhancer complex.

71 d that hnRNP H is a protein component of the splicing enhancer complex.

72 plicing is activated through the activity of splicing enhancer complexes assembled on multiple repeat

73 rs bound at the 5' splice site, assembled in splicing enhancer complexes, or associated with the U4/U

74 ction, SR proteins function as components of splicing enhancer complexes.

75 hat although present in many of our selected splicing enhancers conforming to this motif, a typical p

76 The Drosophila doublesex female-specific splicing enhancer consists of two classes of regulatory

77 iple SF2/ASF binding sites within the exonic splicing enhancer contribute to maximal enhancer activit

78 interaction between Tra2 beta and the exonic splicing enhancer correlates with the activity of this e

79 evolution by demonstrating that three exonic splicing enhancers derived from vertebrates (chicken ASL

80 ulate trans splicing might be similar to cis-splicing enhancers described in other systems.

81 This 24-nucleotide (nt) downstream intronic splicing enhancer (DISE) is located within intron 9 imme

82 the c-src N1 exon is mediated by an intronic splicing enhancer downstream of the N1 5' splice site.

83 Introduction of an exonic splicing enhancer downstream of the PTC mutation restore

84 Two exonic splicing enhancers, each containing two ASF/SF2 (alterna

85 ow show that the change creates a new exonic splicing enhancer element and increases the amount of fu

86 n family of splicing factors, can activate a splicing enhancer element composed of high-affinity ASF/

87 mplex that binds specifically to an intronic splicing enhancer element downstream of the neuron-speci

88 The element UGCAUG is a splicing enhancer element found downstream of numerous n

89 Our results revealed an exonic splicing enhancer element located in exon 10.

90 We identified a specific splicing enhancer element that regulates the inclusion o

91 cally to a previously characterized pre-mRNA splicing enhancer element.

92 ch we term the NISE (Nova-dependent intronic splicing enhancer) element.

93 Analysis of selected splicing enhancer elements and other enhancers in S100 c

94 splice site of E10 is weak and requires exon splicing enhancer elements for efficient E10 inclusion.

95 forms a subrepeat within the repeated 13-nt splicing enhancer elements of fru and dsx RNAs.

96 We have identified multiple distinct splicing enhancer elements within protein-coding sequenc

97 An exonic splicing enhancer (ESE) and an exonic splicing silencer

98 a previously unrecognized multipartite exon splicing enhancer (ESE) composed of an SC35-like binding

99 hat has been attributed to loss of an exonic splicing enhancer (ESE) dependent on the SR protein spli

100 ly, we report the presence of a novel exonic splicing enhancer (ESE) element within the 5'-proximal r

101 Ab initio prediction of functional exon splicing enhancer (ESE) elements based on RNA sequences

102 This regulation involves an exonic splicing enhancer (ESE) in exon 12 of the mRNA.

103 We identify a purine-rich exonic splicing enhancer (ESE) in exon 3 that promotes exon inc

104 ransition functions not to disrupt an exonic splicing enhancer (ESE) in SMN1, as previously suggested

105 In this study, an exonic splicing enhancer (ESE) in the nucleotide (nt) 3520 to 3

106 enhance splicing when the palindromic exonic splicing enhancer (ESE) is mutated, indicating that TIAs

107 tion is not the result of creating an exonic splicing enhancer (ESE) or disrupting a putative seconda

108 iously, we identified a 69-nucleotide exonic splicing enhancer (ESE) required for alpha-exon inclusio

109 e Adam17 gene that ablates a putative exonic splicing enhancer (ESE) sequence in exon 7 resulting in

110 nic mutations that disrupt functional exonic splicing enhancer (ESE) sequences, resulting in exon ski

111 e characterized a novel bidirectional exonic splicing enhancer (ESE) that regulates the expression of

112 ver, a C-->T substitution converts an exonic-splicing enhancer (ESE) to a silencer (ESS), causing fre

113 The presence of a purine-rich exon splicing enhancer (ESE) was required for exon 3 recognit

114 INE1 insertion the inactivation of an exonic splicing enhancer (ESE) within exon 6 is required for sk

115 A variation that disrupts an exonic splicing enhancer (ESE), for example, could cause exon s

116 225 3' splice site and consists of an exonic splicing enhancer (ESE), SE1, followed immediately by a

117 , for example when they inactivate an exonic splicing enhancer (ESE), thereby resulting in exon skipp

118 exonic splicing silencer (ESS) and an exonic splicing enhancer (ESE), which together determine the le

119 requires the presence of a downstream exonic splicing enhancer (ESE).

