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1 ng of a 1.8-kb transcript lacking the second exon.
2 retained intron and overlaps the alternative exon.
3 tween long inverted repeats upstream of each exon.
4 ich differ in the utilization of an internal exon.
5 tial GC content between adjacent introns and exons.
6 nation types, involving initial and terminal exons.
7  of splicing regulatory sequences across the exons.
8 pping or large genomic deletions that delete exons.
9  non-coding introns from pre-mRNAs and joins exons.
10 chinery to a protein modification that marks exons.
11 ng platforms that supply promoters and first exons.
12 y exceeding that found within protein-coding exons.
13  of several protein fragments encoded by HTT exon 1 by using the associative memory, water-mediated,
14 ombination of both terminal additions in HTT exon 1 fragment leads to a complex aggregation mechanism
15 ical free energy profiles are uphill for HTT exon 1 fragments having 20 or 30 glutamines, the aggrega
16 e pathology in mouse models and that the HTT exon 1 gene product can self-assemble into amyloid struc
17 HTTexon1) that encodes the highly pathogenic exon 1 HTT protein.
18 ed CRISPR/Cas9 vectors designed to juxtapose exon 1 of Dnajb1 with exon 2 of Prkaca to create the Dna
19 lants examined, sequences closely resembling exon 1 of SRK have been found, but the function of these
20                We have previously shown that exon 1 of the huntingtin gene does not always splice to
21 e, caused by expansion of the polyQ tract in exon 1 of the Huntingtin protein (Htt), is associated wi
22 mozygous nonsense mutation was identified in exon 1 of the TYR gene, with the substitution of a cytos
23 na-fide T3 phosphorylation alters Huntingtin exon 1 protein conformation and aggregation properties.
24 nsgenes in Hu128/21 mice match the human HTT exon 1 reference sequence.
25  BACHD transgene carries a floxed, synthetic exon 1 sequence.
26 tion of N-terminal fragments (encoded by HTT exon 1) underlies the disease pathology in mouse models
27 e lines introducing premature stop codons in exon 1, as well as obtained an abcd1 allele from the Zeb
28 and (ii) an NF-kappaB p65 driven enhancer in exon 1.
29 mation from the physiologically relevant htt exon-1 (Httex1) protein has been challenging.
30 mics simulations to study the folding of Htt-exon-1 across five different polyQ-lengths.
31  expansion of the polyglutamine tract in the exon-1 domain of the huntingtin protein (htt(e1)).
32 whether the accumulation of an amyloidogenic exon-1 fragment of mutant huntingtin (mHTTx1) modulates
33 n the extended polyglutamines (polyQ) within exon-1 of Huntingtin protein (Htt) and age onset of Hunt
34 anded polyglutamine (polyQ) sequences in the exon-1 region of mutant huntingtin plays a central role
35                  Alternative splicing of tau exon 10 generates tau isoforms with three or four microt
36 ysregulating the alternative splicing of tau exon 10 in AD.
37                      Alternative splicing of exon 10 in the tau primary transcript gives rise to prot
38 found that inhibition of Dyrk1A enhanced tau exon 10 inclusion, leading to an increase in 4R-tau/3R-t
39 phorylation, the alternative splicing of tau exon 10, and cognitive performance.
40 CYP24A1, but also increased expression of an exon 10-skipped CYP24A1 splice variant; in a minigene mo
41 ulates alternative splicing of exogenous tau exon 10.
42 V receptor, we generated mice with humanized exons 10-12 of the mouse Dpp4 locus.
43 d a previously unreported de novo variant in exon 11 (p.Gly487Cys), which we modeled to determine its
44 T mutations, including deletions that affect exon 11 codons 557 and/or 558.
45                            Patients with KIT exon 11 deletion mutations benefit most from the longer
46                                          KIT exon 11 deletion mutations, deletions that involved codo
47            Similarly, in the subset with KIT exon 11 deletion mutations, higher-than-the-median mitot
48                     PDGFRA mutations and KIT exon 11 insertion or duplication mutations were associat
49 ement in GIST patients harboring the non-KIT exon 11 mutation and should be considered the standard o
50                        We concluded that the exon 11 mutations were the most important in both cases
51  largest lesion (smaller), and KIT mutation (exon 11) were significant prognostic factors for the pro
52 f metabolic response (P < 0.001) and non-KIT exon 11-mutated GISTs (P < 0.001).
