ライフサイエンスコーパス: exon

1 ng gene promoter such as within an intron or exon.

2 ic retroelements as promoter and alternative exon.

3 rrelation have been observed at the level of exon.

4 enylation signals (PASs) in introns and last exons.

5 lank many AR-regulated alternatively spliced exons.

6 arely alter the inclusion of highly-included exons.

7 frontal cortex, CpG islands and shores, and exons.

8 t least one gene, and 32.8% interrupt coding exons.

9 disordered peptide regions than constitutive exons.

10 as found, with evidence of weak selection in exons.

11 Notably, most of these mutations create new exons.

12 d with regions of high percent-spliced in of exons.

13 MN1 is encoded by only two exons.

14 ting the splicing pattern of other essential exons.

15 ry motifs, when compared with other types of exons.

16 egulatory sequence downstream of Gdf5 coding exons.

17 Also, OXTR methylation in the exon 1 area could be a potential biomarker of sociabilit

18 Methylation at a CpG site in the exon 1 area was positively related to social responsiven

19 We found that expression of exon 1 HTT fragments with longer polyQ tracts led to the

20 We find that exon 1 HTT is constantly generated but its selective acc

21 T in HD140Q knock-in (KI) mice, we show that exon 1 HTT is stably present in the brain, regardless of

22 Httexon1) that encodes the highly pathogenic exon 1 HTT protein.

23 rapeutic potential in blocking generation of exon 1 HTT.

24 eNcell VM NSCs) stably transduced to express exon 1 huntingtin (HTT) fragments with variable length p

25 A sequence dimorphism in exon 1 of HLA-B gives rise to leader peptides containing

26 dy the formation of fibrils and oligomers by exon 1 of huntingtin protein.

27 re, we describe CRISPR/Cas9-based editing of exon 1 of the HVT079 and HVT096 genes from the HVT genom

28 Caenorhabditis elegans) increases mutant HTT exon 1 phosphorylation and reduces its aggregation and c

29 re targeted to mitochondria independently of exon 1 splicing.

30 deletion (Delta27bp) within the polymorphic exon 1 that occurs frequently in human CRC cells and nei

31 iously shown that the incomplete splicing of exon 1 to exon 2 of the HTT gene results in the producti

32 he terminal exon or the extreme 3' region of exon 1, and are therefore predicted to result in escape

33 hat depending on the alternative splicing of exon 1, type I splice variants (MOCS1A) either localize

34 mous mutation decreased exonic definition of exon 1.

35 Alternative splicing of MOCS1 within exons 1 and 9 produces four different N-terminal and thr

36 ks exons 8 and 10 and NPM1.3 which comprises exons 1-10 (and so lacks the region of sequence mutated

37 This new gene fusion involves exons 1-4 from the 5' end of the Trk fused Gene (TFG) fu

38 e variants with the major variant encoded by exons 1-9 and 11-12 (NPM1.1).

39 that increases the propensity of huntingtin exon-1 to form cross-beta fibrils.

40 patients, respectively, have "canonical" MPL exon 10 driver mutations W515L/K/R/A or S505N, which gen

41 se Familial Mediterranean Fever (FMF) map to exon 10 encoding the B30.2 domain.

42 Other "noncanonical" MPL exon 10 mutations have also been identified in patients,

43 in published and previously unpublished MPL exon 10 sequencing data from MPN patients, demonstrating

44 regions of high sequence identity in ATAD3A exon 11 and ATAD3C exon 7.

45 he KIT receptor tyrosine kinase, such as the exon 11 KIT V559Delta mutation.

46 sis, we used the alternatively spliced BRCA2 exon 12 (E12) as a model system because its in-frame ski

47 erin gene (PgCad1) has a 234-bp insertion in exon 12 encoding a mutant PgCad1 protein that lacks 36 a

48 By deleting exon 13 (which encodes a sterile alpha motif) from the T

49 MET exon 14 alteration defines a molecular subgroup of NSCLC

50 ed MET copy number or the detection of a MET exon 14 alteration in circulating tumor DNA.

51 ice-site region and mutation type of the MET exon 14 alteration, concurrent increased MET copy number

52 therapy in people with lung cancers with MET exon 14 alterations and adds to an expanding list of gen

53 MET exon 14 alterations are oncogenic drivers of non-small-c

54 patients with advanced NSCLCs harboring MET exon 14 alterations.