120 auxiliary cis-acting elements such as exonic splicing enhancers (ESE) and exonic splicing silencers (

121 splicing include weak 3' splice sites, exon splicing enhancers (ESE), and exon splicing silencers (E

122 Such sequences are known as exonic splicing enhancers (ESE).

123 c splicing silencer (ESS3a/b), and an exonic splicing enhancer (ESE3).

124 Exonic splicing enhancers (ESEs) activate pre-mRNA splicing by

125 stitutive SREs, since only 18% of our exonic splicing enhancers (ESEs) are contained in constitutive

126 Exonic splicing enhancers (ESEs) are important cis elements req

127 Exonic splicing enhancers (ESEs) are pre-mRNA cis-acting elemen

128 Exonic splicing enhancers (ESEs) are required for splicing of c

129 Exonic splicing enhancers (ESEs) are sequences that facilitate

130 spliceosome formation by recognizing exonic splicing enhancers (ESEs) during pre-mRNA splicing.

131 Discrete sequence elements known as exonic splicing enhancers (ESEs) have been shown to influence b

132 ice sites in the intron databases and exonic splicing enhancers (ESEs) in S.pombe exons.

133 the purine-rich region found multiple exonic splicing enhancers (ESEs) known to promote splicing thro

134 Exon splicing enhancers (ESEs) overlap with amino acid coding

135 Some exonic splicing enhancers (ESEs) promoted use of intron-proxima

136 ave identified three novel classes of exonic splicing enhancers (ESEs) recognized by human SF2/ASF, S

137 ssors mapped four physically distinct exonic splicing enhancers (ESEs) within HIPK3-T, each containin

138 The SREs include exonic splicing enhancers (ESEs), exonic splicing silencers (ES

139 in a correlated way, whereas specific exonic splicing enhancers (ESEs), including motifs associated w

140 either cis-regulatory motifs, such as exonic splicing enhancers (ESEs), or mRNA secondary structures,

141 plicing when present in exons, termed exonic splicing enhancers (ESEs), play important roles in const

142 as being uniquely densely packed with exonic-splicing enhancers (ESEs), rendering this exon hypersens

143 atory have identified two purine-rich exonic splicing enhancers (ESEs), SE1 and SE2, located between

144 238 hexamers previously identified as exonic splicing enhancers (ESEs).

145 nsistent with their identification as exonic splicing enhancers (ESEs).

146 s and can function through binding to exonic splicing enhancers (ESEs).

147 promote exon inclusion by binding to exonic splicing enhancers (ESEs).

148 gered when nonsense mutations disrupt exonic splicing enhancers (ESEs).

149 effects by disrupting the activity of exonic splicing enhancers (ESEs).

150 s-acting splicing elements-so-called "exonic splicing enhancers" (ESEs).

151 donor-acceptor sites or by disturbing exonic splicing enhancers (ESESs).

152 al to 5'ss D2; and an SRp75-dependent exonic splicing enhancer (ESEVif).

153 of cycled selection was used to characterize splicing enhancers for exon inclusion from a pool of bet

154 Examining exonic splicing enhancers found near the splice junction in the

155 A purine-rich splicing enhancer from a constitutive exon has been show

156 competed by RNAs containing the purine-rich splicing enhancer from cardiac troponin T exon 5.

157 ted by TRA and TRA2 and depends on an exonic splicing enhancer (fruRE) consisting of three 13-nucleot

158 suggest that general dysregulation of Nova's splicing enhancer function may underlie the neurologic d

159 that this purine-rich region provides an RNA splicing enhancer function required for splicing inhibit

160 They do this through a splicing enhancer function, in addition to their apparen

161 f the small U2AF subunit is not required for splicing enhancer function.

162 re, we investigate the role of RS domains in splicing enhancer function.

163 he binding of these proteins is required for splicing enhancer function.

164 se data are consistent with a model in which splicing enhancers function by increasing the local conc

165 We conclude that splicing enhancers function similarly in activating regu

166 suggests that rs12718541 may be an intronic splicing enhancer, further studies are needed to determi

167 C can interfere with the function of an exon splicing enhancer in an open reading frame-dependent man

168 h conventional splicing assays to test for a splicing enhancer in exon 17 of the human MLH1 gene.