53  mutation was a homozygous A > G mutation in exon 12 (amino acid 567) of PDGFR-alpha.
54 ot restricted to patients with JAK2 V617F or exon 12 mutations.
55 two competing alternative 5' splice sites in exon 12 yield Esrp1 isoforms with differential nucleocyt
56 th NMDA receptor gene Grin1 exon 4, and Enah exon 12, all consistent with a change in SCN RBFOX activ
57 ch the first common exon of the ZC3H14 gene, exon 13 is removed (Zc3h14Deltaex13/Deltaex13) leading t
58 nchymal-epithelial transition (MET) near the exon 14 splice sites are recurrent in lung adenocarcinom
59          Our results provide a mechanism for exon 16 3' splice site activation in which a coordinated
60                                              Exon 16 of protein 4.1R encodes a spectrin/actin-binding
61  tumor, which was NSCLC with responsive EGFR exon 19 deleted.
62  with a confirmed, activating EGFR mutation (exon 19 deletion or L858R mutation).
63 rsus EGFR-TKI, age, performance status, EGFR exon 19 mutation, and absence of extracranial metastases
64 nterneurons express only isoforms containing exon 1b, whereas excitatory principal cells express exon
65 , whereas excitatory principal cells express exon 1e alone or both 1e and 1b.
66                         Sequences for Papa-B exon 2 and 3 were determined from the genomic DNA in 255
67  structure of lnc18q22.2 showing an extended exon 2 in liver.
68  designed to juxtapose exon 1 of Dnajb1 with exon 2 of Prkaca to create the Dnajb1-Prkaca gene fusion
69 o-oncogene (c.1799T>A [V600E]; BRAFV600E) or exon 2 of the KRAS proto-oncogene (KRAS) in the primary
70 >isoleucine mutation in the 33rd position of exon 2 of TTR in 1 patient of 1 pedigree, confirming the
71 re5 binds RNA in vivo, with a preference for exon 2 regions of intron-containing pre-mRNAs and poly(A
72 he huntingtin gene does not always splice to exon 2 resulting in the production of a small polyadenyl
73 We describe a pseudogene sharing homology to exons 2 through 5 of human CD59 present in the C. porcel
74 ug resistance in drug-sensitive EGFR or HER2 exon 20 insertion models.
75 f Gly770 into two dacomitinib-resistant EGFR exon 20 insertion mutants restored sensitivity to dacomi
76 igated the effects of specific EGFR and HER2 exon 20 insertion mutations from NSCLC patients that had
77 nd HER2 both occur at analogous positions in exon 20.
78 enome editing efficiently excised the mutant exon 23 in dystrophic mice, and immunofluorescence data
79           Nf123aIN/23aIN mice are viable and exon 23a inclusion approaches 100% in all tissues, inclu
80 N/23aIN mouse brain lysates, confirming that exon 23a inclusion inhibits Nf1 RasGAP activity in vivo
81 n which the splicing signals surrounding Nf1 exon 23a were manipulated to increase exon inclusion.
82 highly regulated alternative splicing of Nf1 exon 23a.
83 C2 mutations - Glu1352Ala and a duplication (exons 24 and 25).
84 C2a and KCC2b along with a novel one lacking exon 25 (KCC2a-S25).
85 tions, we determined that the first 22 bp of exon 3 contain cis-acting elements that enhance the excl
86  is survivin DEx3, in which the exclusion of exon 3 generates a unique carboxyl terminus with specifi
87 cting elements that enhance the exclusion of exon 3 to generate the survivin DEx3 mRNA isoform.