55 Several agents targeting exon 14 skipping alterations are currently in clinical d

56 an rs6128-dependent association between SELP exon 14 skipping and race.

57 28 is a platelet splice QTL that alters SELP exon 14 skipping and soluble versus transmembrane P-sele

58 tracellular domains and those that result in exon 14 skipping.

59 DNA sequencing revealed mutations in exon 15 of the Braf gene identical to the human BRAF(V60

60 cilitating exon 16 skipping and deletions of exon 16 in a subset of these lung tumors and in a number

61 well as splicing site mutations facilitating exon 16 skipping and deletions of exon 16 in a subset of

62 rnative splicing of ERBB2 causes skipping of exon 16, leading to the expression of an oncogenic ERBB2

63 Exon 17b peptides also promote fodrin-actin complex form

64 keleton via a bispecific interaction with an exon 17b-encoded peptide.

65 f seven noncontiguous amino acids encoded in exon 19 that mediates SREBP2's proteasomal degradation i

66 MOCS1A proteins required exon 1a for mitochondrial translocation, but fluorescenc

67 either localize to the mitochondrial matrix (exon 1a) or remain cytosolic (exon 1b).

68 ndrial matrix (exon 1a) or remain cytosolic (exon 1b).

69 We sequenced MHC-DRB exon 2 (IIa) and MHC-DOB exon 2 (IIb) on the MiSeq platf

70 e sequenced MHC-DRB exon 2 (IIa) and MHC-DOB exon 2 (IIb) on the MiSeq platform from an enclosed whit

71 Mutagenesis of exon 2 in Knock-in (KI) mouse models of the R47H variant

72 rein referred to as ORF-Z, was also found in exon 2 of POLG.

73 mutation that introduces a premature stop in exon 2 of the appb gene.

74 wn that the incomplete splicing of exon 1 to exon 2 of the HTT gene results in the production of a sm

75 primary transcription start site and within exon 2 partially mediate the effects of risk variants on

76 , MEFV showed E148Q heterozygous mutation in exon 2.Since an adult case of PFAPA syndrome is likely t

77 of disease-correlated mutations that map to exons 2 and 3 of POLG but also affect ORF-Y provides pot

78 coding signature in an alternative frame in exons 2 and 3 of POLG, herein referred to as ORF-Y that

79 ed allele approach, demarcated by dystrophin exons 2-79, in complementation with a cardiac and skelet

80 hose on the African mainland, with seventeen exon-2 haplotypes unique to bushpigs in Madagascar (2/28

81 tive to H1047R (A3140G) missense mutation in exon 20 in breast cancer as the model target.

82 fluorescence only when skipping of mdx-type exon 23 is induced by ASOs.

83 addition, we show that a Smn protein lacking exon 2B can rescue iMEF survival and snRNP assembly in t

84 embly in the absence of flwt-Smn, indicating exon 2B is not required for the essential function of Sm

85 Here, we explored BRCA2 exon 3 (BRCA2e3) as a model for calibrating variant-indu

86 A pathogenic RYR2 exon 3 in-frame deletion was identified in the third pro

87 ndromic repeats)/Cas9 to introduce indels in exon 3 of FMR1, we generated an isogenic human pluripote

88 Furthermore, two SNPs located within exon 3 of IGHM (rs45471499, P(combined) = 1.15 x 10(-9))

89 IRXA) gene cluster, where hypomethylation in exon 3 of IRX2 in neuronal nuclei was associated with co

90 Finally, targeted disruption of PTCHD1-AS exon 3 recapitulated diminished miniature excitatory pos

91 associated with a higher abundance of CYP2D6 exon 3 skipping junctions.

92 rated in vitro that the GH1 variant leads to exon 3 skipping, predicting a mutant protein known to ca

93 re derived from alternative 3' splicing from exon 3 to alternative sites within exon 5.

94 se in levels of a shorter transcript missing exon 3, suggestive of an incompletely penetrant splice d

95 cture for Drosophila EMB, indicates that the exon 3-encoded region in the myosin head is part of the

96 Cas9 technology by introducing a deletion of exons 3 and 4.

97 This region is encoded by alternative exons 3a and 3b and includes part of the N-terminal beta

98 ense mutation increased exonic definition of exon 4 and the MMP20 synonymous mutation decreased exoni

99 (TE) sequences at precisely the same site in exon 4 in nine of the 10 cnr alleles.

