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1                                              Pol III acts on lifespan downstream of TORC1, and limiti
2                                              Pol III inhibition affects gene reactivation status alon
3                                              Pol III is a determinant of cellular growth and lifespan
4                                              Pol III regulation is thus sensitive to environmental cu
5                                              Pol III subunits Rpc53 and Rpc37 (C53/37) form a heterod
6                                              Pol III transcription at tRNA genes (tDNAs) requires the
7                                              Pol III-dependent transcription was independent of the i
8 o determine the intranuclear positions of 13 Pol III-transcribed genes.
9 ng RNA-seq data and built an atlas of 17,249 Pol III-transcribed Alu elements.
10 orresponding to the Rpc82/34/31 and Rpc53/37 Pol III-specific subcomplexes.
11            The ancestral eukaryotic RPR is a Pol III transcript generated with mature termini.
12           Conversely, ectopic insertion of a Pol III-transcribed gene in the vicinity of a centromere
13 opriate access to the replication fork via a Pol III*-Pol IV switch relying on both the rim and cleft
14                                 Accordingly, Pol III activity is tightly regulated with cell growth a
15                   To reach maximum activity, Pol III binds to the DNA sliding clamp beta and the exon
16 mental defects cluster in hotspots affecting Pol III stability and/or biogenesis, whereas mutations a
17    A 2000-fold purification of Pol III* (all Pol III HE subunits except beta) from this strain contai
18 units are common to Pol I (a.k.a. Pol A) and Pol III (a.k.a. Pol C) and are encoded by single genes.
19  factors (GRFs) Reb1p, Rap1p, and Abf1p, and Pol III transcription factors enhance the efficiency of
20 ed that alcohol increases TBP expression and Pol III gene transcription to promote liver tumor format
21  new nomenclature system for plant Pol I and Pol III subunits in which the 12 subunits that are struc
22 me that the major DNA polymerases (Pol I and Pol III) and DNA ligase are directly involved with oligo
23 st that RNA polymerases I and III (Pol I and Pol III) are the only enzymes that directly mediate the
24 ymerases I and III (abbreviated as Pol I and Pol III), the first analysis of their physical compositi
25 ted to parts of these factors (for Pol I and Pol III).
26 der identical conditions, purified Pol I and Pol III, but not Pol II, could transcribe nucleosomal te
27  which are normally transcribed by Pol I and Pol III.
28 with the functional divergence of Pol I- and Pol III-specific AC40 paralogs.
29 on factor, which regulates Pol I, Pol II and Pol III gene activity.
30  functional conservation of human Pol II and Pol III pre-initiation complexes.
31 ted mechanism of exchange between Pol II and Pol III that occurs outside the replication fork.
32 target negative regulators of RNA Pol II and Pol III to coordinately increase the transcription of ho
33 or a close similarity between the Pol II and Pol III transcription complexes, and additionally explai
34 s reveal that the interactions of Pol II and Pol III with beta allow for rapid exchange during DNA sy
35 olymerases, abbreviated as Pol I, Pol II and Pol III.
36 somal barrier with those of yeast Pol II and Pol III.
37 ed transcription to a mixture of Pol II- and Pol III-, or to a solely Pol III-dependent initiation of
38 s reveal a novel mechanism by which MAF1 and Pol III regulate the activity of a protein-coding gene t
39           Our study links mutated POLR3E and Pol III to an innate immune deficiency state in humans.
40 transcription by interfering with TFIIIB and Pol III.
41 ntially, the drugs did not affect Pol-II and Pol-III transcription, demonstrating a high selectivity.
42 e circadian clock, which allows anticipatory Pol III transcription.
43 lear accumulation, binding to RNA Pol III at Pol III genes and transcriptional repression.
44               All but the INR also reside at Pol III promoters, where TBP makes similar contacts.
45 ) II-transcribed promoters, slow turnover at Pol III promoters, and very slow turnover at the Pol I p
46                                   Autonomous Pol III transcription was also revealed for Alus nested
47 th minimal Pol II activity, thereby boosting Pol III activity to a level that is higher than that of
48 span; in flies, longevity can be achieved by Pol III inhibition specifically in intestinal stem cells
49  insertions upstream of genes transcribed by Pol III indicated that Ty1 preferentially integrates int
50              Outside of genes transcribed by Pol III, Ty1 avoids coding sequences, a pattern that is
51 -dependent and -independent transcription by Pol III.
