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1                                              snRNA Psis are guided by single hairpin snoRNAs, also im
2                                              snRNA-seq achieves comparable gene detection to scRNA-se
3 NA (different subunits) and 5250 miRNA, 3747 snRNA, gene sequences from 9282 complete genome chromoso
4 n (snRNP), which contains, additionally, 7SK snRNA, methyl phosphate-capping enzyme (MePCE), and La-r
5                             Depletion of 7SK snRNA or Larp7 disrupts LEC integrity, inhibits RNAPII r
6                                      The 7SK snRNA specifically associates with a fraction of RNAPII
7             We demonstrate that two abundant snRNAs, WsnRNA-46 and WsnRNA-49, are expressed in Wolbac
8 east, the U2 small nuclear ribonucleic acid (snRNA) component of the spliceosome is targeted for addi
9 riptional modification of U56 and U93 alters snRNA conformational dynamics by distinct mechanisms and
10  view that 21U RNA biogenesis is built on an snRNA-related pathway.
11 implications for understanding canonical and snRNA 3'-end processing.
12 ur in the 5' splice-site binding region, and snRNA-mutant tumours have significantly disrupted RNA sp
13 pression datasets with both bulk RNA-seq and snRNA-seq data, Bisque replicates previously reported as
14                                scRNA-Seq and snRNA-Seq from matched samples recovered the same cell t
15 n clinical tumor samples using scRNA-Seq and snRNA-Seq, respectively.
16 iety of noncoding RNAs-snoRNAs, scaRNAs, and snRNAs-that are dependent on Cajal bodies for stability
17 ence for small RNA genes (tRNAs, snoRNAs and snRNAs) suggesting a putative role for RNA in its recrui
18 RNAs), and alters the occupancy of Pol II at snRNA loci.
19 ther, our results draw new parallels between snRNA and piRNA biogenesis in nematodes and provide evid
20                      In addition, DSP1 binds snRNA loci and interacts with Pol-II in a DNA/RNA-depend
21   The analysis revealed 42 Psis on T. brucei snRNAs, which is the highest number reported so far.
22                                  Analysis by snRNA-seq identified transcript profiles and inferred fu
23  least four additional proteins, to catalyze snRNA 3' end maturation in Arabidopsis.
24        Here, we identified and characterized snRNAs from the endosymbiotic bacteria, Wolbachia, which
25                             We then compared snRNA-seq of myoblasts before and after differentiation.
26                                 By contrast, snRNA-seq from all three platforms captured a diversity
27 ived from core promoter elements controlling snRNA transcription.
28 o increases the levels of assembly-defective snRNAs and suppresses some splicing defects seen in SMN-
29          To determine how assembly-defective snRNAs are degraded, we first demonstrate that yeast U1
30 antling of the Prp3-binding site on U4/U6 di-snRNA but leaves the Prp31- and Snu13-binding sites on U
31                    In solution, the U4/U6 di-snRNA forms a 3-helix junction with a planar Y-shaped st
32                                 The U4/U6 di-snRNA is conserved in eukaryotes and is part of the U4/U
33 sing factor 31 (Prp31), and Prp3 to U4/U6 di-snRNA leads to a stepwise decrease of Brr2-mediated U4/U
34 i-snRNAs and inhibits Brr2-mediated U4/U6 di-snRNA unwinding in vitro.
35 yses that Prp3 contains a bipartite U4/U6 di-snRNA-binding region comprising an expanded ferredoxin-l
36 f a 92-nt 3-helix junction from the U4/U6 di-snRNA.
37 operatively with Snu13 and Prp31 on U4/U6 di-snRNAs and inhibits Brr2-mediated U4/U6 di-snRNA unwindi
38  strongly inhibited by mutations in U4/U6 di-snRNAs that diminish the ability of U6 snRNA to adopt an
39 the spliceosome from unstable genome-encoded snRNA variants.
40 s ptRNA-subclasses that exist in eukaryotes: snRNA, snoRNA, RNase P, RNase MRP, Y RNA or telomerase R
41                          It consists of five snRNAs and more than 200 proteins.
42               Although DIEM was designed for snRNA-seq, our clustering strategy also successfully fil
43  subunits, which are largely dispensable for snRNA processing, also have regulatory roles at these pr
44 CESSING 1 (DSP1) is an essential protein for snRNA 3' end maturation in Arabidopsis.
45 de evidence for the production of functional snRNAs by Wolbachia that play roles in cross-kingdom com
46 metal cofactors of the spliceosome alter how snRNAs respond to these modifications.