88 nsitive alternative splicing of its terminal exon 3' untranslated region, generating an oncogenic, C-
89 tected a heterozygous c.305T>C alteration in exon 3, which causes a leucine to serine substitution at
90 nd over 90% of these fusions occurred in ERG exons 3 or 4.
91  identified a deletion in a patient spanning exon 35 as a result of a recombination event between fla
92 roximately 17Kb large deletion including the exon 4 and exon 5 of RP2 gene was found in an XLRP famil
93 ite cluster for this transcription factor on exon 4 of APOE.
94 o exclusion of both NMDA receptor gene Grin1 exon 4, and Enah exon 12, all consistent with a change i
95 ut altering physical dependence, whereas the exon 4-associated truncation in mE4M-B6 mice facilitated
96  over G protein activation compared with the exon 4-associated variant, suggesting an interaction of
97 studies indicated a relatively high ratio of exon 4-excluded neuro-oncological ventral antigen 1 (Nov
98 g, with the most abundant transcript lacking exon 4.
99 g (AS) that occurs at the final coding exon (exon 47) of the Cav2.1 voltage-gated calcium channel (VG
100 0 indexed by a nonsynonymous SNP mutation on exon 5 of a bHLH transcription factor was found to eleva
101 17Kb large deletion including the exon 4 and exon 5 of RP2 gene was found in an XLRP family.
102 ed when targeting each allele of rs362331 in exon 50 of the HTT transcript; this selectivity was also
103 rsen, an antisense oligonucleotide targeting exon 51: an open label study including 12 patients; a ph
104 an receptor CD44V6 (CD44 containing variable exon 6 (v6)) for differentiation of lung fibroblast to m
105 hanistic insight into the regulation of IL7R exon 6 splicing and its impact on MS risk.
106 17 (P =1.27 x 10-303), a known coding SNP in exon 6 that is associated with a 0.06 g/l ( approximatel
107 an receptor, CD44V6 (CD44 variant containing exon 6), which enhances the TGFbeta1 autocrine signaling
108 onal epistasis with allelic variants in IL7R exon 6.
109 avours the production of transcripts lacking exon 7 and a rapidly degraded non-functional SMNDelta7 p
110 usly reported the c.859G > C variant in SMN2 exon 7 as a positive modifier in several patients.
111 at binds the SMN2 messenger RNA and promotes exon 7 inclusion and thus increases full length SMN expr
112  a novel approach for the restoration of SMN exon 7 inclusion for a potential therapy of SMA.
113 y to reprogram pre-mRNA splicing and restore exon 7 inclusion in SMN1 carrying a broad spectrum of pa
114 brain stem and hypothalamus, consistent with exon 7 involvement in morphine tolerance.
115      Here, we have identified 3 mutations in exon 7 of NTN1 in 2 unrelated families and 1 sporadic ca
116 e-stranded (ds) oligonucleotide representing exon 7 of the p53 gene.
117  SMN2 cannot compensate for SMN1 loss due to exon 7 skipping.
118 -N1, which controls survival of motor neuron exon 7 splicing.
119 n SCN gene transcripts; inclusion of Cacna1c exon 7, and also exclusion of both NMDA receptor gene Gr
120 ciated variant, suggesting an interaction of exon 7-associated C-terminal tails with beta-arrestin 2
121                         In mE7M-B6 mice, the exon 7-associated truncation diminished morphine toleran
122                       In cell-based studies, exon 7-associated variants shifted the bias of several m
123 ydrolysis) of primary oxidation sites of p53 exon 7.
124 ne coupled with predominant skipping of SMN2 exon 7.
125 c mutations at both the 3'ss and 5'ss of the exon 7.
