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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
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
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
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
19 ther, our results draw new parallels between snRNA and piRNA biogenesis in nematodes and provide evid
28 o increases the levels of assembly-defective snRNAs and suppresses some splicing defects seen in SMN-
30 antling of the Prp3-binding site on U4/U6 di-snRNA but leaves the Prp31- and Snu13-binding sites on U
33 sing factor 31 (Prp31), and Prp3 to U4/U6 di-snRNA leads to a stepwise decrease of Brr2-mediated U4/U
35 yses that Prp3 contains a bipartite U4/U6 di-snRNA-binding region comprising an expanded ferredoxin-l
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
40 s ptRNA-subclasses that exist in eukaryotes: snRNA, snoRNA, RNase P, RNase MRP, Y RNA or telomerase R
43 subunits, which are largely dispensable for snRNA processing, also have regulatory roles at these pr
45 de evidence for the production of functional snRNAs by Wolbachia that play roles in cross-kingdom com
47 1 and U2 genes as models, we show that human snRNA genes are more similar to mRNA genes than yeast sn
49 Production of snR-DPGs required the Pol II snRNA promoter (PIIsnR), and CPL4RNAi plants showed incr
53 uantify contamination and filter droplets in snRNA-seq experiments, called Debris Identification usin
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
66 monstrated that a new class of human U1-like snRNAs, the variant (v)U1 snRNAs (vU1s), also participat
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
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
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-
81 ding to snRNAs are known to reduce levels of snRNAs, suggesting an unknown quality control system for
84 al defects, impairs the 3' end processing of snRNAs, increases the levels of snRNA primary transcript
86 RNAi compromised the guided modification on snRNA and reduced parasite growth at elevated temperatur
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.
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
101 complex delivers pre-small nuclear RNAs (pre-snRNAs) to the heptameric Sm ring for the assembly of th
103 the levels of snRNA primary transcripts (pre-snRNAs), and alters the occupancy of Pol II at snRNA loc
106 promotes maturation and stability of regular snRNAs while leaving snRNA variants unprocessed and expo
108 hese data suggest that U6 small nuclear RNA (snRNA) and RtcB participate in the formation of chimeric
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
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
125 tion of 3'-extensions of small nuclear RNAs (snRNAs) and biogenesis of novel transcripts from protein
127 3A>G) of U1 spliceosomal small nuclear RNAs (snRNAs) in about 50% of Sonic hedgehog (SHH) medulloblas
129 host RNAs, particularly small nuclear RNAs (snRNAs), and avoidance of host transcripts encoding host
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
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
139 A-seq (scRNA-seq) or single-nucleus RNA-seq (snRNA-seq) data to generate a reference expression profi
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
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
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
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
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
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.
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
181 ites and modest delays at some histone and U snRNA genes, suggesting that the torpedo mechanism is no
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
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,
191 e U1 snRNP core particle (Sm proteins and U1 snRNA), but not the mature U1 snRNP-specific proteins (U
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
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
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
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
213 the AU dincucleotide at the 5'-end of the U1 snRNA is highly conserved, despite the absence of an app
216 eraction between stem-loop 4 (SL4) of the U1 snRNA, which recognizes the 5' splice site, and a compon
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
223 We show that Cr1-activating engineered U1 snRNAs (eU1s) have the unique ability to reprogram pre-m
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
232 er, our results indicate that the Psis in U2 snRNA contribute to pre-mRNA splicing by directly alteri
236 s open conformation in U2 snRNP, and that U2 snRNA forms a BSL that is sandwiched between PRP5, TAT-S
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
243 ase relocation to its loading sequence in U4 snRNA, enabling Brr2 to unwind the U4/U6 snRNA duplex to
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
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
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
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
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
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
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.
277 e ability of Delta247-Brr2 to bind the U4/U6 snRNA duplex at high pH and increases Delta247-Brr2's RN
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,
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
289 rated that the 3' stem-loop region of U6atac snRNA contains a U12-dependent spliceosome-specific targ
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
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