52 cription is observed in cancer and causative Pol III mutations have been described in neurodevelopmen
53 II (Pol III) transcription enhances cellular Pol III gene production, leading to an increase in trans
54 ination by isolated Saccharomyces cerevisiae Pol III.
55 redominantly to the WH1 domain of the citrus Pol III subunit C34 (CsC34) and that its phosphoregulato
56 ing primer strand is stabilized by conserved Pol III residues along the fingers, thumb and exonucleas
57 , we show that POLR3G and POLR3GL containing Pol III complexes bind the same target genes and assume
58 promoter being directly responsive to a core Pol III transcription factor complex.
59 sceptibility to challenge by exogenous D403E Pol III*.
60                              Only when D403E Pol III was bound to a tau-containing DnaX complex did e
61 lar interactions occurring at Brf2-dependent Pol III promoters and highlighting the general structura
62 same beta clamp and to positively dissociate Pol III from beta clamp in a concentration-dependent man
63  enzymatic activities of the replicative DNA Pol III are well understood, its dynamics within the rep
64 tion and stress conditions by Maf1 to enable Pol III regulation.
65 er, and germline mutations in genes encoding Pol III subunits or tRNA processing factors cause neurog
66 esis under normal conditions but facilitates Pol III displacement from the primer terminus following
67 t RNA secondary structure, which facilitates Pol III release.
68 ith dNTPs at the active site of the C-family Pol III replicase at a step that does not require correc
69 t corroborate their findings using bona fide Pol III from two laboratory sources.
70 herefore identify a radical new function for Pol III in the regulation of macrophage function which m
71 einitiation complex but are not required for Pol III recruitment.
72 -IN but not two other complexes required for Pol III transcription, transcription initiation factors
73 t can activate p53, this is not required for Pol III transcriptional inhibition.
74 y recovered via two sequential switches from Pol III to Pol IV and back to Pol III.
75 ranscription of RNA Pol III-dependent genes (Pol III genes), tRNA(Leu), tRNA(Tyr), 5S rRNA and 7SL RN
76                        Here we report global Pol III expression/methylation profiles and molecular me
77 lamp), in the presence of primase, helicase, Pol III core, clamp loader, and beta-clamp initiates DNA
78                                       Hence, Pol III is a pivotal mediator of this key nutrient-signa
79                               Whereas higher Pol III occupancy during the night reflects a MAF1-depen
80 hether or not DNA polymerase III holoenzyme (Pol III HE) contains gamma.
81 ts showed an increase in Pol III holoenzyme (Pol III HE) foci post-UV that do not colocalize with the
82 al replicase, DNA polymerase III holoenzyme (Pol III HE).
83                            Understanding how Pol III-dependent microRNAs subvert cellular and viral p
84                          Initiation of human Pol III from TATA box-containing Pol II promoters under
85 o-EM reconstruction at 4.0 angstrom of human Pol III, allowing mapping and rationalization of reporte
86 odule in the assembly and stability of human Pol III.
87 oinformatic pipeline allowing us to identify Pol III-dependent transcripts of individual Alu elements
88 ism whereby MPA inhibits RNA polymerase III (Pol III) activity, in both yeast and mammalian cells.
89 an antimutator allele of DNA polymerase III (Pol III) alpha-subunit (dnaE915) and either chromosomal
90  snRNA is transcribed by RNA polymerase III (Pol III) and has an external upstream promoter that cons
91 ation that involves both RNA polymerase III (Pol III) elements and CCCTC binding factor (CTCF) sites.
