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 ice site, cryptic branch point and an exonic splicing enhancer.

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

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

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

24 These could serve as intronic splicing enhancers.

25 ndidate sequences for assessment as intronic splicing enhancers.

26 ive RNA splicing mediated by multiple exonic splicing enhancers.

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

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

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

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

31 clusion in regulated splicing through exonic splicing enhancers.

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

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

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

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

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

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

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

39 The splicing enhancer activity of CA21 in vivo is abolished

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

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

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

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

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

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

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

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

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

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

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

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

52 Bioinformatic searches for splicing enhancers and repressors mapped four physically

53 Intronic splicing enhancers and silencers (ISEs and ISSs) are two

54 antisense oligonucleotide tiling to identify splicing enhancers and silencers in its flanking introns

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

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

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

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

59 equence, loss or gain of exonic and intronic splicing enhancers and silencers, complete intron retent

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

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

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

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

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

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

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

67 Splicing enhancers are RNA sequences consisting of one o

68 Splicing enhancers are RNA sequences required for accura

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

95 osine to thymine transition within an exonic splicing enhancer element within exon 7.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

112 region around RAS Q61 is enriched in exonic splicing enhancer (ESE) motifs and we designed mutant-sp

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

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

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

116 reviously identified set of hexameric exonic splicing enhancer (ESE) sequences compared to their spli

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

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

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

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

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

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

123 225 3' splice site and consists of an exonic splicing enhancer (ESE), SE1, followed immediately by a

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

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

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

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

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

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

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

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

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

133 Exonic splicing enhancers (ESEs) are enriched in exons relative

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

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

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

137 Exonic splicing enhancers (ESEs) are sequences that facilitate

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

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

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

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

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

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

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

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

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

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

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

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

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

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

152 238 hexamers previously identified as exonic splicing enhancers (ESEs).

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

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

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

156 r induce exon skipping by disruption of exon splicing enhancers (ESEs).

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

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

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

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

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

162 ce of CA(G/C/A)CC(C/A) as a potential exonic splicing enhancer for these SRSF3-regulated exons.

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

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

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

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

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

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

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

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

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

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

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

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

175 We conclude that splicing enhancers function similarly in activating regu

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

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

178 egulatory role for SNRPA1 as a prometastatic splicing enhancer in breast cancer.

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

180 cing factor 6 (SRSF6) binding to an intronic splicing enhancer in intron 20.

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

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

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

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

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

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

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

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

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

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

191 This fru splicing enhancer is sufficient to promote the activatio

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

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

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

195 5' donor site that functions as an intronic splicing enhancer (ISE) required for efficient large-int

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

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

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

199 1 because of a crucial mutation in an exonic splicing enhancer, leading to alternative splicing and e

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

201 HIN1 bound to a GAA-repeat, Exonic Splicing Enhancer-like RNA motif enriched in flanking se

202 2 repeat elements that are part of an exonic splicing enhancer located immediately upstream of the fe

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

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

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

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

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

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

209 istics, including enrichment of hnRNPH-bound splicing enhancer motifs and a propensity for G-quadrupl

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

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

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

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

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

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

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

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

218 We traced this event to a mutation in a splicing enhancer of the DNA repair gene Aplf in the fis

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

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

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

222 85 deep intronic mutations indicated gain of splicing enhancers or loss of splicing silencers.

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

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

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

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

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

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

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

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

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

232 how that rs6043409 alters a predicted exonic splicing enhancer, resulting in significant shifts in th

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

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

235 er with molecular QTLs data, including mRNA, splicing, enhancer RNA (eRNA), and protein expression da

236 native HIV-1 splicing revealed an unexpected splicing enhancer role for hnRNP H1 through binding to i

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

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

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

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

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

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

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

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

245 e exon inclusion, SRSF1 by binding to exonic splicing enhancer sequences (ESEs) and U1 snRNPs by bind

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

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

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

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

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

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

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

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

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

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

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

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

258 e discovered a previously unknown structural splicing enhancer that is enriched near cassette exons w

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

260 RIF1-Ex32 splice-in is mediated by an exonic splicing enhancer that is recognized by the serine and a

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

262 rich splicing factor arginine SRSF5, a major splicing enhancer that regulates alternative splicing.

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

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

265 eam of the introns contain pre-mRNA-specific splicing enhancers, the substitution or hybridization of

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

267 oaches, we found that SRSF1 and PTBP1 act as splicing enhancers to increase CD33 exon 2 inclusion in

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

269 ed to the cryptic branch point and an exonic splicing enhancer, U7.BP + 623, was the most effective i

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

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

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

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

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

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

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

277 Functional splicing enhancers were then selected by multiple rounds

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

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

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

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

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

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

284 1p recognizes introns that contain the Mer1p splicing enhancer, while the N-terminal domain interacts

285 exclusively recognize single-stranded exonic splicing enhancers, while RS lacks RNA-binding specifici

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

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

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

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

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

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