コーパス検索結果 (1語後でソート)
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 regulatory element for genes transcribed by RNA polymerase II.
2 ccessibility for transcription initiation by RNA polymerase II.
3 uired for the transcription of most genes by RNA polymerase II.
4 that Cuff prevents premature termination of RNA polymerase II.
5 the same time and place as transcription by RNA polymerase II.
6 in particular, contribute to the pausing of RNA polymerase II.
7 ation of the start site for transcription by RNA polymerase II.
8 d by binding defects to both nucleosomes and RNA polymerase II.
9 osphorylating the carboxy-terminal domain of RNA polymerase II.
10 and in the transcription of coding genes by RNA polymerase II.
11 minal domain (CTD) of the largest subunit of RNA polymerase II.
12 o the expression of all genes transcribed by RNA polymerase II.
13 associate with the core mediator complex of RNA polymerase II.
14 ike domain (PLD) to the C-terminal domain of RNA polymerase II.
15 recruited a significant fraction of cellular RNA polymerase II.
16 ted with Set1 (COMPASS) to promoter-proximal RNA polymerase II.
17 or (Inr), direct transcription initiation by RNA polymerase II.
18 ex, which regulates transcription pausing of RNA-polymerase II.
19 ve genes and disrupted recruitment of active RNA polymerase II, a property shared with pan-BETis that
21 ortem brain, and pharmacologic modulation of RNA polymerase II activity altered repetitive element ex
23 lement expression positively correlated with RNA polymerase II activity in postmortem brain, and phar
24 ay decreased heterochromatin domains, a high RNA-polymerase II activity and enhanced c-Fos expression
26 einitiation complex (PIC), which consists of RNA polymerase II and general transcription factors.
28 erexpression of FOXC1 hinders recruitment of RNA polymerase II and increases histone H3K9 trimethylat
29 machinery allowing O-GlcNAc accumulation on RNA polymerase II and numerous chromatin factors includi
31 EJ proteins form a multiprotein complex with RNA polymerase II and preferentially associate with the
33 ere was a significantly reduced occupancy of RNA polymerase II and the essential mitotic transcriptio
34 ntified transcriptome-wide binding sites for RNA polymerase II and the exosome cofactors Mtr4 (TRAMP
38 romatin reassembly in the wake of elongating RNA polymerase II and transcriptional elongation, thus r
40 to form mediator complexes, phosphorylating RNA polymerase II, and by its intrinsic histone acetyltr
41 tes as a "speed bump" against advancement of RNA polymerase II, and temperature stress releases the b
42 be a master coordinator of transcription by RNA polymerase II, and this complex is recruited by tran
43 ive viral transcription by focal assembly of RNA polymerase II around Kaposi's sarcoma-associated her
45 a, C/EBPalpha, PPARgamma), coactivator MED1, RNA polymerase II, as well as epigenome (H3K4me1/2/3, H3
48 function of VIP proteins, components of the RNA polymerase II-associated factor 1 complex (Paf1c).
50 suppressed the initiation and elongation of RNA polymerase II at active genes genome-wide, with pron
51 mine the first room-temperature structure of RNA polymerase II at high resolution, revealing new stru
54 EFb and thereby prevented phosphorylation of RNA polymerase II at Ser2 and productive elongation.
55 n, both FUS and TDP43 colocalize with active RNA polymerase II at sites of DNA damage along with the
57 al factories" decreased the pool of cellular RNA polymerase II available for cellular gene transcript
60 ion experiments showed that the abundance of RNA polymerase II binding to the intron-less construct i
61 ssin treatment was associated with increased RNA polymerase II binding to the promoter proximal regio
64 In addition, through its interaction with RNA Polymerase II C-terminal domain (CTD) and affecting
66 ylglucosamine (O-GlcNAc) modification of the RNA polymerase II C-terminal domain was described 20 yea
68 pitation experiments revealed that the Ssu72 RNA polymerase II carboxyl-terminal domain phosphatase,
69 ifferent physiological signals manifested by RNA polymerase II carboxyl-terminal domain phosphorylati
70 A) silencing by inhibiting recombination and RNA polymerase II-catalyzed transcription in the rDNA of
71 that both enhancer classes are enriched for RNA Polymerase II, CBP, and architectural proteins but t
72 of higher-order chromatin structure data and RNA polymerase II ChIA-PET data from MCF-7 cells did not
82 ive elongation factor (NELF) associates with RNA polymerase II during early elongation and causes RNA
83 Convergent transcription causes stalling of RNA polymerase II during transcription, which permits ER
84 3 binding, recruitment of BRG1, and enhanced RNA polymerase II elongation and SALL4 transcription.