100 narily conserved ATF-C/EBP composite site in exon 4 of the Gadd45a gene.

101 na: Ca(v)1.4 splice variants with or without exon 47 (Ca(v)1.4+ex47 and Ca(v)1.4Deltaex47, respective

102 manner that is strengthened by exclusion of exon 47 and inclusion of beta(2X13) and alpha(2)delta-4.

103 y, were generally larger in channels lacking exon 47.

104 5, that lowers the 607:558 ratio by altering exon 5 inclusion in SmgGDS pre-mRNA (messenger RNA).

105 Exon 5 inclusion triggers nonsense-mediated mRNA decay (

106 Germline heterozygous ablation of exon 5 increases BAK1 proteins exclusively in the brain,

107 Therefore, neural-specific exon 5 splicing and depletion of BAK1 proteins uniquely

108 The functional relevance of these exon 5-associated MOR-1Bs has been demonstrated in mu ag

109 Both mouse and human OPRM1 have five exon 5-associated seven transmembrane full-length carbox

110 A single treatment of neonatal mice with an exon 5-targeted ASO-induced robust exon skipping for mor

111 hipathic helix-forming (AH) motif encoded by exon 5.

112 cing from exon 3 to alternative sites within exon 5.

113 rough a motif within the sequence encoded by exon 5.

114 s of skeletal muscle of mice with dystrophin exon 51 deletion.

115 mutation p.Ser6366Ile and a deletion of NEB exon 55, the Compound-Het model that resembles typical N

116 nd 993 corresponding to the junction between exons 6 and 7.

117 point mutation in intron 6, upstream of the exon 7 acceptor site.

118 s, containing 333 nt of the C8alpha intron 6/exon 7 boundary, in an in vitro splicing assay.

119 showing more robust initial effects on SMN2 exon 7 inclusion, but less persistence in the central ne

120 quence identity in ATAD3A exon 11 and ATAD3C exon 7.

121 ith CLN3 Batten have a deletion encompassing exons 7 and 8 (CLN3(Deltaex7/8)), creating a reading fra

122 Skipping of exons 7 and 8 is predicted to delete critical amino acid

123 2RX7L, that is, characterized by skipping of exons 7 and 8.

124 also shows direct benefit for DDEB caused by exon 73 mutations.

125 sense oligonucleotide specifically targeting exon 73.

126 ined by an exon-exon splice junction between exons 8 and 10 (junc8.10) and that is predicted to encod

127 Further variants include NPM1.2 which lacks exons 8 and 10 and NPM1.3 which comprises exons 1-10 (an

128 n of the alternatively spliced 25-amino acid exon 9* mimicking a splice variant of alpha(1C) upregula

129 In contrast, introduction of the exon 9* splice variant in the alpha(1C) I-II loop, which

130 for a previously reported point mutation in exon 9.

131 rter that are encoded for by MHC alternative exons 9 and 11, respectively, directly contribute to inc

132 genetically engineered mouse model to delete exons 9/10 of Bcor (Bcor (DeltaE9-10) ) in GNPs during d

133 n weakly and highly evolutionarily conserved exons, a proxy for functional importance.

134 lation (poly(A)) sites, alternative terminal exons account for much of the variation between human tr

135 dentify novel cell type-specific alternative exons across the nervous system and leverage ENCODE and

136 We propose that exon-activated functional rescue is a more widespread me

137 Alternatively spliced exons also overlap more frequently with intrinsically di

138 ing events: skipped exon, mutually exclusive exons, alternative 5' splice site, alternative 3' splice

139 a bifunctional nsp14 protein which possesses ExoN and guanine-N-7 methyltransferase (G-N-7 MTase) act

140 ere a method for the coordinated analysis of exon and intron data by investigating their relationship

141 This coordinated analysis of exon and intron data offers strong evidence for signific

142 e for the simultaneous consideration of both exon and intron data.

143 exon-only expression data from the combined exon and intron data.

144 model to analyze the differences between the exon and intron definition scenarios and find that exon

145 ct promoters that are separated by the first exon and intron.

146 e discovered a collaboration between LASV NP ExoN and L protein in limiting dsRNA accumulation.

147 RNA promotes inclusion of a poison cassette exon and transcript degradation via nonsense-mediated de

148 quence of CpMMS19 is 62 kb, consisting of 20 exons and 19 introns.

149 mplex than appreciated, identifying 38 novel exons and 241 novel transcripts.