92 BocaSR is transcribed by RNA polymerase III (Pol III) from an intragenic promoter at levels similar t
93 equired for Escherichia coli polymerase III (Pol III) holoenzyme association at the replication origi
94                          RNA polymerase III (Pol III) is an essential enzyme responsible for the synt
95                          DNA polymerase III (Pol III) is the catalytic alpha subunit of the bacterial
96  al. characterized their RNA polymerase III (Pol III) preparation and concluded that it requires an R
97                          RNA polymerase III (Pol III) promoters, such as 7SK, U6, and H1, are widely
98 AF1 (CsMAF1) protein, an RNA polymerase III (Pol III) repressor that controls ribosome biogenesis and
99                          RNA polymerase III (Pol III) synthesizes short noncoding RNAs, many of which
100                          RNA polymerase III (Pol III) synthesizes tRNAs and other small noncoding RNA
101  contain two isoforms of RNA polymerase III (Pol III) that differ in only a single subunit, with POLR
102 a conserved inhibitor of RNA polymerase III (Pol III) that influences phenotypes ranging from metabol
103                          RNA polymerase III (Pol III) transcribes medium-sized non-coding RNAs (colle
104          Deregulation of RNA polymerase III (Pol III) transcription enhances cellular Pol III gene pr
105 he 'master' repressor of RNA polymerase III (Pol III) transcription in yeast, and is conserved in euk
106                          RNA polymerase III (Pol III) transcription of tRNA genes is essential for ge
107 ansposon Ty3 is found at RNA polymerase III (Pol III) transcription start sites of tDNAs.
108  non-coding RNA genes by RNA polymerase III (Pol III), but the precise role of this ribonucleoprotein
109 hase of transcription by RNA polymerase III (Pol III), the enzyme that synthesizes the majority of RN
110       The association of RNA polymerase III (Pol III)-transcribed genes with nucleoli seems to be an
111 e integrates upstream of RNA polymerase III (Pol III)-transcribed genes, yet the primary determinant
112 oduction of noncanonical RNA polymerase III (Pol III)-transcribed viral microRNAs in leukemic B cells
113 scripts that are made by RNA polymerase III (Pol III).
114  of genes transcribed by RNA polymerase III (Pol III).
115 ransposon transcribed by RNA polymerase III (Pol III).
116    We have approached this using immobilized Pol III-nucleic acid scaffolds to examine the two major
117 ings provide the first evidence for impaired Pol III transcription in cellular models of POLR3-HLD an
118  two potential C31 variants were detected in Pol III.
119  hypothesis have claimed that gamma found in Pol III HE might be a proteolysis product of tau.
120 prisingly, our results showed an increase in Pol III holoenzyme (Pol III HE) foci post-UV that do not
121                  We find that a reduction in Pol III extends chronological lifespan in yeast and orga
122  that, for the first time, alcohol increases Pol III gene transcription through a response element, w
123  have reported that alcohol intake increases Pol III gene transcription to promote cell transformatio
124 les of Pol III genes suggest that individual Pol III genes are exquisitely regulated by transcription
125 alysis has demonstrated that alcohol induces Pol III gene transcription.
126 FIIIB and that overexpression of p65 induces Pol III-dependent transcription.
127  MAF1 is also not responsible for inhibiting Pol III in response to MPA treatment.
128  Hyper-methylation of Pol III genes inhibits Pol III binding to DNA via inducing repressed chromatin
129            We show that MPA rapidly inhibits Pol III by depleting GTP.
130 subunit and either protein can assemble into Pol III.
131  Pol I and the other of which assembles into Pol III.
132 n lifespan downstream of TORC1, and limiting Pol III activity in the adult gut achieves the full long
133 tal anomalies, suggesting that BRF1-mediated Pol III transcription is required for normal cerebellar
134 ghly resistant to dilution in the absence of Pol III* in solution.
135                   Inhibiting the activity of Pol III in the gut of adult worms or flies is sufficient
136 y; the growth-promoting anabolic activity of Pol III mediates the acceleration of ageing by TORC1.
137 al DNA arrays resulted in the association of Pol III-transcribed genes with nucleoli.
138          We conclude that the association of Pol III-transcribed genes with the nucleolus, when permi
139 s catalytic inactivation and backtracking of Pol III, thus committing the enzyme to termination and t
140 MAF1 knockdown indicated enhanced binding of Pol III and BRF1, as well as of CFP1, p300, and PCAF, wh
141 ionally integrated with the active center of Pol III during termination.