85 troller for transcription activation through RNA polymerase II elongation at a subset of genomic piRN
86 ucleoprotein (snRNP) plays a central role in RNA polymerase II elongation control by regulating the a
88 several lines of evidence showing that slow RNA polymerase II elongation increases both cotranscript
89 Moreover, we demonstrate that altering the RNA polymerase II elongation rate in either direction co
91 undance of the active/elongating form of the RNA polymerase-II enzyme (RNAPII-Ser2P), together with C
93 a "non-canonical" form of RdDM dependent on RNA polymerase II expression to initiate and re-establis
96 trotransposons, begins with transcription by RNA polymerase II followed by reverse transcription and
97 eneral transcriptional machinery required by RNA polymerase II for the initiation of eukaryotic gene
100 LR2A, which encodes the catalytic subunit of RNA polymerase II, hijack this essential enzyme and driv
101 n cryo-electron microscopy map of a Mediator-RNA polymerase II holoenzyme reveals that changes in the
102 TREX is loaded on nascent RNA transcribed by RNA polymerase II in a splicing-dependent fashion; howev
103 ncy of GR, the p65 subunit of NF-kappaB, and RNA polymerase II in airway epithelial cells treated wit
107 ation by confiscation of a limited supply of RNA polymerase II in infected cells.IMPORTANCE B cells i
109 H3 trimethylated at lysine 27 (H3K27me3) and RNA polymerase II in wild-type and piwi mutant ovaries d
110 wnregulated CDK7-mediated phosphorylation of RNA polymerase II, indicative of transcriptional inhibit
112 tor protein) is an unconventional prefoldin, RNA polymerase II interactor that functions as a transcr
115 matin occupancy of serine 2-unphosphorylated RNA polymerase II is increased, and that of topoisomeras
118 finding revealed that the exosomes increase RNA polymerase II loading onto the HIV-1 promoter in the
127 H3K4me3, and H3K27me3, DNA methylation, and RNA polymerase II occupancy and perform transcriptome an
128 tome profiling, chromatin accessibility, and RNA polymerase II occupancy demonstrate that BTBD18 faci
130 chromatin immunoprecipitation (ChIP) assays RNA polymerase II occupancy of SALL4 gene, as a function
131 Although dexamethasone treatment reduced RNA polymerase II occupancy of TNF targets such as IL8 a
133 ablation of FHL2 facilitates recruitment of RNA polymerase II on the TGF-beta1 promoter, suggesting
137 rovide new insights into the contribution of RNA polymerase II pausing in mammalian gene regulation a
138 n be activated by decreasing the duration of RNA polymerase II pausing in the promoter-proximal regio
139 many proteins, and mechanisms, ranging from RNA Polymerase II pausing to cotranscriptional histone m
140 tion between one specific enhancer state and RNA Polymerase II pausing, linking transcription regulat
141 tes inclusion of weak upstream exons through RNA polymerase II pausing, whereas 5-methylcytosine evic
143 acts with transcription initiation-competent RNA polymerase II phosphorylated at Ser-5 in a DNA templ
146 oding genes in eukaryotes are transcribed by RNA polymerase II (Pol II) and introns are removed from
148 ge preinitiation complex (PIC) that includes RNA polymerase II (Pol II) and the general transcription
149 genes there was constitutive association of RNA polymerase II (Pol II) and the general transcription
152 nitiation, the TFIIH-kinase Kin28/Cdk7 marks RNA polymerase II (Pol II) by phosphorylating the C-term
154 orylates the termination factor PCF11 on its RNA polymerase II (Pol II) C-terminal domain (CTD)-inter
155 n between mRNA synthesis and the dynamics of RNA Polymerase II (Pol II) clusters at a gene locus.