150 All six exons and adjacent regions of the NAGLU gene were sequen

151 Cassette exons and alternative 3' splice sites were the most freq

152 rforming deep mutagenesis of highly-included exons and by analysing the association between genome se

153 panning 18,048,877 bp, some of which disrupt exons and known regulatory elements.

154 their siblings without ASD, particularly in exons and near splice junctions, and in genes related to

155 inct KO strategies, for example, by skipping exons and reinitiating translation to potentially yield

156 sgenic (TG) mice containing all the introns, exons, and 5'- and 3'-flanking regions of the hCYP11B2 g

157 pliced dPix isoforms that contain a specific exon are necessary and sufficient for postsynaptic diffe

158 Interestingly, these exons are enriched in NMD signals, and, accordingly, ZMA

159 essentiality and cancer relevance of poison exons are likely to contribute to their unusually high c

160 s, whereas pLoF variants in highly expressed exons are most strongly enriched among cases.

161 Moreover, regulated exons are often shorter than constitutive exons but are

162 Among these tissue-regulated exons are several highly conserved microexons <27 nt in

163 , 399, 250, and 299 differentially expressed exons (AS exons) at 4, 24, 48, and 72 hpi, respectively,

164 , and 299 differentially expressed exons (AS exons) at 4, 24, 48, and 72 hpi, respectively, showing t

165 ecture to predict the inclusion of a spliced exon based on adjacent epigenetic signals, and we showed

166 We find that exons biased toward prenatal and postnatal expression pr

167 ed exons are often shorter than constitutive exons but are flanked by longer intron sequences.

168 pping, are significantly enriched in mencRNA exons, but not the promoters or introns.

169 r identity across species than nearby coding exons, but their physiological role and molecular regula

170 Here, the recognition of the adjacent exons by the spliceosome is required for removal of an i

171 over driver fusions beyond canonical exon-to-exon chimeric transcripts, we develop CICERO, a local as

172 he inclusion levels of alternatively spliced exons, consistent with the concept that altered splicing

173 FF replicates, with 98% agreement in coding exon coverage and a median correlation of whole transcri

174 We collected genome-wide exon data for 110 (~80%) species in the group and aggreg

175 et sequence, typically elements that control exon definition and/or splice-site recognition.

176 nd intron definition scenarios and find that exon definition prevents the accumulation of deleterious

177 Our analysis suggests that exon definition promotes robust and reliable splicing ou

178 intron, causing intron retention or partial exon deletion, thereby eliminating male-determining XOL-

179 deletions were predicted to result in coding exon disruption.

180 This leads to alternative splicing of target exons due to the RNA helicase activity of DDX17.

181 ffer for 2 extra exons in HP2 that result in exon duplication undetectable by classic genome-wide ass

182 A synonymous substitution that results in exon eight skipping in most mRNA molecules, ultimately l

183 al properties of one of the four alternative exon-encoded regions within the Drosophila myosin cataly

184 (GenBank # KU304333.1) consists of a single exon, encoding a putative membrane protein of 127 amino

185 he latter (rs13266634) locates in an SLC30A8 exon, encoding a tryptophan-to-arginine substitution tha

186 ith incorporation of a set of 1,039 cassette exons enriched in genes encoding RNA binding proteins.

187 d identified 13,149 high-confidence cassette exon events with variable incorporation across samples.

188 s they only weakly affected expression of an exon-exon junction that tags the majority of abundant tr

189 ing expression features to genes (eGene) and exon-exon junctions (eJunction).

190 predicted to be overexpressed, defined by an exon-exon splice junction between exons 8 and 10 (junc8.

191 However, most exons expressed in any cell are highly-included in matur

192 ion analysis currently relies primarily upon exon expression data.

193 ystematically incorporates information about exon expression into the interpretation of variants.

194 We documented 1263 TEs containing exon fragments from 1629 donor genes.

195 ncoding the ELAV paralog FNE acquires a mini-exon, generating a new protein able to translocate to th

196 genetic variants typically reside outside of exons has inspired widespread investigation into the gen

197 when restricting to LOF variants located in exons highly expressed in cardiac tissue (TTN(LOF)).

198 Nevertheless, the function of NP ExoN in arenavirus infection remains to be defined.

199 rnative splicing of a functionally validated exon in normal and disease states - and reveal a potenti

200 s data obtained for an alternatively spliced exon in the proto-oncogene RON and determine the functio

201 ient to activate many photoreceptor-specific exons in HepG2 liver cancer cells.

