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1                                              RNA pol II chromatin immunoprecipitation was combined wi
2                                              RNA pol II is converted into an elongating form shortly
3 e coding region of the rtfA gene, encoding a RNA-pol II transcription elongation factor-like protein,
4 e ability to block enhancers from activating RNA pol II transcribed promoters.
5 ensed chromatin regions together with active RNA pol II for the first time using super-resolution mic
6 ent of African Sleeping Sickness, deploys an RNA pol II that contains a non-canonical CTD to accompli
7 as inhibited after gene activation, Adr1 and RNA pol II remained at promoters, and RNA pol II remaine
8 uppressed by defects in the Paf1 complex and RNA pol II.
9 gested that S. cerevisiae growth control and RNA pol II transcription might be coupled by using the R
10 w that HIV-1 Tat protein stimulated DSIF and RNA pol II phosphorylation by P-TEFb during elongation.
11 that an intimate association between MLL and RNA pol II occurs at MLL target genes in vivo that is re
12 ed Mediator contained some kinase module and RNA pol II, Mediator purified through F-Med26 contained
13 r1 and RNA pol II remained at promoters, and RNA pol II remained in the ORF with associated nascent t
14  assess the relative contributions of RT and RNA pol II to HIV-1 mutagenesis, a system was establishe
15 te the relative contribution of HIV-1 RT and RNA pol II to viral mutagenesis.
16         We have applied the method to arrest RNA pol II elongation complexes on a DNA template contai
17  triplex structure and isolation of arrested RNA pol II elongation complexes should be generalizable
18      However, the fusion proteins as well as RNA pol II were recruited to heat shock puffs during hea
19 in activated Th cells by promoter-associated RNA pol II.
20 , such as Fas/APO1, have low levels of bound RNA pol II but undergo damage-induced activation through
21                                        BRCA1-RNA pol II complexes showed evidence of a multiply phosp
22 show that the non-canonical CTD of T. brucei RNA pol II is important for normal protein-coding gene e
23 episome, suggesting that it is controlled by RNA pol II.
24 longation factors, which block elongation by RNA pol II shortly after the initiation of transcription
25 s a strong block to transcript elongation by RNA pol II.
26 ted by the quality of pre-mRNAs generated by RNA pol II.
27 er and terminator and triggers initiation by RNA pol II.
28 nd in the DHFR gene, which is transcribed by RNA pol II.
29 ein-coding gene expression, likely directing RNA pol II to the TSSs within the genome.
30 at functioned in concert with the CTD during RNA pol II transcription.
31 tion complex and travels with the elongating RNA pol II, whereas TFIIH is released from the elongatio
32  important for the progression of elongation RNA pol II on the egr1 gene.
33                                       First, RNA pol II transcription in poliovirus-infected cell ext
34 C sites but not with intervening or flanking RNA pol II transcribed genes.
35 GlcNAc-transferase activity is essential for RNA pol II promoter recruitment and that pol II goes thr
36 tion completes the set of human homologs for RNA pol II subunits defined in yeast and should provide
37 icing may have uncoupled the requirement for RNA pol II-mediated mRNA production.
38 I (IIO), in preference to hypophosphorylated RNA pol II (IIA) expected at promoters.
39 asic transcription factor RNA polymerase II (RNA pol II) and the coactivator p300 on the endogenous M
40  transcriptionally active RNA polymerase II (RNA pol II) at super-resolution is still lacking.
41  a general coactivator of RNA polymerase II (RNA pol II) bridging enhancer-bound transcriptional fact
42 e that phosphorylates the RNA polymerase II (RNA pol II) C-terminal domain (CTD) within a transcripti
43 homogeneous population of RNA polymerase II (RNA pol II) elongation complexes arrested at a DNA damag
44 epair factor TFIIH to the RNA polymerase II (RNA pol II) initiation complex to facilitate promoter cl
45                       The RNA polymerase II (RNA pol II) interacted with the Ifng gene promoter in an
46       A unique feature of RNA polymerase II (RNA pol II) is its long C-terminal extension, called the
47 r level, AT7519 inhibited RNA polymerase II (RNA pol II) phosphorylation, a CDK9, 7 substrate, associ
48 ly and the recruitment of RNA polymerase II (RNA pol II) to the promoter.