156 te the degradation of Rpb1, a subunit of the RNA polymerase II (Pol II) complex, and therefore hamper
158 n (ChIP) and chemical inhibitor studies that RNA polymerase II (Pol II) elongation is important for e
160 acts upstream of promoter-proximally paused RNA polymerase II (Pol II) formation (likely at the step
162 omatin immunoprecipitation of histone H3 and RNA polymerase II (Pol II) in mutants lacking single or
163 facilitate ubiquitylation and degradation of RNA polymerase II (pol II) in response to multiple stimu
165 rs promoter-proximal accumulation/pausing of RNA polymerase II (Pol II) independently of its capping
172 association of DSIF and NELF with initiated RNA Polymerase II (Pol II) is the general mechanism for
174 e identification and characterization of the RNA polymerase II (Pol II) kinase Cdk12 as a factor that
175 The carboxy-terminal domain (CTD) of the RNA polymerase II (Pol II) large subunit cycles through
176 trap optical tweezers to study single yeast RNA polymerase II (Pol II) molecules transcribing along
177 n of this mechanism unexpectedly showed that RNA polymerase II (Pol II) occupancy changes at FLC did
178 diated PRC eviction occurs in the absence of RNA polymerase II (Pol II) occupancy, transcription, and
179 minal domain (CTD) of the largest subunit of RNA polymerase II (Pol II) orchestrates dynamic recruitm
183 OGA is physically associated with the known RNA polymerase II (pol II) pausing/elongation factors SP
186 Gene expression in metazoans is regulated by RNA polymerase II (Pol II) promoter-proximal pausing and
190 iption is regulated at many steps, including RNA polymerase II (Pol II) recruitment, transcription in
194 tory step in gene expression, which requires RNA polymerase II (pol II) to escape promoter proximal p
198 tisense RNAs are a mechanistic by-product of RNA polymerase II (Pol II) transcription or biologically
202 Termination of Saccharomyces cerevisiae RNA polymerase II (Pol II) transcripts occurs through tw
204 eal globally elevated levels of transcribing RNA Polymerase II (Pol II) within genes in both species.
205 atin reorganization surrounding transcribing RNA polymerase II (Pol II), and using asymmetric nucleos
206 n that directly binds the largest subunit of RNA polymerase II (pol II), Rpb1, in response to phospho
207 By profiling the genome-wide binding of RNA polymerase II (Pol II), TaDa can also identify trans
208 D) plays a central role in the initiation of RNA polymerase II (Pol II)-dependent transcription by nu
209 t a robust genome-wide approach for studying RNA polymerase II (Pol II)-mediated transcription in hum
211 find that 6mA is exclusively associated with RNA polymerase II (Pol II)-transcribed genes, but is not
217 ucers and their relationship to transcribing RNA polymerase II (Pol2) could provide new insights abou
219 tudy, we identified carboxyl-terminal domain RNA polymerase II polypeptide A small phosphatase 1 (SCP
220 te, 52-protein, 2.5 million dalton, Mediator-RNA polymerase II pre-initiation complex (Med-PIC) was a
221 structure and promoter recruitment of poised RNA polymerase II preinitiation complex (RNAPII PIC), wh
223 in wild-type and mutant yeast cells in which RNA polymerase II promoter escape is blocked, allowing d
225 non-coding RNA hyperproduction from cryptic RNA polymerase II promoters; (ii) alterations in recombi
226 cient binding to DNA templates, facilitating RNA polymerase II recruitment and frequent reutilization
227 sses such as transcription factor occupancy, RNA polymerase II recruitment and initiation, nascent tr
228 pho-p65 or phospho-CREB and CBP bindings and RNA polymerase II recruitment to these promoters in mesa
231 hock-induced genes and does so by increasing RNA polymerase II release from promoter-proximal pause.