142 e formation of the initiation sub-complex of Pol III.
143 ssembly of defective initiation complexes of Pol III.
144             The evolutionary conservation of Pol III affirms its potential as a therapeutic target.
145 ical role in alcohol-induced deregulation of Pol III genes in liver tumor development.
146 ociated with alcohol-induced deregulation of Pol III genes.
147  class of mutant mapped to the PHP domain of Pol III alpha, ablating interaction with the proofreadin
148                             Dysregulation of Pol III transcription has been linked to cancer, and ger
149                               Examination of Pol III* with varying composition of tau or the alternat
150                          A three-tau form of Pol III HE would contain three Pol IIIs.
151 sembly, indicating that the dominant form of Pol III* in cells is Pol III2tau2 gammadeltadelta'chipsi
152      Intriguingly, a significant fraction of Pol III transcription from non-coding regions is not sub
153 , of RNase P is critical for the function of Pol III in cells and in extracts.
154 binding regions, suggesting an impairment of Pol III cytosolic viral DNA-sensing.
155 emonstrate the role of BRCA1 in induction of Pol III genes by alcohol and uncover a novel mechanism o
156 of these effects, we show that inhibition of Pol III activity in macrophages restrains cytokine secre
157 representing a third species of this kind of Pol III-dependent viral noncoding RNA and the first nonc
158 evealed an overall decrease in the levels of Pol III-transcribed tRNAs and an imbalance in the levels
159 However, the genetic and functional links of Pol III to innate immunity in humans remain largely unkn
160 yeast extracts revealed that the majority of Pol III subunits co-purify with Ty1-IN but not two other
161 Similarity between termination mechanisms of Pol III and bacterial RNA polymerase suggests that hairp
162 ylation profiles and molecular mechanisms of Pol III regulation that have not been as extensively stu
163                         Hyper-methylation of Pol III genes inhibits Pol III binding to DNA via induci
164 o coordinate transcription and processing of Pol III transcripts in C. elegans.
165 environmental cues, yet a diurnal profile of Pol III transcription activity is so far lacking.
166                  A 2000-fold purification of Pol III* (all Pol III HE subunits except beta) from this
167        TFIIIB is required for recruitment of Pol III and to promote the transition from a closed to a
168  the clamp loader, suggesting recruitment of Pol III HE at sites of DNA repair.
169 f the gene, but the nucleolar recruitment of Pol III-transcribed genes required active transcription.
170 tions were associated with the 5' regions of Pol III transcribed genes; alignment of Ty1 insertion si
171 ear localization and the rapid repression of Pol III in the nucleus.
172                       MAF1 is a repressor of Pol III transcription whose activity is controlled by ph
173 1-dependent response to feeding, the rise of Pol III occupancy before the onset of the night reflects
174                    Emerging diverse roles of Pol III genes suggest that individual Pol III genes are
175 f protein-coding genes has left the roles of Pol III in organismal physiology relatively unexplored.
176 nucleosome-bound factor enriched at sites of Pol III transcription, determines preferred target sites
177 ture of chromatin characteristic of sites of Pol III transcription.
178 ere, we show that the extensive structure of Pol III-synthesized transcripts dictates the release of
179 etween Ty1 integrase and the AC40 subunit of Pol III and demonstrate that AC40 is the predominant det
180 s in POLR3A, encoding the largest subunit of Pol III, cause POLR3-related hypomyelinating leukodystro
181 POLR3E gene, coding for a protein subunit of Pol III, in a child with recurrent and systemic viral in
182 ion affects alcohol-induced transcription of Pol III genes.
183 , PTEN and Maf1 repress the transcription of Pol III genes.
184                              Upregulation of Pol III transcription is observed in cancer and causativ
185 ediate insertion of Ty1 elements upstream of Pol III-transcribed genes.
186 ng Ty1-IN to insert Ty1 elements upstream of Pol III-transcribed genes.
187 minant targeting Ty1 integration upstream of Pol III-transcribed genes.