49      In eukaryotic cells, RNA polymerase II (RNA pol II) transcription and pre-mRNA processing are co
50 such functions coupled to RNA polymerase II (RNA pol II) transcription, perhaps by affecting the comp
51 anscription initiation by RNA polymerase II (RNA pol II) via direct interaction with the basal transc
52 -PK promoter occupancy by RNA polymerase II (RNA pol II), acetylated histone H3 (Ac-H3), and acetylat
53 -terminal domain (CTD) of RNA polymerase II (RNA pol II), as well as negative elongation factors, whi
54 scription Factors (GTFs), RNA polymerase II (RNA pol II), co-activators, co-repressors, and more.
55 e transcribed by cellular RNA polymerase II (RNA pol II), ICP4 must interact with components of the p
56 gene delivery systems for RNA polymerase II (RNA pol II)-based promoters have been developed and are
57 d template containing the RNA polymerase II (RNA pol II)-dependent adenovirus major late promoter.
58 d functional complex with RNA polymerase II (RNA pol II).
59 e two largest subunits of RNA polymerase II (RNA pol II).
60 onal machinery, including RNA polymerase II (RNA pol II).
61   Loss of function Mll results in defects in RNA pol II distribution.
62 everal approaches to show a role for WRNp in RNA pol II transcription, possibly as a transcriptional
63  rho termination factor from E. coli induces RNA pol II to release at all of these pause sites.
64 ional activity assay, where F-Med26 Mediator/RNA pol II was the most active.
65  purified through F-Med26 contained the most RNA pol II and the least kinase module as demonstrated b
66 f1 in tRNA gene-mediated silencing of nearby RNA pol II transcription.
67 irects 3' end formation of nonpolyadenylated RNA pol II transcripts, such as snoRNAs.
68 erestingly, localization studies of numerous RNA pol II transcription and pre-mRNA processing factors
69 red after the phosphorylation of serine 5 of RNA pol II C-terminal domain (CTD) has occurred, but bef
70 y enhances the phosphorylation of the CTD of RNA pol II by holo-TFIIH in vitro.
71 s demonstrate a critical role for the CTD of RNA pol II LS in the intranuclear targeting of splicing
72 In mammalian cells, truncation of the CTD of RNA pol II LS prevents the targeting of the splicing mac
73  regulatory carboxy-terminal domain (CTD) of RNA pol II disrupts transcriptional silencing, indicatin
74      In WT mES cells, the elongating form of RNA pol II accumulates near Vezf1 binding sites within t
75             The initiation competent form of RNA pol II and general transcription factors appeared in
76 rs, whereas the elongation competent form of RNA pol II was detected even later.
77 of Set2 with the hyperphosphorylated form of RNA pol II.
78 ollowing chemical or genetic inactivation of RNA pol II.
79      GSK-3beta activation was independent of RNA pol II dephosphorylation confirmed by alpha-amanitin
80  endogenous CDKN1C mediates an inhibition of RNA pol II CTD phosphorylation in HeLa cells upon treatm
81  II inihibitor, showing potent inhibition of RNA pol II phosphorylation without corresponding effects
82 ciation can dramatically reduce the level of RNA pol II CTD phosphorylation at both Ser-2 and Ser-5 o
83 R3 transcription, as predicted by a model of RNA pol II engagement with DPE-containing Drosophila pro
84 at domain in the catalytic subunit (p220) of RNA pol II, and the complex was highly functional in tra
85 he clearance of promoter-proximal pausing of RNA pol II on the HIV-1 long terminal repeat at differen
86                           Phosphorylation of RNA pol II CTD by TFIIH is thought to play an important
87 k7, SNS-032 inhibited the phosphorylation of RNA pol II in all four lines and blocked RNA synthesis.
88 sed H3K9me3 and H3K27me3, and a reduction of RNA pol II occupancy on viral genes.
89 , we find that CDKN1C-mediated repression of RNA pol II phosphorylation is E2F1-dependent, suggesting
90  function, occurs exclusively as a result of RNA pol II-mediated transcription.
91 e showed that two of the largest subunits of RNA pol II coprecipitated with the N-terminal 315-residu
92 cyclin A2 as a key transcriptional target of RNA pol II during HU-induced centriole overduplication.
93  We infer that the lack of ubiquitylation of RNA pol II LS in Cockayne's syndrome cells does not caus
94 ol II LS), suggesting that ubiquitylation of RNA pol II LS may be necessary for TCR in eukaryotes.
95 nctional Rsp5, there is no ubiquitylation of RNA pol II LS.
96                              This control on RNA pol II-dependent transcription rate is obtained by c
97  Collectively, our results show that ongoing RNA pol II transcription is required for centriole overd
98 h could have been introduced by either RT or RNA pol II, whereas the other eleven mutations were only
99 during which growth is inhibited and overall RNA pol II transcription is reported to be inhibited.