232 lymerase in cycling and quiescent cells: (i) RNA polymerase II release mediates heterochromatin forma
235 in an interactome predominantly comprised of RNA Polymerase II (RNA Pol II) transcriptional machinery
236 is essential for transcription initiation by RNA polymerase II (RNA pol II) via direct interaction wi
237 ng the General Transcription Factors (GTFs), RNA polymerase II (RNA pol II), co-activators, co-repres
238 f recent studies detailing the mechanisms of RNA polymerase II (RNA Pol II)-based transcriptional ini
239 Eukaryotic gene expression requires that RNA Polymerase II (RNAP II) gain access to DNA in the co
240 (ChIP) studies illustrated that M inhibited RNA polymerase II (RNAP II) recruitment to gene promoter
241 nactive clusters based on the enrichment for RNA polymerase II (RNAPII) and H3K9me3, respectively.
242 is a conserved protein that colocalizes with RNA polymerase II (RNAPII) and has been shown to be impo
243 ssociated with genes actively transcribed by RNA polymerase II (RNAPII) and is catalyzed by Saccharom
245 IS-only sites) are, on average, enriched for RNA polymerase II (RNAPII) binding and histone retention
246 nt and the accumulation of P-TEFb-associated RNA polymerase II (RNAPII) C-terminal domain (CTD)-Ser7
247 (H3K4me3) in transcriptional events such as RNA polymerase II (RNAPII) elongation and alternative sp
248 nitiation and regulation of transcription by RNA polymerase II (RNAPII) in eukaryotes rely on the tra
249 transcript elongation of subsets of genes by RNA polymerase II (RNAPII) in the chromatin context.
253 B) is a BRCA1-binding protein that regulates RNA polymerase II (RNAPII) pausing and transcription elo
254 es are at promoters that have high levels of RNA polymerase II (RNAPII) stalling and DNA accessibilit
256 7, regulates the mRNA elongation capacity of RNA polymerase II (RNAPII) through controlling the nucle
259 ion of the carboxyl-terminal-domain (CTD) of RNA polymerase II (RNAPII) with stimulation of TOP1 abov
264 e beta-tubulin (BenA), calmodulin (CaM), and RNA polymerase II second largest subunit (RPB2) genes.
265 ar large subunit (LSU) of ribosomal DNA, the RNA polymerase II second-largest subunit (RPB2), and the
266 bed with 12 pure proteins (80 polypeptides): RNA polymerase II, six general transcription factors, TF
267 assembly of large protein complexes, such as RNA polymerase II, small nucleolar ribonucleoproteins an
268 increased binding of total and phospho-Ser2 RNA polymerase II specifically at the intron retained un
270 revisiae Spt6 binds the linker region of the RNA polymerase II subunit Rpb1 rather than the expected
271 tyrosyl-DNA-phosphdiesterase, and TAF12, an RNA polymerase II TATA-box binding factor, cause CIN whe
272 as established a role of base J in promoting RNA polymerase II termination in Leishmania spp. where t
276 e super-enhancer signature and elongation of RNA polymerase II through the Hand2 enhancer locus.
278 based mutagenesis reduced the recruitment of RNA polymerase II to ENL-target genes, leading to the su
280 tion of DNA replication per se or loading of RNA polymerase II to late promoters and subsequent reduc
281 merase II during early elongation and causes RNA polymerase II to pause in the promoter-proximal regi
282 in reduced binding of actively transcribing RNA polymerase II to the endogenous Asc gene, resulting
285 eneral cofactor required for essentially all RNA polymerase II transcription and is not consistent wi
286 nd found a positive correlation between both RNA polymerase II transcription and mRNA degradation wit
291 tion prevents the enrichment of Mediator and RNA polymerase II transcription machinery, but not that
292 d role of CKII and FACT in the regulation of RNA polymerase II transcription through chromatin via ph
293 d TFIID are alternative factors that promote RNA polymerase II transcription, with about 10% of genes
295 somerase 1 (Top1) as a positive regulator of RNA polymerase II transcriptional activity at pathogen-i
296 f translation-competent mRNA is dependent on RNA polymerase II transcripts being modified by addition
298 ChIP-Seq quantification of binding sites for RNA polymerase II was combined with RNA-Seq quantificati
300 ntial mitotic transcription factor FoxM1 and RNA polymerase II were found to occupy the cyclin B1 gen
WebLSDに未収録の専門用語(用法)は "新規対訳" から投稿できます。