169 icating that SE1 also functions as an exonic splicing enhancer in its normal context.

170 tem, we previously showed that a purine-rich splicing enhancer in the alternative exon functions as a

171 d in vitro, and results from disruption of a splicing enhancer in the coding sequence.

172 the 5' half of the N1 exon itself acts as a splicing enhancer in vivo.

173 This motif served as strong splicing enhancers in a heterogeneous exon.

174 and GT are predicted to function as intronic splicing enhancers in fish but are not enriched in mamma

175 ector morpholino that blocked Fox2-dependent splicing enhancers in intron 16 or a splice-blocking mor

176 urine-rich region reminiscent of purine-rich splicing enhancers in other genes that stimulate the rem

177 equired a high density of GAA/CAA-containing splicing enhancers in the exonized segment and was promo

178 termed this element ISE/ISS-3 (for "intronic splicing enhancer-intronic splicing silencer 3").

179 This fru splicing enhancer is sufficient to promote the activatio

180 We find that the strength of splicing enhancers is determined by the relative activit

181 ed that only one of the following two exonic splicing enhancers is sufficient for inclusion of the KI

182 G-rich M2 and a G-rich splicing enhancer (ISE) in intron 3 share similarities i

183 5' donor site that functions as an intronic splicing enhancer (ISE) required for efficient large-int

184 , exonic splicing silencers (ESSs), intronic splicing enhancers (ISEs), and intronic splicing silence

185 es of functional elements, possibly intronic splicing enhancers (ISEs).

186 e novel and may represent conserved intronic splicing enhancers (ISEs).

187 1 because of a crucial mutation in an exonic splicing enhancer, leading to alternative splicing and e

188 propose that these sequences are large exon splicing enhancers (LESEs).

189 2 repeat elements that are part of an exonic splicing enhancer located immediately upstream of the fe

190 ceptors is directed exclusively by redundant splicing enhancers located in the adjacent introns.

191 pproaches underscore the relevance of exonic splicing enhancer loss and silencer gain in inherited di

192 splicing patterns by disruption of an exonic splicing enhancer may be a frequent mechanism by which p

193 ubstantially inhibited by interfering with a splicing enhancer mechanism using a target protector mor

194 e change), which lies in a suggestive exonic splicing enhancer motif in exon 1, was common only in Af

195 n exon 5 and also disrupts a putative exonic splicing enhancer motif.

196 This method was used to isolate particular splicing enhancer motifs from a previously enriched pool

197 altering the recognition of specific exonic splicing enhancer motifs to drive recurrent mis-splicing

198 onin T minigenes in vivo via muscle-specific splicing enhancer (MSE) sequences.

199 , these elements function as muscle-specific splicing enhancers (MSEs) and are the first muscle-speci

200 ple intronic elements called muscle-specific splicing enhancers (MSEs) that flank the alternative exo

201 s previously identified four muscle-specific splicing enhancers (MSEs) that promote exon inclusion sp

202 We previously described four muscle-specific splicing enhancers (MSEs) within introns flanking exon 5

203 ncing led to the identification of an exonic splicing enhancer mutation in exon 7 of CIZ1 (c.790A>G,

204 Mutagenesis of either a purine-rich splicing enhancer or a pyrimidine tract element within e

205 r to the loss of an SF2/ASF-dependent exonic splicing enhancer or to the creation of an hnRNP A/B-dep

206 substitutions that disrupt predicted exonic splicing enhancers or create predicted exonic splicing s

207 cleotide polymorphisms (cSNPs) within exonic splicing enhancers or silencers may affect the patterns

208 We identified 456 putative splicing enhancers or silencers, of which 221 were predi

209 mately 2,000 RNA octamers as putative exonic splicing enhancers (PESEs) based on a statistical compar

210 exons, and we propose that the Fox family of splicing enhancers plays an important role in alternativ

211 ely due to the action of a putative intronic splicing enhancer present in intron 25, which appeared t

212 These results suggest that exonic splicing enhancers recruit multiple spliceosomal compone

213 egion and RBM4 interacting with the intronic splicing enhancer region.