47 1 and U2 genes as models, we show that human snRNA genes are more similar to mRNA genes than yeast sn
48                                  Thus, human snRNA genes may use chromatin structure as an additional
49   Production of snR-DPGs required the Pol II snRNA promoter (PIIsnR), and CPL4RNAi plants showed incr
50 s a previously unknown function of CPSF73 in snRNA maturation.
51 , reflecting a strong and specific defect in snRNA 3'-end formation.
52              Here, we show that DEFECTIVE in snRNA PROCESSING 1 (DSP1) is an essential protein for sn
53 uantify contamination and filter droplets in snRNA-seq experiments, called Debris Identification usin
54 r7, which is a hallmark of RNAPII engaged in snRNA synthesis.
55 a Hypoplasia Type 7 (PCH7) and implicated in snRNA and hTR processing.
56                 snoRNA species implicated in snRNA pseudouridylation were identified by a genome-wide
57 nteraction is crucial for the role of INT in snRNA 3'-end processing.
58 chment for long non-coding RNAs (lncRNAs) in snRNA-seq.
59 were particularly sensitive to variations in snRNA abundance in a breast cancer cell line model were
60 As with highly structured 3' ends, including snRNAs and histone mRNAs, are naturally resistant to RNa
61  of non-polyadenylated transcripts including snRNAs and mRNAs encoding replication-dependent histone
62 ogically relevant perturbation of individual snRNAs drove widespread gene-specific differences in alt
63 nd stability of regular snRNAs while leaving snRNA variants unprocessed and exposed to degradation in
64 A turnover at short transcription units like snRNA-, replication-dependent histone-, promoter upstrea
65 identified the presence of expressed U1-like snRNAs in multiple species, including humans.
66 monstrated that a new class of human U1-like snRNAs, the variant (v)U1 snRNAs (vU1s), also participat
67 d noncoding RNAs (e.g., mRNA, miRNA, lncRNA, snRNA, tRNA, yRNA), DNA, proteins, and enzymes.
68 ere, we present an approach for multiplexing snRNA-seq, using sample-barcoded antibodies to uniquely
69 we first demonstrate that yeast U1 Sm-mutant snRNAs are degraded either by Rrp6- or by Dcp2-dependent
70 pecific sn/snoRNA genes, and reduces nascent snRNA and snoRNA synthesis.
71 operate to protect and chaperone the nascent snRNA during its journey to the spliceosome.The mechanis
72  for introns and various RNA classes (ncRNA, snRNA, snoRNA) and less variability after degradation.
73  single cells (scRNA-seq) and single nuclei (snRNA-seq) and found them comparable, with a distinct en
74 rocessing of snRNAs, increases the levels of snRNA primary transcripts (pre-snRNAs), and alters the o
75 se results identify a conserved mechanism of snRNA quality control, and also suggest a general paradi
76 r a key factor involved in the processing of snRNA 3' ends.
77 ecreases the occupancy of LEC at a subset of snRNA genes and results in a reduction in their transcri
78 ole in the recruitment of LEC to a subset of snRNA genes through direct interaction of EAF and the N-
79 ongation during transcription of a subset of snRNA genes.
80                           However, levels of snRNAs did not follow the expression of splicing protein
81 ding to snRNAs are known to reduce levels of snRNAs, suggesting an unknown quality control system for
82            The biogenesis of the majority of snRNAs involves 3' end endonucleolytic cleavage of the n
83 plex was sufficient for 3'-end maturation of snRNAs.
84 al defects, impairs the 3' end processing of snRNAs, increases the levels of snRNA primary transcript
85 ulated pre-mRNA processing requires study of snRNAs, as well as protein splicing factors.
86  RNAi compromised the guided modification on snRNA and reduced parasite growth at elevated temperatur
87 t of the snRNP code to which Gemin5 binds on snRNAs.
88 otein WDR79, is essential for guiding Psi on snRNAs but not on rRNAs.