126       In particular, mouse uses the terminal exon 8 T, while Human uses terminal exon 9, which is abs
127                    Alternate splicing in the exon-8 of vascular endothelial growth factor (VEGF)-A re
128 interaction with the intronic 3 site of NUMB exon 9 contributing to regulation of the Notch pathway i
129 e associated with favorable RFS, whereas KIT exon 9 mutations were associated with unfavorable outcom
130 terminal exon 8 T, while Human uses terminal exon 9, which is absent in rodents.
131  the two newly discovered exons of the gene, exons 9beta and 9gamma, generated by alternative splicin
132                                              Exon Ab inclusion correlated with predicted free energie
133 d BPs next to a long polypyrimidine tract of exon Ab.
134 lpha6 helix of U2AF35, and was fine-tuned by exon Ab/3 variants.
135  coverage is both local (coverage of a given exon across different platforms) and global (coverage of
136 erent platforms) and global (coverage of all exons across the genome in the given platform).
137 ansferase (MTase) and 3'-5' exoribonuclease (ExoN) activities.
138 ught to determine the contributions of nsp14 ExoN activity in the induction of and resistance to the
139 ur data suggest murine hepatitis virus (MHV) ExoN activity is required for resistance to the innate i
140 r an RNA modification act on viruses lacking ExoN activity.IMPORTANCE CoVs encode multiple antagonist
141 dentified protein-coding genes, with skipped exon and alternative first exon being the most frequentl
142 pplied to three case studies concerning both exon and HTA arrays.
143                            To understand how exon and intron length and splice site recognition mode
144 e spliceosomal C complex with the cleaved 5' exon and lariat-3'-exon bound to the catalytic centre re
145 show that m(6)A methylations are enriched in exons and are added to transcripts prior to splicing.
146                                          The exons and exon-intron junctions of present day higher pl
147 proximately 39%) with relatively long coding exons and few coding introns.
148 y only one gene, titin comprises hundreds of exons and has the potential for enormous diversity.
149  of a large 2-kb transcript composed of four exons and one consisting of a 1.8-kb transcript lacking
150            The mutation removes the last two exons and part of the 3' UTR of DSTYK.
151  the proximity of alternatively spliced (AS) exons and poly(A) sites.
152 s a diverse set of RNA motifs in introns and exons and regulates alternative splicing.
153 accuracy in rice (0.5648 for CDS, 0.4468 for exon, and 0.6695 nucleotide structure) and A. thaliana (
154  and A. thaliana (0.5808 for CDS, 0.5955 for exon, and 0.8839 nucleotide structure).
155 andem duplicate of the CAG repeat-containing exon, and a corrected model, introduced here.
156 integrative GWAS-eQTL analysis against gene, exon, and splice-junction quantifications.
157 gene coding, which removes introns and joins exons, and splicing branchpoints are indicators for the
158               Ig heavy-chain variable region exons are assembled developmentally from V, D, J gene se
159                                      Bimodal exons are flanked by more conserved intronic sequences h
160 and after selection confirmed that all HPRT1 exons are needed.
161                In summary, m(6)A is added to exons before or soon after exon definition in nascent pr
162 nes, with skipped exon and alternative first exon being the most frequently utilised.
163 mplex with the cleaved 5' exon and lariat-3'-exon bound to the catalytic centre revealed that branchi
164 only explain diversity gradients near intron-exon boundaries if the conversion template comes from ou
165  avoid conserved functional regions, such as exons, but, somewhat surprisingly, also avoid introns.
166        However, DNA methylation in the first exon can prevent CTCF binding in most cancers, but the m
167 the unique elements regulating NDE1 terminal exon choice.
168       Special categories of splicing such as exon circularization, first and last intron processing,
169 68 RNA binding sites flank the Neurexin2 AS4 exon, compared with those flanking the Neurexin1 and Neu
170                          PIECE (Plant Intron Exon Comparison and Evolution) is a web-accessible datab
171 8 isoforms, including three from novel first exons consistent with existing transcription start site
172        Due to titin's large size (363 coding exons), current web applications are unable to map titin
173 lated with splicing efficiencies, suggesting exon definition as the step affected by most mutations.