214 n synonymous codons that are associated with splicing enhancers remains after controlling for this bi

215 We report here the identification of a splicing enhancer required for IIIc inclusion.

216 ontaining either a constitutive or regulated splicing enhancer revealed that U2AF35 directly mediates

217 Characterization of the selected splicing enhancers revealed a highly heterogeneous popul

218 BPV-1 late pre-mRNAs two purine-rich exonic splicing enhancers (SE1 and SE2) which also stimulate sp

219 Two purine-rich exonic splicing enhancers, SE1 and SE2, are essential for prefe

220 tite element consisting of an AC-rich exonic splicing enhancer (SE4) and an exonic splicing suppresso

221 In addition, a potent splicing enhancer sequence isolated in the selection spe

222 seven nucleotides in length including novel splicing enhancer sequence motifs.

223 ding of the SF2/ASF protein to a purine-rich splicing enhancer sequence that is located in the 3' exo

224 e central RNA recognition motif to an exonic splicing enhancer sequence, a phenomenon reversed by SRP

225 -exon splicing, indicating the presence of a splicing enhancer sequence.

226 ly we showed that E10 splicing involved exon splicing enhancer sequences at the 5' and 3' ends of E10

227 e regulatory specificity of predicted exonic splicing enhancer sequences that may control splicing re

228 n, KSRP, activates splicing through intronic splicing enhancer sequences.

229 regulate splicing from a number of intronic splicing enhancer sequences.

230 on 9 skipping by reducing the binding of the splicing enhancer SF2.

231 hese SNPs, rs10185378, is a predicted exonic splicing enhancer; significant alteration in the express

232 ly spliced large exons had a higher ratio of splicing enhancers/silencers and were more conserved acr

233 the binding of RBFOX2 to downstream intronic splicing enhancers stabilizes the pre-mRNA-U1 snRNP comp

234 ice sites or accessory sequences that act as splicing enhancers, suggesting steric interference betwe

235 holino antisense oligonucleotides to the two splicing enhancers surrounding the second donor site led

236 vealed that Ins44 disrupts a putative exonic splicing enhancer that allows for skipping of exon 2, wh

237 These elements include an exon splicing enhancer that can either be strengthened (mutat

238 studies have identified UGCAUG as an intron splicing enhancer that is frequently located adjacent to

239 splicing enhancers and a G/GU-rich intronic splicing enhancer that lies adjacent to the second donor

240 ied antisense oligonucleotides targeted to a splicing enhancer that regulates STAT3 exon 23 alternati

241 h point, a polypyrimidine tract and suitable splicing enhancers-that may be distributed over hundreds

242 rine/arginine-rich (SR) protein to an exonic splicing enhancer, thereby inhibiting splicing at that e

243 e that these enhancers function as multisite splicing enhancers to specify 3' splice-site selection.

244 d the functional significance of an intronic splicing enhancer, UGCAUG, and its cognate splicing fact

245 n the second intron by targeting an intronic splicing enhancer using a Morpholino antisense oligonucl

246 ate the sequence specificity of these exonic splicing enhancers, various mutant SE1 or SE2 elements w

247 The activity of this AG-rich splicing enhancer was altered by N279K and Del280K mutat

248 found that the poly-G run, a known intronic splicing enhancer, was the most significantly enriched m

249 ing of SR proteins observed on the doublesex splicing enhancer, we found that Rbp1 and Tra2 bind to t

250 Two purine-rich exonic splicing enhancers were identified downstream of nt 3225

251 Functional splicing enhancers were then selected by multiple rounds

252 Mutant exon 6D sequences function as a splicing enhancer when inserted into an enhancer-depende

253 t have been shown to bind a number of exonic splicing enhancers where they function to stimulate the

254 element to a region coincident with the Env splicing enhancer, which binds SR proteins, and inactiva

255 occurs within a heptamer motif of an exonic splicing enhancer, which in SMN1 is recognized directly

256 In contrast, the activity of the intronic splicing enhancer, which is necessary for PLP splicing,

257 xonic GGG motif overlapped a critical exonic splicing enhancer, which was predicted to bind the SR pr

258 1p recognizes introns that contain the Mer1p splicing enhancer, while the N-terminal domain interacts

259 he exonic N279K mutation which strengthens a splicing enhancer within E10.

260 at this exon/exon association depends on the splicing enhancer within exon 5.

261 s due to the disruption of an SC35-dependent splicing enhancer within exon 51.

262 jacent to the 5' element of a bipartite exon splicing enhancer within the NS2-specific exon of minute

263 ort, we further identified 3 putative exonic splicing enhancers within exon 16 and investigated the f

264 g an inefficient splice donor from essential splicing enhancers within exon 5, with the result that i