89 s restore snRNP assembly of Sm proteins onto snRNA and completely rescue both survival of Smn null mi
90  faithful delivery of seven Sm proteins onto snRNA and the formation of the common core of snRNPs.
91 utations did not affect pre-mRNA splicing or snRNA levels.
92 an cells lack antisense elements to rRNAs or snRNAs; thus, their targets remain unknown.
93                                          Our snRNA-seq protocol yielded 20-fold more podocytes compar
94  and a few other small RNA types like piRNA, snRNA and snoRNA.
95 complex with the Sm site or m(7)G cap of pre-snRNA, which reveal that the WD40 domain of Gemin5 recog
96 vels of TOE1 accumulated 3'-end-extended pre-snRNAs, and the immunoisolated TOE1 complex was sufficie
97 nd sufficient for binding the Sm site of pre-snRNAs by isothermal titration calorimetry (ITC) and mut
98  recognizes the Sm site and m(7)G cap of pre-snRNAs via two distinct binding sites by respective base
99  for the assembly of the ring complex on pre-snRNAs at the conserved Sm site [A(U)4-6G].
100  complex, is responsible for recognizing pre-snRNAs.
101 complex delivers pre-small nuclear RNAs (pre-snRNAs) to the heptameric Sm ring for the assembly of th
102                                    These pre-snRNAs contained 3' genome-encoded tails often followed
103 the levels of snRNA primary transcripts (pre-snRNAs), and alters the occupancy of Pol II at snRNA loc
104 5 in escorting the truncated forms of U1 pre-snRNAs for proper disposal.
105 ent CPSF73-I-containing complexes to process snRNAs and pre-mRNAs.
106 promotes maturation and stability of regular snRNAs while leaving snRNA variants unprocessed and expo
107                       The small nuclear RNA (snRNA) activating protein complex (SNAPc) is essential f
108 hese data suggest that U6 small nuclear RNA (snRNA) and RtcB participate in the formation of chimeric
109                       The small nuclear RNA (snRNA) components of the spliceosome undergo many confor
110 ption of Pol II-dependent small nuclear RNA (snRNA) genes.
111 ncluding c-myc and LEC to small nuclear RNA (snRNA) genes.
112                  Yeast U2 small nuclear RNA (snRNA) nucleotides that form base pairs with the branch
113  Mg(2+) site in the U2/U6 small nuclear RNA (snRNA) triplex, and the 5'-phosphate of the intron nucle
114 mal complex comprising U5 small nuclear RNA (snRNA), extensively base-paired U4/U6 snRNAs and more th
115 RNP), composed of the 7SK small nuclear RNA (snRNA), MePCE, and Larp7, regulates the mRNA elongation
116 e for the U6 spliceosomal small nuclear RNA (snRNA).
117 atalytic metal site in U6 small nuclear RNA (snRNA).
118 authentic pre-mRNA and U7 small nuclear RNA (snRNA).
119 stemloops in U1 and/or U2 small nuclear RNA (snRNA).
120 on a functional U2 snRNP (small nuclear RNA [snRNA] plus associated proteins), as H2A.Z shows extensi
121 l nucleolar RNA [snoRNA], small nuclear RNA [snRNA], small Cajal body-specific RNA [scaRNA], and tran
122 xpression of modified U1 small nuclear RNAs (snRNA) complementary to the splice donor sites strongly
123 ly downstream from viral small nuclear RNAs (snRNA).
124        In prokaryotes, small noncoding RNAs (snRNAs) of 50-500 nt are produced that are important in
125 tion of 3'-extensions of small nuclear RNAs (snRNAs) and biogenesis of novel transcripts from protein
126             Uridine-rich small nuclear RNAs (snRNAs) are the basal components of the spliceosome and
127 3A>G) of U1 spliceosomal small nuclear RNAs (snRNAs) in about 50% of Sonic hedgehog (SHH) medulloblas
128 hat TOE1 associated with small nuclear RNAs (snRNAs) incompletely processed spliceosomal.
129  host RNAs, particularly small nuclear RNAs (snRNAs), and avoidance of host transcripts encoding host
130 , transfer RNAs (tRNAs), small nuclear RNAs (snRNAs), and RMRP.
131 rsors to specific tRNAs, small nuclear RNAs (snRNAs), and small nucleolar RNAs (snoRNAs) are all enri
132  in 3' end processing of small nuclear RNAs (snRNAs), attenuates MtnA transcription during copper str
133 methylation of rRNAs and small nuclear RNAs (snRNAs), respectively.