202 leles of HP, HP1 and HP2, differ for 2 extra exons in HP2 that result in exon duplication undetectabl

203 Transcribed regions and exons in RTR account for ~42% and ~6.5% of the genome, r

204 prevented the use of photoreceptor-specific exons in transcripts critical for outer segment morphoge

205 ith distinct expression profiles of specific exons, in the hippocampus.

206 iation between genome sequence variation and exon inclusion across the transcriptome, we report that

207 Preventing cytosine-rich exon inclusion in mutant KRAS/p53 PDACs decreases tumor

208 filing reveals that ZMAT3 directly modulates exon inclusion in transcripts encoding proteins of diver

209 ivity disorder are located in protein-coding exons, indicating a more substantial role of regulatory

210 analysis, gene set enrichment analysis, and exon-intron landscape analysis, we examined the impact o

211 omosomal regions including promoters, coding exons, introns and distal intergenic regions.

212 distributed in all genomic regions including exons, introns, intergenic, TTS (transcription terminati

213 , coq-2a and coq-2e, and the coq-2e-specific exon is only found in species that synthesize RQ.

214 Grouping exons is essential in splicing analysis of scRNA-seq dat

215 Exon junction complexes (EJCs) are deposited on mRNAs du

216 g protein - possibly in association with the exon-junction complex (EJC) - expands the capacity of ce

217 produce short reads that only span up to two exon junctions per read.

218 Exon-level analysis (including noncoding exons) revealed

219 We subjected these samples to exon-level analysis with rMATS-turbo, purpose-built soft

220 Both gene-level and exon-level coverage can be immediately appreciated and t

221 ly aggregates spliced reads across different exons, making it possible to detect splicing events even

222 confirmed the Myc regulation of 147 of these exons, many of which introduced frameshifts or encoded p

223 Following nerve injury, exon methylation is increased, and splicing is disrupted

224 Although JUNV and MACV NPs also have the ExoN motif, dsRNA readily accumulated in infected cells

225 ugh the NPs of JUNV and MACV also harbor the ExoN motif, dsRNA readily formed during JUNV and MACV in

226 navirus NPs contain a highly conserved DEDDh ExoN motif, through which LASV NP degrades virus-derived

227 contain a highly conserved exoribonuclease (ExoN) motif, through which LASV NP has been shown to deg

228 ypes of alternative splicing events: skipped exon, mutually exclusive exons, alternative 5' splice si

229 g sites cover more of the genome than coding exons; nevertheless, most noncoding variant prioritizati

230 a heterozygous mutation in the first coding exon of Hnrnph1 (H1(+/-)) showed reduced methamphetamine

231 Remarkably, methylation of the second exon of HR4 is not only reduced in ago4-1 but also in pl

232 ion of the polyglutamine domain in the first exon of huntingtin (HttEx1).

233 e termination codon at position +5 in leader exon of Igh (Ter5H) allele.

234 p.E455K (c.1363 C > T) mutation in the same exon of PLCD1.

235 entire genes, PLEK and CNRIP1, and the first exon of PPP3R1 (protein coding), in addition to four unc

236 consequences of deleting a single conserved exon of PTCHD1-AS.

237 leterious mutations (102C > A), in the first exon of the GBE1 gene (GBE1(102C>A)).

238 ent noncoding mutations surrounding a single exon of the HNRNPH1gene.

239 at is caused by a CAG expansion in the first exon of the huntingtin gene.

240 s alternative splicing of mRNA, which allows exons of a gene to be expressed at varying levels across

241 Specifically, the exons of protein-coding genes harbor more than 90% of va

242 etions mapping to the PTCHD1 locus disrupted exons of PTCHD1-AS.

243 erences that distinguish the profiles of the exon-only expression data from the combined exon and int

244 erved in 8/21 probands, fall in the terminal exon or the extreme 3' region of exon 1, and are therefo

245 put to plot the concerned data on promoters, exons or any other user-defined genome locations and gen

246 SFs contain ultraconserved poison exon (PE) sequences that exhibit greater identity across

247 ution: How did ESE motifs become enriched in exons prior to the evolution of ESE recognition?

248 ic splicing enhancers (ESEs) are enriched in exons relative to introns and bind splicing activators.