174 m(6)A is added to exons before or soon after exon definition in nascent pre-mRNA, and while m(6)A is
175 ceosome A complex formation, and facilitates exon definition through RBM39-mediated splicing regulati
176 icing factor 2 (SRSF2), a crucial protein in exon definition, but only when Lys-77 is unmethylated.
177 algorithm to detect rare, intragenic, single-exon deletion CNVs using WES data; this tool can be usef
178 nables direct editing of the mutation, multi-exon deletion or complete gene correction via homologous
179 n (EBNA-LP) resides predominantly within the exons downstream of IR1.
180   Prp22 binds nucleotides 15 to 21 in the 3' exon, enabling it to pull the intron-exon or ligated exo
181            Here we use a conserved alternate exon encoding part of the first domain of sodium channel
182 c regions to genomic annotations (promoters, exons, enhancers, etc.).
183 rimary breast tumors, confirming many of the exon events identified in the TCGA cohort.
184                                              ExoN excises nucleotide mismatches at the RNA 3'-end in
185 rentiation, we discover that up to 20% of AS exons exhibit bimodality.
186 hly expressed genes with distant alternative exons exhibit coordination, showcasing the need for long
187 plicing (AS) that occurs at the final coding exon (exon 47) of the Cav2.1 voltage-gated calcium chann
188 encing data, utilizing information from both exon-exon junctions and discordant paired-end reads.
189 ng RNA-seq, we examined whole-exome gene and exon expression in non-psychiatric controls (CON, N=29),
190 L investigation of microarray-based gene and exon expression levels in whole blood in a cohort of 525
191 of CRAM, bigwig and bedGraph files, gene and exon expression quantification matrices (Fragments Per K
192 d standardized alignment as well as gene and exon expression quantification of all public bulk (and i
193 .g., conditional knockout alleles containing exons flanked by LoxP sites).
194                                              Exon flanks, which are enriched for sequences required f
195 ity of miR-122 binding on 3' UTRs and coding exons followed by extensive binding to other genic and n
196 undergo somatic hypermutation (SHM) of V(D)J exons followed by selection for SHMs that increase antig
197 mbinatorial assembly of IgH and IgL V region exons from gene segments generates preimmune Ig repertoi
198             Given that the majority of multi-exon genes generate diverse functional products, it is i
199                      Over 95% of human multi-exon genes undergo alternative splicing, a process impor
200 ch higher percentage of genes ( 20% of multi-exon genes) undergo AS than previously reported (3-5%).
201 ition; moreover, flanks at the 5' end of the exons have significantly lower SSM density than at the 3
202 the COMT promoter at a conserved CpG site in exon II.
203 t case of alternative splicing of duplicated exon in a mollusc that produces a novel variant adaptive
204 abling it to pull the intron-exon or ligated exons in a 3' to 5' direction to achieve 3'-ss proofread
205 ve splicing, including inclusion of A-T rich exons in target genes, a phenomenon that has previously
206 ass 2A member 1 gene (MAN2A1) and the last 6 exons in the FER tyrosine kinase gene (FER), called MAN2
207 the product of a fusion between the first 13 exons in the mannosidase alpha class 2A member 1 gene (M
208 s with G-quadruplex-forming capacity promote exon inclusion.
209 ng Nf1 exon 23a were manipulated to increase exon inclusion.
210 lls RNA polymerase II occupancy of all SALL4 exons increased, suggesting CpG demethylation downstream
211 b-accessible database that houses intron and exon information of plant genes.
212 serting functional rearranged human variable exons into the mouse IgH and IgL loci has been used to e
213 n the transcription start site and the first exon-intron junction.