134           Although these small nuclear RNAs (snRNAs), termed U1, U2, U4, U5, and U6 snRNA, are presen
135 sis) on the spliceosomal small nuclear RNAs (snRNAs), which may enable growth at the very different t
136 compartments enriched in small nuclear RNAs (snRNAs)-and promotes efficient spliceosomal snRNP assemb
137 oteins plus U4/U6 and U5 small nuclear RNAs (snRNAs).
138 As such as small nuclear and nucleolar RNAs (snRNAs and snoRNAs).
139 A-seq (scRNA-seq) or single-nucleus RNA-seq (snRNA-seq) data to generate a reference expression profi
140                      Single-nucleus RNA-seq (snRNA-seq) enables the interrogation of cellular states
141 d from fresh tumors, single-nucleus RNA-Seq (snRNA-Seq) is needed to profile frozen or hard-to-dissoc
142     Here, we report a single-nuclei RNA-seq (snRNA-seq) transcriptomic study on human retinal tissue,
143 ghts, we used single nuclear RNA sequencing (snRNA-seq) and translating ribosome affinity purificatio
144  by performing single nuclei RNA sequencing (snRNA-seq) at multiple stages of mouse embryonic develop
145               Single-nucleus RNA sequencing (snRNA-seq) measures gene expression in individual nuclei
146 roplet-based, single-nucleus RNA sequencing (snRNA-seq) of A1 across three developmental time points
147 rmed unbiased single-nucleus RNA sequencing (snRNA-seq) on cryopreserved human diabetic kidney sample
148   We utilized single nucleus RNA sequencing (snRNA-seq) to examine the transcriptomes of over 16 000
149 platform with single-nucleus RNA sequencing (snRNA-seq) using sNuc-DropSeq, DroNc-seq, and 10X Chromi
150   Here we use single-nucleus RNA-sequencing (snRNA-seq) analysis in mice and humans to characterize a
151 whole-cell and single-nuclei RNA-sequencing (snRNA-seq) methods, here we show that snRNA-seq faithful
152 , we utilized single-nucleus RNA-sequencing (snRNA-seq) to determine the extent of transcriptional di
153 otein-coding genes downstream of the snRNAs (snRNA-downstream protein-coding genes [snR-DPGs]).
154 irst high-throughput mapping of spliceosomal snRNA Psis by small RNA Psi-seq.
155 ranscription of RNAPII-specific spliceosomal snRNA and small nucleolar RNA (snoRNA) genes.
156                                  In summary, snRNA-seq of activated neurons enables the examination o
157 hat the Integrator complex, which terminates snRNA transcription, is recruited to piRNA loci.
158                  Our study demonstrates that snRNA-seq provides reliable transcriptome quantification
159            Our results further indicate that snRNA-seq has unique advantage in capturing nucleus-enri
160                              We observe that snRNA-seq is commonly subject to contamination by high a
161 ncing (snRNA-seq) methods, here we show that snRNA-seq faithfully recapitulates transcriptional patte
162 udy identifies a complex responsible for the snRNA 3' end maturation in plants and uncovers a previou
163                We show here that Gemin5, the snRNA-binding protein of the SMN complex, binds directly
164    In the wild type, salt stress induced the snRNA-to-snR-DPG switch, which was associated with alter
165  plants showed increased read-through of the snRNA 3'-end processing signal, leading to continuation
166 tinuation of transcription downstream of the snRNA gene.
167 ell Integrator complex, which recognizes the snRNA 3' end processing signal (3' box), generates the 5
168 ive binding of all protein components to the snRNA duplex during di-snRNP assembly by electrophoretic
169 l for transcription of genes that encode the snRNAs.
170  from protein-coding genes downstream of the snRNAs (snRNA-downstream protein-coding genes [snR-DPGs]
171 ar splicing speckles and associates with the snRNAs that are involved in splice site recognition.
172                We evaluated DIEM using three snRNA-seq data sets: (1) human differentiating preadipoc
173                 Surprisingly, in contrast to snRNA 3' end processing, HVS pre-miRNA 3' end processing
174 tment of Integrator or Heat Labile Factor to snRNA or RDH genes, respectively.