100 fraction colocalized with the phosphorylated RNA pol II decreased with the inhibition of transcriptio
101 actions: one colocalized with phosphorylated RNA pol II and the other as nascent aggregates.
102 molecular switch for transcription of poised RNA pol II.
103 ed using either ACTB (beta-actin) or POLR2A (RNA pol II large subunit), but not when RNA levels are n
104 ated with a large fraction of the processive RNA pol II activity present in undamaged cells, and the
105     Preferential interaction with processive RNA pol II in undamaged cells places BRCA1 in position t
106  interacts with both CDK7 and CDK9 (putative RNA pol II CTD kinases) and that CDKN1C blocks their abi
107  provide direct evidence of a 9-fold reduced RNA pol II binding capacity for the -63C allele.
108 itment to the promoter, resulting in reduced RNA pol II loading.
109 se gaps were enriched with phosphorylated S5 RNA pol II, and were sensitive to the cellular transcrip
110 tion confirmed by alpha-amanitin, a specific RNA pol II inihibitor, showing potent inhibition of RNA
111 ted by alpha-amanitin, a potent and specific RNA pol II inhibitor.
112                          Isolation of stable RNA pol II elongation complexes arrested at DNA damage s
113                      We developed a stepwise RNA pol II walking approach and used Western blotting to
114                      We have used a stepwise RNA pol II walking approach and Western blotting to dete
115 itro transcription assay markedly stimulates RNA pol II-dependent transcription carried out by nuclea
116 tylation of RNA polymerase II large subunit (RNA pol II LS), suggesting that ubiquitylation of RNA po
117 ivity by n-3 PUFA correlated with suppressed RNA pol II, Ac-H3, and Ac-H4 occupancy on the L-PK promo
118 orylation may be a prerequisite for targeted RNA pol II degradation.
119 ous observations, these results suggest that RNA pol II may terminate by a mechanism closely related
120 ions among ERalpha, its coactivators and the RNA pol II machinery are all required for ERalpha- media
121 sphorylation-driven interactions between the RNA pol II CTD and the WW domain of Ess1/Pin1, we sugges
122         We further show that deletion of the RNA pol II C-terminal domain (CTD) kinase Ctk1, or parti
123  data all point to OGA as a component of the RNA pol II elongation machinery regulating elongation ge
124 to support a model in which the entry of the RNA pol II gene expression machinery into newly forming
125 to the carboxyl-terminal domain (CTD) of the RNA pol II large subunit.
126 endent on the carboxy-terminal domain of the RNA pol II largest subunit.
127 CR, demonstrating that ubiquitylation of the RNA pol II LS is not required for TCR.
128 rved post-translational modifications on the RNA pol II C-terminal domain (CTD) and the chromatin tem
129      Following exposure to UV radiation, the RNA pol II elongation complex is blocked at sites of UV-
130 ched at a DSB were the phosphatase Sit4, the RNA pol II degradation factor Def1, the mRNA export prot
131 atin landscape is a central function of this RNA pol II-distinguishing domain.
132  ubiquitin-protein ligase that ubiquitylates RNA pol II LS in cells exposed to DNA-damaging agents.
133                                       Unlike RNA pol II-dependent promoter repression, overexpressing
134 ber of the Paf1 complex that associates with RNA pol II and regulates transcription elongation.
135 s demonstrate that DSIF/NELF associates with RNA pol II complexes during early transcription elongati
136 Here we report that p16INK4A associates with RNA pol II CTD and TFIIH.
137 op1-lacZ fusion protein was colocalized with RNA pol II in some but not all of the nonpuff, interband
138  polymerase II (pol II) and colocalizes with RNA pol II at a subset of actively transcribed target in
139  enhancer-bound transcriptional factors with RNA pol II.
140    The head and middle modules interact with RNA pol II, and the tail module interacts with transcrip
141        We demonstrated that interaction with RNA pol II is a conserved feature of BRCA1 proteins from
142        The yeast Paf1 complex interacts with RNA pol II and mediates histone modifications during elo
143 t blocks gene activation by interfering with RNA pol II, activator and coactivator recruitment, and e
144 NA and needs to gain access to Ig loci, with RNA pol II transcription possibly providing both aspects
145  of genes, showing considerable overlap with RNA pol II, SPT5, TRIM28-KAP1-TIF1beta, and O-GlcNAc its
146 mechanistically linked to transcription with RNA pol II serving as a platform to recruit RNA processi
147 o interact functionally with the other yeast RNA pol II subunits in vivo.

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