214                                The exons and exon-intron junctions of present day higher plant's Rca,
215 of a transcription factor through changes in exon-intron organization and thereby supported the evolu
216                           An analysis of the exon-intron structures and conserved motifs provided fur
217                           An analysis of the exon/intron structure and protein domains was conducted
218  all tissues, including the brain, where the exon is normally almost completely skipped.
219      We found that selection of the terminal exon is regulated in a cell dependent manner and relies
220 cases, such as MAPT Coordination of internal exons is found to be extensive among protein coding gene
221 ve usage of a 3' splice site in the terminal exon) is protective for kidney function.
222 icing complexes assembled at the alternative exon lead to inefficient splicing and intron retention.
223 scriptome assemblies: incomplete annotation, exon level differences, transcript fragmentation and inc
224 2-, ER- HER2-, and HER2+, many events on the exon level were subtype specific.
225 st frequency of candidate-causal eQTLs using exon-level RNA-Seq, and identified novel SLE susceptibil
226 but lacked information on 3'-ss recognition, exon ligation, and exon release.
227                Slu7 and Prp18, which promote exon ligation, bind together to the Prp8 RNase H-like do
228 east P-complex spliceosome immediately after exon ligation.
229 or 3'-splice site docking, thereby promoting exon ligation.
230  transesterification reactions-branching and exon ligation.
231 nucleotides that is inserted into the coding exon of a target gene using CRISPR/Cas9 technology and h
232 tretch of guanine-rich sequence in the first exon of hTERT and located within the CTCF-binding region
233 f Imprinted Sites (BORIS) at the alternative exon of Pyruvate Kinase (PKM) is associated with cancer-
234  mutation c.796C>T (p.Arg266Ter) in the last exon of SERPINB7.
235 ominant 7-base-pair duplication in the first exon of the forkhead box I3 gene (FOXI3) shared by all t
236       Two families had mutations in the last exon of the gene and a third family was identified with
237  of CCCTC-binding factor (CTCF) to the first exon of the hTERT gene can down-regulate its expression.
238  generated a mouse in which the first common exon of the ZC3H14 gene, exon 13 is removed (Zc3h14Delta
239 (c.2737C>T [p.Arg913Ter]) in the penultimate exon of ZSWIM6 who have severe-profound intellectual dis
240 Damaging, nonsynonymous PZMs within critical exons of prenatally expressed genes were more common in
241 and cytosine DNA methylation are elevated at exons of spliced genes and have been implicated in the r
242                 METHODS AND We sequenced the exons of the CETP gene in 58 469 participants from 12 ca
243 riants reveals that the two newly discovered exons of the gene, exons 9beta and 9gamma, generated by
244                                 We sequenced exons of this gene in DNA from a total of 134 nonsyndrom
245 ulti-region' track display configuration for exon-only, gene-only and custom regions visualization; n
246  the 3' exon, enabling it to pull the intron-exon or ligated exons in a 3' to 5' direction to achieve
247 fication matrices (Fragments Per Kilobase Of Exon Per Million Fragments Mapped, Transcripts Per Milli
248 y identify quadruplex formation in the first exon promoted by CpG dinucleotide methylation as a regul
249                    The in vitro formation of exon-protein complexes between the mutant molecules and
250      When bound upstream or within regulated exons PTBP1 tends to promote their skipping, whereas bin
251 ompounds that act transcriptionally, enhance exon recognition, or stabilize the SMN protein.
252  expression levels of 20 genes and sequenced exon regions of 8 genes (HNF1A, IL6ST, CTNNB1, FRK, STAT
253                         Finally, analysis of exons regulated by ancient CELF family homologs in chick
254       Finally, we identify tandem homologous exons regulated by U2AF and show that their preferential
255 ' direction to achieve 3'-ss proofreading or exon release, respectively.
256 ion on 3'-ss recognition, exon ligation, and exon release.
