コーパス検索結果 (left1)
通し番号をクリックするとPubMedの該当ページを表示します
1 nome-wide studies revealed that KAP1 and 7SK snRNP co-occupy most promoter-proximal regions containin
2 f an unprecedented mechanism controlling 7SK snRNP delivery to promoter-proximal regions to facilitat
3 pathway, calpain 2 cleavage of the core 7SK snRNP component MePCE promoted P-TEFb release and conseq
6 oop, liberating P-TEFb from the inactive 7SK snRNP, and inducing the formation of the Tat-SEC complex
11 ARP7) is a constitutive component of the 7SK snRNP and localizes to the 3' terminus of the 7SK long n
12 on elongation factor b (P-TEFb) from the 7SK snRNP in a manner that is dependent on its helicase acti
13 elongation and sn/snoRNA synthesis, the 7SK snRNP is a key regulator of nuclear RNA production by RN
15 Here, we show that the assembly of the 7SK snRNP is preceded by an intermediate complex between HEX
16 is study, the release of P-TEFb from the 7SK snRNP led to increased synthesis of HEXIM1 but not HEXIM
19 regulator KAP1 continuously tethers the 7SK snRNP to PRG promoters to facilitate P-TEFb recruitment
23 lacking exon 2B can rescue iMEF survival and snRNP assembly in the absence of flwt-Smn, indicating ex
25 ted WT mice showed elevated anti-dsDNA, anti-snRNP, CXCL1, and MCP-1 levels compared to untreated mic
26 ed to untreated mice; however levels of anti-snRNP, MCP-1, and CXCL1 were reduced in pristane-treated
27 ts that have been characterized thus far are snRNP proteins because, in contrast to individual snRNPs
28 proliferating cells, which actively assemble snRNPs, as a readout for unperturbed SMN complex functio
29 d intracellular localization of autoantibody snRNP complexes was measured by flow cytometry and confo
31 ith both in vitro-reconstituted and cellular snRNPs led to similar changes in SHAPE reactivities, con
33 e small nuclear ribonucleoprotein complexes (snRNPs) U2, U5 and U6 and the so-called NineTeen complex
35 /U6 di-small nuclear RNA-protein complex (di-snRNP) during spliceosome activation via ATP-driven tran
36 ein components to the snRNA duplex during di-snRNP assembly by electrophoretic mobility shift assay a
37 Base-pairing of U4 and U6 snRNAs during di-snRNP assembly requires large-scale remodeling of RNA st
38 of human RNPC3, also known as the U11/U12 di-snRNP 65-kDa protein, a unique component of the U12-type
40 6 helix II and an interface between U4/U6 di-snRNP and the U2 snRNP SF3b-containing domain, which als
42 set up a recombinant Brr2-mediated U4/U6 di-snRNP disruption system, showing that sequential additio
43 of the function played by SART3 in U4/U6 di-snRNP formation, our discovery points to a direct link b
55 proteins because, in contrast to individual snRNPs, purification of intact spliceosomes has not been