175 se of a neurodegenerative syndrome linked to snRNA maturation and uncover a key factor involved in th
176     Defects in Sm protein complex binding to snRNAs are known to reduce levels of snRNAs, suggesting
177 of all regular RNA polymerase II transcribed snRNAs of the major and minor spliceosomes by removing p
178  plants, suggesting that the transcriptional snRNA-to-snR-DPG switch may be a ubiquitous mechanism to
179 erns similar to canonical ncRNAs (e.g. tRNA, snRNA, miRNA, etc) on approximately 70% of human long nc
180 nctional RNA molecules including rRNA, tRNA, snRNA and ribozymes.
181 ites and modest delays at some histone and U snRNA genes, suggesting that the torpedo mechanism is no
182 omplex, to processing bodies, thus forming U snRNA bodies (U bodies).
183 , and Listeria interfere with spliceosomal U snRNA maturation in the cytosol.
184  to the decline in the cytosolic levels of U snRNAs and of the SMN complex proteins SMN and DDX20 tha
185 ial infection resulted in the rerouting of U snRNAs and their cytoplasmic escort, the survival motor
186              Mechanistically, targeting of U snRNAs to U bodies was regulated by translation initiati
187 than an overall reduction in Uridyl-rich (U)-snRNAs, may contribute to the specific neuromuscular dis
188 Strikingly, we have been unable to find a U1 snRNA candidate or any predicted U1-associated proteins,
189 esigned several U1 snRNA vectors to adapt U1 snRNA binding sequences of the mutated DDC gene.
190               Therefore, mutation-adapted U1 snRNA gene therapy can be a promising method to treat ge
191 e U1 snRNP core particle (Sm proteins and U1 snRNA), but not the mature U1 snRNP-specific proteins (U
192 ins to a lesser extent than the canonical U1 snRNA.
193 at ALS-associated FUS aberrantly contacts U1 snRNA at the Sm site with its zinc finger and traps snRN
194 gether, these data suggest that the human U1 snRNA variants analyzed here are unable to efficiently b
195  we identified these hotspot mutations in U1 snRNA in only <0.1% of 2,442 cancers, across 36 other tu
196 s the 3' introns, compensatory changes in U1 snRNA rescue trans-splicing of TSA mutants, demonstratin
197           We found that only the modified U1 snRNA (IVS-AAA) that completely matched both the introni
198   Alternative splicing mediated by mutant U1 snRNA inactivates tumour-suppressor genes (PTCH1) and ac
199 omplex (CBC) to the 5' end of the nascent U1 snRNA, which ultimately influences the utilization of U1
200 e saw reciprocal changes in the levels of U1 snRNA and U1 snRNP proteins.
201  splice sites, and exhibit high levels of U1 snRNA binding compared with cytoplasm-localized messenge
202 rpholino that base-pairs to the 5' end of U1 snRNA blocks splicing in the coupled system and complete
203 tion of U5, U6 snRNAs and accumulation of U1 snRNA in the B(act) complex.
204                        Acute depletion of U1 snRNA or of the U1 snRNP protein component SNRNP70 marke
205 duplex between pre-mRNA and the 5'-end of U1 snRNA.
206  removal, although MBNL1 has no effect on U1 snRNA recruitment.
207        In this study, we designed several U1 snRNA vectors to adapt U1 snRNA binding sequences of the
208                 U1 snRNP inserts the 5'SS-U1 snRNA helix between the two RecA domains of the Prp28 DE
209                              We find that U1 snRNA is the primary RNA target of FUS via its interacti
210 ticles (snRNPs) that are comprised of the U1 snRNA and 10 core components, including U1A, U1-70K, U1C
211 e found that this interaction between the U1 snRNA and SF3A1 occurs within prespliceosomal complexes
212                                       The U1 snRNA is highly conserved across a wide range of taxa; h
213 the AU dincucleotide at the 5'-end of the U1 snRNA is highly conserved, despite the absence of an app
214                          Thus, SL4 of the U1 snRNA is important for splicing, and its interaction wit
215                                       The U1 snRNA mutations occur in the 5' splice-site binding regi
216 eraction between stem-loop 4 (SL4) of the U1 snRNA, which recognizes the 5' splice site, and a compon
217  site of a pre-mRNA and the 5' end of the U1 snRNA.