257 HL tumor samples lacking either 1 or several exon sequences.
258 conducted genome-wide mRNA profiling and DNA exon sequencing of two cell lines (TMD and BMD) derived
259                             Deep ( 500X) NF1 exon sequencing was also conducted on tumor DNA.
260                                           By exon shuffling, this mechanism leads to the production o
261  Rgs16 Interestingly, the lack of the second exon significantly decreased AK144841's inhibitory effec
262 e recurrent in lung adenocarcinoma and cause exon skipping (METDelta14).
263 processing, alternative 5 and 3'ss usage and exon skipping are marked by distinct patterns of ordered
264 ory circuit of sense-antisense pairs and the exon skipping during alternative splicing, through inter
265 p a new target function for AS prediction in exon skipping events and show it significantly improves
266                                Although SMN2 exon skipping is the principal contributor to SMA severi
267 t some single-guide RNAs (sgRNAs) can induce exon skipping or large genomic deletions that delete exo
268                                 Drug-induced exon skipping preferentially affects shorter alternative
269                                  AON-induced exon skipping resulted in specific Alk4 down-regulation,
270    Mutations at splice junctions often cause exon skipping, short deletions, or insertions in the mat
271 ention, and Sudemycins more acute effects on exon skipping.
272 es, higher expression of hDBR1 only affected exon-skipping activity in malignant cells.
273  splicing modulator-induced intron-retention/exon-skipping profile, which correlates with the differe
274              The identification of an intron/exon-spanning promoter in a hosting gene, resulting in p
275 le sequence variants (n = 16,384) of the HIV exon splicing silencer 3 (ESS3) 7-nt apical loop.
276 HC reduces insertion of the stress-regulated exon (STREX) in the KCNMA1 gene, permitting protein kina
277  more KCNMA1 containing the stress-regulated exon (STREX), a splice-variant of the alpha-subunit that
278 show that in ants such as H. saltator, the 9-exon subfamily of odorant receptors (HsOrs) responds to
279 ions were located in the last or penultimate exon, suggesting escape from nonsense-mediated mRNA deca
280 us, and an isoform containing an alternative exon that targets the transcript for nonsense mediated d
281 6029 revealed an 11-bp deletion in the first exon that was predicted to result in a premature stop co
282  (that can be assembled into variable region exons that encode bnAb precursors), have been engineered
283 es a large fraction of alternatively spliced exons throughout the human genome.
284  produces 34.5% and 36.3% more correct multi-exon transcripts than StringTie and TransComb, and respe
285                                              Exon-trapping assays with constructs containing splice s
286 e we show the consequences of germline final-exon-truncating mutations in REST for organismal develop
287 ose flanking the Neurexin1 and Neurexin3 AS4 exons under joint control by both Sam68 and SLM2.
288 g human myogenesis reveals that CDM-relevant exons undergo prenatal RNA isoform transitions and are p
289                                  Alternative exon usage was widespread, and although common events we
290  alteration from membrane to secreted IgH-mu exon usage, similar to in mammals.
291 orms in SCN and cerebral cortex that exhibit exon variation across two protein domains, we found a 3-
292 nce of an IFN-beta-mediated antiviral state, ExoN(-) viral RNA levels were not substantially reduced
293  decreased relative fitness, suggesting that ExoN(-) virus generated during an antiviral state is les
294                                     However, ExoN(-) virus generated from IFN-beta-pretreated cells h
295                                              ExoN(-) virus replication did not result in IFN-beta gen
296                                 In addition, ExoN(-) virus replication was attenuated in wild-type bo
297 ) encodes 3'-to-5' exoribonuclease activity (ExoN), which performs a proofreading function and is req
298 uses are the only RNA viruses that encode an ExoN, which functions to degrade double-stranded RNA (ds
299 ich an MT LTR provided a promoter and the 5' exon with a functional start codon while the bulk of the
300 scribed genes that, in rare cases, comprised exons with orientations and frames compatible with expre
301  were developed primarily for detecting gene exons within eukaryotic genomes and were therefore optim

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