57 PN1, which is essential for TMG cap-mediated snRNP import in humans, is not well conserved in flies.
58 ges of SMN give rise to loss of SMN-mediated snRNP assembly and support the hypothesis that this loss
62 lfils essential functions in the assembly of snRNPs, which are key components in the splicing of pre-
65 le of cells subjected to knockdown of Gro or snRNP-U1-C (a component of U1 snRNP) showed a significan
66 er tri-snRNP complex proteins, but not other snRNP spliceosome complexes, selectively abrogated growt
67 U2 small nuclear ribonucleoprotein particle (snRNP) are also subunits of the Spt-Ada-Gcn5 acetyltrans
68 U2 small nuclear ribonucleoprotein particle (snRNP) associates with U4/U6.U5 tri-snRNP through the U2
69 U2 small nuclear ribonucleoprotein particle (snRNP) complex, which assembles across the intron at the
71 and U2 small nuclear ribonucleic particles (snRNPs) and suggested that RBM20-dependent splicing repr
72 in the form of ribonucleoprotein particles (snRNPs) that are comprised of the U1 snRNA and 10 core c
73 2 small nuclear ribonucleoprotein particles (snRNPs), and transforms into a catalytically active spli
75 Gemin5 in small nuclear ribonucleic protein (snRNP) biogenesis as well as, potentially, other cellula
78 izes the U1 small nuclear ribonucleoprotein (snRNP) and is essential for the localization of reporter
79 urvival and small nuclear ribonucleoprotein (snRNP) assembly, demonstrating intragenic complementatio
82 wed that U1 small nuclear ribonucleoprotein (snRNP) associates with RNAP II, and both RNAP II and U1
83 ccurs by U1 small nuclear ribonucleoprotein (snRNP) binding the 5' SS and recognition of the BS by th
86 and coilin/small nuclear ribonucleoprotein (snRNP) co-localization are significantly impaired in SH-
88 of the 7SK small nuclear ribonucleoprotein (snRNP) complex, is recruited to the promoters of Pol II-
92 oSNP1, a U1 small nuclear ribonucleoprotein (snRNP) component, likely in a manner dependent on direct
95 The 7SK small nuclear ribonucleoprotein (snRNP) plays a central role in RNA polymerase II elongat
96 The 7SK small nuclear ribonucleoprotein (snRNP) sequesters and inactivates the positive transcrip
98 in the 7SK small nuclear ribonucleoprotein (snRNP), which contains, additionally, 7SK snRNA, methyl
101 omposed of small nuclear ribonucleoproteins (snRNPs) and accessory proteins that excises introns from
103 U1 and U2 small nuclear ribonucleoproteins (snRNPs) bound to the precursor messenger RNA 5' splice s
105 U1 and U2 small nuclear ribonucleoproteins (snRNPs) mark an intron and recruit the U4/U6.U5 tri-snRN
107 RNA-protein complexes, including ribosomes, snRNPs, snoRNPs, telomerase, microRNAs, and long ncRNAs.
108 ated huge protein) and U7 small nuclear RNP (snRNP) are HLB components that participate in 3' process
113 es (CBs), major NBs involved in spliceosomal snRNP assembly and their role in genome organization.
114 n orchestrating the assembly of spliceosomal snRNP particles and subsequently regulating the alternat
118 though mechanisms of P-TEFb release from the snRNP are becoming clearer, how P-TEFb remains in the 7S
119 nd that msk-null mutants are depleted of the snRNP assembly factor, survival motor neuron, and the Ca
121 y of PPM1G blocks P-TEFb reassembly onto the snRNP to sustain NF-kappaB-mediated Pol II transcription
123 t the Sm site with its zinc finger and traps snRNP biogenesis intermediates in human and murine motor
126 construction of Saccharomyces cerevisiae tri-snRNP at 5.9 A resolution to reveal the essentially comp
127 e either reverses assembly by discarding tri-snRNP or proceeds to activation by irreversible U4 loss.