218                                     These U1 snRNA mutations provide an example of highly recurrent a
219 rt defined by sequence complementarity to U1 snRNA, we identify RNA secondary structural elements nea
220 ed predominantly through basepairing with U1 snRNA whilst U1-C fine-tunes relative affinities of mism
221  (snRNP) through strong base-pairing with U1 snRNA.
222                                           U1 snRNAs associate with 5' splice sites in the form of rib
223    We show that Cr1-activating engineered U1 snRNAs (eU1s) have the unique ability to reprogram pre-m
224                     Compensatory modified U1 snRNAs, complementary to mutated donor splice sites, wer
225 one case, we also evaluated exon-specific U1 snRNAs that, by targeting nonconserved intronic sequence
226 s of human U1-like snRNAs, the variant (v)U1 snRNAs (vU1s), also participate in pre-mRNA processing e
227 terminal RNA recognition motif of p65, a U12 snRNA binding protein, also binds to the distal 3' stem-
228  p65 protein-binding apical stem-loop of U12 snRNA can be replaced by this U6atac distal 3' stem-loop
229 ecular helix I region between U6atac and U12 snRNAs, several other regions within these RNA molecules
230 icates that Prp5 has reduced affinity for U2 snRNA that lacks Psi42 and Psi44 and that Prp5 ATPase ac
231 stem-loop (BSL)(8), but whether the human U2 snRNA folds in a similar manner is unknown.
232 er, our results indicate that the Psis in U2 snRNA contribute to pre-mRNA splicing by directly alteri
233 me formation was blocked by a mutation in U2 snRNA.
234 hens U4/U6 RNA-RNA and U2B"/U2A' proteins-U2 snRNA interaction at elevated temperatures.
235 intaining interactions with the keto-rich U2 snRNA.
236 s open conformation in U2 snRNP, and that U2 snRNA forms a BSL that is sandwiched between PRP5, TAT-S
237 iometric association of U2 snRNPs and the U2 snRNA is base-paired to the pre-mRNA.
238                             U6 folds with U2 snRNA into an RNA-based active site that positions the 5
239                                     Yeast U2 snRNA contains three conserved Psis (Psi35, Psi42, and P
240  k-turns from ribosomes, riboswitches and U4 snRNA, finding a strong conservation of properties for a
241 d predispose them to ion-induced folding, U4 snRNA are strongly biased to an inability to such foldin
242 snRNA triggers unwinding of U6 snRNA from U4 snRNA.
243 ase relocation to its loading sequence in U4 snRNA, enabling Brr2 to unwind the U4/U6 snRNA duplex to
244             The single-stranded region of U4 snRNA between its 3' stem-loop and the U4/U6 snRNA stem
245 ves the Prp31- and Snu13-binding sites on U4 snRNA unaffected.
246 nu13-U4/U6 RNP into an intact Prp31-Snu13-U4 snRNA particle, free Prp3, and free U6 snRNA.
247 ffold during the entire assembly, but the U4 snRNA 5' stem-loop adopts alternative orientations each
248 anslocates only a limited distance on the U4 snRNA strand and does not actively release RNA-bound pro
249 ation via ATP-driven translocation on the U4 snRNA strand.
250  interact with the exon binding loop 1 of U5 snRNA.
251 he amino-terminal domain of Prp8 position U5 snRNA to insert its loop I, which aligns the exons for s
252  mutations in PRP16, PRP8, SNU114 and the U5 snRNA that affect this process interact genetically with
253 l and linker domains, and base-pairs with U5 snRNA loop 1.
254                                           U6 snRNA is transcribed by RNA polymerase III (Pol III) and
255                                           U6 snRNA undergoes post-transcriptional 3' end modification
256 to unwind the U4/U6 snRNA duplex to allow U6 snRNA to form the catalytic center of the spliceosome.
257 ruitment, packaging of both pre-tRNAs and U6 snRNA requires the nuclear export receptor Exportin-5.
258 RNAs (snRNAs), termed U1, U2, U4, U5, and U6 snRNA, are present in equal stoichiometry within the spl
259 lic phosphates at the ends of 5S rRNA and U6 snRNA.