188  human cell lines and assessed its impact on Pol III biogenesis, nuclear import, DNA occupancy, trans
189        Given the opposite effects of RecA on Pol III and TLS replisomes, we propose that RecA acts as
190 does not affect the ability of repression on Pol III genes.
191 mote the transition from a closed to an open Pol III pre-initiation complex, a process dependent on t
192 crease is observed in mutants of TF(III)B or Pol III subunits, demonstrating a specific role for the
193 s and, most prominently, pre-tRNAs and other Pol III transcripts are targeted for oligoadenylation an
194 get regions upstream of tRNA genes and other Pol III-transcribed genes when retrotransposing to new s
195       To determine the extent to which other Pol III-transcribed genes serve as genomic targets for T
196 n contained one molecule of gamma-C(tag) per Pol III* assembly, indicating that the dominant form of
197 states of E. coli replicative DNA polymerase Pol III.
198 omplex of Pol II, the replicative polymerase Pol III core complex and the dimeric processivity clamp,
199  Using a dominant negative D403E polymerase (Pol) III alpha that can form initiation complexes and se
200  replication is performed by DNA polymerase (Pol) III.
201 ultaneously bind the replicative polymerase (Pol) III and the conserved Y-family Pol IV, enabling exc
202  as the central regulator of RNA polymerase (Pol) III activity.
203                              RNA polymerase (Pol) III has a noncanonical role of viral DNA sensing in
204               In eukaryotes, RNA Polymerase (Pol) III is specialized for the transcription of tRNAs a
205                              RNA polymerase (Pol) III is the essential, evolutionarily conserved enzy
206 ion of gene transcription by RNA polymerase (Pol) III requires the activity of TFIIIB, a complex form
207 Transcription termination by RNA polymerase (Pol) III serves multiple purposes; it delimits interfere
208                Brf2 recruits RNA polymerase (Pol) III to type III gene-external promoters, including
209 ration of precursor tRNAs by RNA polymerase (Pol) III transcription to end maturation and modificatio
210 e active in transcription by RNA polymerase (Pol) III.
211 As) and tRNAs transcribed by RNA polymerase (Pol) III.
212 A sensors (DAI, AIM2, DDx41, RNA polymerase [Pol] III, and IFI16 [p204]) have been identified in rece
213     Compared to the alternative polymerases, Pol III transcription dominates during mid-exponential p
214 -circle synthesis by the fully reconstituted Pol III replisome.
215 ping effect, which indicates that recruiting Pol III was required for activation of Pol II-mediated t
216 ription factor IIIB (TFIIIB), which recruits Pol III to target genes.
217              Moreover, BRF1 mutations reduce Pol III-related transcription activity in vitro.
218 rapamycin kinase complex 1 (TORC1) regulates Pol III activity, and is also an important determinant o
219 ng module capable of specifically regulating Pol III transcriptional output in living cells.
220 h both a stalled and an actively replicating Pol III* in a manner that was independent of the rim con
221 ely studied, using nc886 as a representative Pol III gene.
222 propose a mechanism for how CsMAF1 represses Pol III transcription and how phosphorylation controls t
223 ch is a BRCA1 deficient cell line, represses Pol III gene transcription.
224                               MAF1 represses Pol III-mediated transcription by interfering with TFIII
225  occurs upstream of genes transcribed by RNA Pol III, requires the Ty1 element-encoded integrase (IN)
226 ortion of Alu elements is transcribed by RNA Pol III, whereas the remaining ones are part of Pol II t
227 omatin environment with marked peaks for RNA Pol III and a number of histone modifications, suggestin
228 1 is a specific transcription factor for RNA Pol III genes.
229                   CsMAF1 bound the human RNA Pol III and rescued the yeast maf1 mutant by repressing
230                          The products of RNA Pol III (RNA polymerase III) dependent genes are elevate
231  is not strongly inhibited in absence of RNA Pol III activity, it compromises the translation of key
232 significantly increased transcription of RNA Pol III-dependent genes (Pol III genes), tRNA(Leu), tRNA
233 inding studies with bacterially purified RNA Pol III proteins demonstrate that Rpc31, Rpc34, and Rpc5
234 dependent CK2 stimulation and subsequent RNA Pol III activation are therefore key for the acquisition
235 Trap purification of multiple GFP-tagged RNA Pol III subunits from yeast extracts revealed that the m
236 lation, nuclear accumulation, binding to RNA Pol III at Pol III genes and transcriptional repression.