133 nd protrudes over the concave surface of tri-snRNP, where the U1 snRNP may reside before its release
136 0 can be successfully assembled into the tri-snRNP (albeit at a lower level than the WT Brr2) and the
137 e first time that PRPF6, a member of the tri-snRNP (small ribonucleoprotein) spliceosome complex, dri
138 rtant bridge between U4/U6 and U5 in the tri-snRNP and comparison with a Prp24-U6 snRNA recycling com
139 in FgSad1 increase the stability of the tri-snRNP and/or the affinity of FgSad1 with U2 snRNP and th
142 aracterized spontaneous mutations in the tri-snRNP-specific protein, FgSad1, which suppressed the gro
145 ure of Saccharomyces cerevisiae U4/U6.U5 tri-snRNP at 3.7 A resolution led to an essentially complete
146 s in assembly of the megaDalton U4/U6.U5 tri-snRNP complex, and lead to a dynamic model for U4/U6 pai
148 ron microscopy structure of the U4/U6.U5 tri-snRNP illustrates how proteins scaffold the RNA and dram
151 article (snRNP) associates with U4/U6.U5 tri-snRNP through the U2/U6 helix II and an interface betwee
152 t sequence, associates with the U4/U6.U5 tri-snRNP to form the fully assembled precatalytic pre-B spl
153 n eukaryotes and is part of the U4/U6.U5 tri-snRNP, a large ribonucleoprotein complex that comprises
163 t this interaction between the galectin-3-U1 snRNP particle and the pre-mRNA results in a productive
164 ct can be reconstituted by the galectin-3-U1 snRNP particle, isolated by immunoprecipitation of the 1
165 hese results indicate that the galectin-3-U1 snRNP-pre-mRNA ternary complex is a functional E complex
167 0S particle that contained galectin-3 and U1 snRNP and this particle was sufficient to load the galec
168 ciates with RNAP II, and both RNAP II and U1 snRNP are also the most abundant factors associated with
169 flanking introns allowed normal U2AF and U1 snRNP binding to the target exon splice sites but blocke
172 f the human pre-B complex captured before U1 snRNP dissociation at 3.3-angstrom core resolution and t
173 mpletely disrupts the association between U1 snRNP and both FUS and RNAP II, but has no effect on the
175 election of 5'-splice site nucleotides by U1 snRNP is achieved predominantly through basepairing with
179 varying degrees and associated with core U1 snRNP proteins to a lesser extent than the canonical U1
181 g an essential canonical splicing factor (U1 snRNP) to this pathway provides strong new evidence that
182 Our findings underscore a wider role for U1 snRNP in splicing regulation and reveal a novel approach
183 factors transiently associate with human U1 snRNP and are not amenable for structural studies, while
185 essential subunits of the yeast and human U1 snRNP, respectively, that are implicated in the establis
189 roteins and U1 snRNA), but not the mature U1 snRNP-specific proteins (U1-70K, U1A and U1C), co-misloc
192 ve uncovered a previously unknown role of U1 snRNP beyond the processing of precursor mRNA, and provi
196 of splicing proteins, and in the case of U1 snRNP we saw reciprocal changes in the levels of U1 snRN
198 down of Gro or snRNP-U1-C (a component of U1 snRNP) showed a significant overlap between genes regula
200 in the majority of human genes depends on U1 snRNP (U1) to co-transcriptionally suppress transcriptio
201 of these transcripts, suggesting that PSI-U1 snRNP interactions coordinate the behavioral network und
206 ing Gems, and motor neurons indicate that U1 snRNP is a component of a molecular pathway associated w
207 omplex is a functional E complex and that U1 snRNP is required to assemble galectin-3 onto an active
210 Here, we report that components of the U1 snRNP core particle (Sm proteins and U1 snRNA), but not
211 e concave surface of tri-snRNP, where the U1 snRNP may reside before its release from the pre-mRNA 5'
212 Acute depletion of U1 snRNA or of the U1 snRNP protein component SNRNP70 markedly reduces the chr
213 interaction between the pre-mRNA and the U1 snRNP, in which a short RNA duplex is established betwee
216 bserved with FUS, knockdown of any of the U1 snRNP-specific proteins results in a dramatic loss of SM
220 Thus, our results demonstrate unique U1 snRNP pathology and implicate abnormal RNA splicing in A