260 e observations suggest that the conserved U6 snRNA methyltransferase evolved an additional function i
261 of the same gRNA expressed from different U6 snRNA promoters, with the previously untested U6:3 promo
262 then completed by the partially displaced U6 snRNA adopting an alternative conformation, which leads
263 13-U4 snRNA particle, free Prp3, and free U6 snRNA.
264 from U1 to U6 snRNA triggers unwinding of U6 snRNA from U4 snRNA.
265 U6 di-snRNAs that diminish the ability of U6 snRNA to adopt an alternative conformation but leave the
266 e fold, which recognizes a 3'-overhang of U6 snRNA, and a preceding peptide, which binds U4/U6 stem I
267         The invariant ACAGAGA sequence of U6 snRNA, which base-pairs with the 5'-splice site during c
268 the tri-snRNP and comparison with a Prp24-U6 snRNA recycling complex suggests how Prp3 may be involve
269 can activate the spliceosome by stripping U6 snRNA of all precatalytic binding partners, while minimi
270 he pairing of the 5' splice site with the U6 snRNA ACAGAGA region.
271 n nucleotides +3 to +6 base-pair with the U6 snRNA ACAGAGA sequence.
272                                 While the U6 snRNA catalytic core remains firmly held in the active s
273  yeasts rely on hyperstabilization of the U6 snRNA-5' splice site interaction to impede the 2nd step
274 r of the 5' splice site (5'SS) from U1 to U6 snRNA triggers unwinding of U6 snRNA from U4 snRNA.
275 t one function of Cwc2 is to stabilize U2-U6 snRNA helix I during splicing.
276 ju2 and Cwc25 as well as destabilizing U2-U6 snRNA helix I.
277 e ability of Delta247-Brr2 to bind the U4/U6 snRNA duplex at high pH and increases Delta247-Brr2's RN
278 ependent ATPase required to unwind the U4/U6 snRNA duplex during spliceosome assembly.
279  U4 snRNA, enabling Brr2 to unwind the U4/U6 snRNA duplex to allow U6 snRNA to form the catalytic cen
280 snRNA between its 3' stem-loop and the U4/U6 snRNA stem I is loaded into the Brr2 helicase active sit
281 n Prp16 stabilizes Cwc2 interactions with U6 snRNA and destabilizes Cwc2 interactions with pre-mRNA,
282                                The U4 and U6 snRNAs are incorporated into the spliceosome as a base-p
283                       The U2, U4, U5, and U6 snRNAs contain expected conserved sequences and have the
284                    Base-pairing of U4 and U6 snRNAs during di-snRNP assembly requires large-scale rem
285 P contains extensively base paired U4 and U6 snRNAs, Snu13, Prp31, Prp3 and Prp4, seven Sm and seven
286 r RNA (snRNA), extensively base-paired U4/U6 snRNAs and more than 30 proteins, including the key comp
287 n, leading to a dramatic reduction of U5, U6 snRNAs and accumulation of U1 snRNA in the B(act) comple
288 ggered by unwinding of the U4 and U6 (U4/U6) snRNAs.
289 rated that the 3' stem-loop region of U6atac snRNA contains a U12-dependent spliceosome-specific targ
290 of various regions in the Sm proteins and U7 snRNA in 3' end processing of histone pre-mRNAs.
291  proof of concept of using the engineered U7 snRNA lentiviral vector for treatment of beta-thalassaem
292  of two core components: a ~60-nucleotide U7 snRNA and a ring of seven proteins, with Lsm10 and Lsm11
293 g these noncoding RNAs, regulation of the U7 snRNA by tRF-GG modulates heterochromatin-mediated trans
294 trate long-term splicing correction using U7 snRNA lentiviral vectors engineered to target several pr
295                A double-target engineered U7 snRNAs targeted to the cryptic branch point and an exoni
296                                 We validated snRNA-seq on fibrotic kidney from mice 14 days after uni
297 pressed, it is unclear whether these variant snRNAs have the capacity to form snRNPs and participate
298 little to no maturation of tested U1 variant snRNAs, which are instead targeted by the nuclear exosom
299 s host RNAs, including those associated with snRNA transcription, and avoidance of host transcripts e
300 omal activation through its interaction with snRNAs and possibly other spliceosomal proteins, reveali
301 es are more similar to mRNA genes than yeast snRNA genes with respect to termination.

 
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