249 be pgFARM (paired guide RNAs for alternative exon removal), a CRISPR-Cas9-based method to manipulate

250 ding length of introns flanking circularized exons, repetitive elements such as Alu elements and SINE

251 ng ZMAT3 increased inclusion of CD44 variant exons, resulting in significant up-regulation of oncogen

252 Autism-associated disruption of this exon results in increased protein production, likely thr

253 Exon-level analysis (including noncoding exons) revealed decreased 5' UTR usage of Hnrnph1 and im

254 how that RNase H ASOs targeted to introns or exons robustly reduce the level of spliced RNA associate

255 eir N-termini through tandem duplications of exon segments.

256 These include ORF assignment of exon skipped transcript, studies of lost protein functio

257 Exon skipping (ES) is reported to be the most common alt

258 We present an exon skipping event in HDAC7, which is a candidate gene

259 al features due to ES events, and studies of exon skipping events associated with mutations and methy

260 ities to identify therapeutically targetable exon skipping events.

261 nts with Becker MD and mdx mice subjected to exon skipping exhibited inhibited dystrophin degradation

262 e with an exon 5-targeted ASO-induced robust exon skipping for more than a year, improved motor coord

263 Indeed, antisense oligonucleotide-based exon skipping has shown promise for RDEB.

264 ASOs also induced exon skipping in cell lines derived from patients with C

265 , antisense oligonucleotides (ASOs) mediated exon skipping is a promising therapeutic approach.

266 Exon skipping is a widespread phenomenon occurring acros

267 further confirmed that all 3 variants caused exon skipping resulting in frameshifts that lead to prem

268 antisense oligonucleotide (ASO) that induces exon skipping to restore the open reading frame.

269 repeatability of platelet RNA expression and exon skipping, a readily measured alternative splicing e

270 oration through micro-dystrophin delivery or exon skipping, preclinical models have shown that incomp

271 We also described an exon-skipping mechanism for CARD11 dominant-negative act

272 an AKT-p300 HAT epigenetic cascade, induces exon-specific Bdnf expression, which in turn is indispen

273 We find that cell and exon-specific DNA hypomethylation permits CTCF binding,

274 fications, but not DNA methylation, underlie exon-specific transcription of the Bdnf gene induced by

275 In vivo, hypomethylation of an alternative exon specifically in nociceptors, likely permits CTCF bi

276 ications (hPTMs) have been shown to regulate exon splicing by either directly recruiting splice machi

277 ession patterns of RNA binding proteins with exon splicing profiles, we uncovered likely causal varia

278 ents, conserved motif identification, intron/exon structural patterns and gene ontology classificatio

279 The intron-exon structure of the NPIP gene family has changed drama

280 ting of a small deletion in the first coding exon supported Hnrnph1 as a quantitative trait gene.

281 This indicates that exon-targeted ASOs achieve full activity after the pre-m

282 ntron-targeted ASOs and, to a lesser extent, exon-targeted ASOs cause RNA polymerase II (Pol II) tran

283 ated with chromatin to a greater extent than exon-targeted ASOs.

284 eptor (BCR) and of antibodies are encoded by exons that are assembled in developing B cells by V(D)J

285 We hypothesize that the high exon to intron motif ratios necessary for ESE function w

286 To discover driver fusions beyond canonical exon-to-exon chimeric transcripts, we develop CICERO, a

287 ckground noise in terms of length, number of exons, transposable element composition, and sequence co

288 ernative splicing events, CHyMErA identifies exons underlying human cell line fitness.

289 nnotations of ES events based on the skipped exon units in cancer and normal tissues are not availabl

290 This also identified differential exon usage and phasing for these genes between the diffe

291 Interestingly, alternative exon usage by PTEN null cells is increased under metabol

292 ese mutations would trigger an alteration of exon usage during RNA splicing, causing the enamel malfo

293 anges in alternative splicing (AS) and first exon usage, increasing the diversity of transcripts expr

294 lly long first intron and the other spanning exons, we identify two classes of active transcription s

295 Many poison exons were essential for the growth of both cultured cel

296 (also known as FGF13) has alternative first exons which produce multiple protein isoforms that diffe

297 he functional relevance of 'poison' cassette exons, which disrupt their host genes' reading frames ye

298 in of collagen VII is encoded by 82 in-frame exons, which makes splice-modulation therapies attractiv

299 e two forces retain certain coding motifs in exons while passively depleting them from introns.

300 ice site, resulting in splicing to a cryptic exon with a premature termination codon.