221 alectin-3 molecules not in a complex with U1 snRNP (fraction 1 of the same gradient), failed to resto
222 otein and RNA-protein interactions within U1 snRNP, and show how the 5' splice site of pre-mRNA is re
223 rroring yeast Prp42/Prp39, supports yeast U1 snRNP as a model for understanding how transiently assoc
224 , we report the cryoEM structure of yeast U1 snRNP at 3.6 A resolution with atomic models for ten cor
226 ron microscopy structure of the human 17S U2 snRNP at a core resolution of 4.1 angstrom and combine i
232 are especially dependent on a functional U2 snRNP (small nuclear RNA [snRNA] plus associated protein
233 1, and maintains its open conformation in U2 snRNP, and that U2 snRNA forms a BSL that is sandwiched
234 Pcbp1, and RBM39 stabilizes or increases U2 snRNP recruitment, enhances spliceosome A complex format
236 ior data showing that loss of function of U2 snRNP components can interfere with cell growth and indu
237 udemycin E interferes with the ability of U2 snRNP to maintain an H3K36me3 modification in actively t
238 nRNP, as H2A.Z loss results in persistent U2 snRNP association and decreased recruitment of downstrea
244 in facilitating interactions between the U2 snRNP complex and ATP-dependent helicases, we examined c
245 nked to interactions of alphaCPs with the U2 snRNP complex and may be mediated by cooperative interac
249 interface between U4/U6 di-snRNP and the U2 snRNP SF3b-containing domain, which also transiently con
251 s essential for stable association of the U2 snRNP with the intron branch site (BS) sequence during s
252 n, the proteins U2AF35 and U2AF65 and the U2 snRNP, are able to recognize alternative candidate sites
253 spliceosomal rearrangements involving the U2 snRNP, as H2A.Z loss results in persistent U2 snRNP asso
261 -snRNP and/or the affinity of FgSad1 with U2 snRNP and therefore potentially facilitate the docking o
262 shows extensive genetic interactions with U2 snRNP-associated proteins, and RNA sequencing (RNA-seq)
263 ylation strengthens the interaction among U2 snRNPs and affects global pre-mRNA splicing pattern and
264 e expression of core components of U1 and U2 snRNPs, splicing regulators and other post-transcription
265 forms with stoichiometric association of U2 snRNPs and the U2 snRNA is base-paired to the pre-mRNA.
268 Sudemycin E induces a dissociation of the U2 snRNPs and decreases their interaction with nucleosomes.
272 entosa assemble less efficiently with the U5 snRNP and bind more strongly to R2TP, with one mutant re
273 PRP31 regulates its interaction with the U5 snRNP component PRP8, which is required for the efficien
274 th RNA splicing regulators, including the U5 snRNP components of the spliceosome, such as EFTUD2.
276 actor PRPF8 is a crucial component of the U5 snRNP, and together with EFTUD2 and SNRNP200, it forms a
282 ively, these data identify domains of the U6 snRNP that are critical for one of the first steps in as
283 exes (designated B(028)) revealed that U4/U6 snRNP proteins are released during activation before the
284 te post-transcriptional assembly of yeast U6 snRNP in vitro, and propose a model for U6 snRNP assembl
285 he post-transcriptional assembly of yeast U6 snRNP in vitro, which occurs through a complex series of
286 seems to be critical for retaining U5 and U6 snRNPs during/after spliceosomal activation through its
287 Thus, the HLB concentrates FLASH and U7 snRNP, promoting efficient histone mRNA biosynthesis and
288 ne pre-mRNAs are cleaved at the 3' end by U7 snRNP consisting of two core components: a ~60-nucleotid
289 at the 3' end by a complex that contains U7 snRNP, the FLICE-associated huge protein (FLASH) and his
291 n and functional properties as endogenous U7 snRNP, and accurately cleaves histone pre-mRNAs in a rec
293 We demonstrate that semi-recombinant holo U7 snRNP reconstituted in this manner has the same composit
295 hat distinct domains of FLASH involved in U7 snRNP binding, histone pre-mRNA cleavage, and HLB locali
297 that failure to concentrate FLASH and/or U7 snRNP in the HLB impairs histone pre-mRNA processing.
298 LASH interacts with the N terminus of the U7 snRNP protein Lsm11, and together they recruit the HCC.
299 re-mRNA 3'-end processing by facilitating U7-snRNP recruitment through physical interaction with the