237 1-IN interacts in vivo and in vitro with RNA Pol III-specific subunits to mediate insertion of Ty1 el
238 t upon MPA treatment, the levels of selected Pol III subunits decrease, but this is secondary to tran
239 o Pol III, establishing that Maf1 sequesters Pol III elements involved in transcription initiation an
240             Although an interplay of several Pol III subunits is known to collectively control these
241                                   Similarly, Pol III occupancy of amino acid isotypes is almost invar
242 ture of Pol II- and Pol III-, or to a solely Pol III-dependent initiation of transcription from Pol I
243 ctive Pol II transcription sites and at some Pol III-transcribed genes, as demonstrated microscopical
244 elics (iYGR033c and ZOD1), and six non-tDNA, Pol III-transcribed types of genes (RDN5, SNR6, SNR52, R
245 m-sized non-coding RNAs (collectively termed Pol III genes).
246  add more direct evidence to the notion that Pol III elements are able to directly influence Pol II g
247             This raises the possibility that Pol III is involved in ageing.
248                          Here, I report that Pol III can, like Pol II, initiate transcription from mo
249 noprecipitation (ChIP) experiments show that Pol III does not fully dissociate from tRNA genes in yea
250                                 We show that Pol III efficiently terminates transcription in the abse
251                            Here we show that Pol III limits lifespan downstream of TORC1.
252                            We then show that Pol III occupancy of its target genes rises before the o
253                  These findings suggest that Pol III stalled at the transpososome is exploited for co
254                   These results suggest that Pol III transcription is involved in chromatin structure
255                                          The Pol III repressor MAF1 is also not responsible for inhib
256                             In addition, the Pol III mutation was found to exert complex downstream e
257 rmation of an initiation complex between the Pol III HE and primed DNA.
258 easing concentrations of Pol II displace the Pol III core during DNA synthesis in a minimal reconstit
259 essed chromatin and is a determinant for the Pol III repertoire.
260 e results provide compelling support for the Pol III*-Pol IV two-step switch model and demonstrate im
261 itive, it has been difficult to identify the Pol III-transcribed elements and quantify their expressi
262 n sharp contrast, RecA severely inhibits the Pol III replisome.
263 equence recognized by the TBP subunit of the Pol III basal transcription factor IIIB and a proximal s
264      Here, we discuss potential roles of the Pol III gene-mediated genome organization during interph
265 omponents bind immediately downstream of the Pol III preinitiation complex but are not required for P
266 alled "extra-transcriptional effects" of the Pol III system are reviewed here, and a model is put for
267 ere, we characterize the architecture of the Pol III-clamp-exonuclease complex by chemical crosslinki
268 zing purified components to reconstitute the Pol III*-Pol II switch in vitro indicated that Pol II sw
269 DmSNAPc) bound to the U6 PSE can recruit the Pol III general transcription factor Bdp1 to form a stab
270     Here, we test the accepted view that the Pol III holoenzyme remains stably associated within the
271 Previous work in vitro demonstrated that the Pol III transcription factor (TF) IIIB is important for
272  labeled polymerases to demonstrate that the Pol III* complex (holoenzyme lacking the beta2 sliding c
273 h fluorescence microscopy, we found that the Pol III* subassembly frequently disengages from the repl
274 how that Rrn7 is most closely related to the Pol III general factor Brf1.
275 vered that PR physically associated with the Pol III holoenzyme.
276 how that p65 can directly associate with the Pol III transcription factor TFIIIB and that overexpress
277 e-tau form of Pol III HE would contain three Pol IIIs.
278                                        Thus, Pol III expression during tumorigenesis is delineated by
279                                        Thus, Pol III transcription during the diurnal cycle is regula
280  switches from Pol III to Pol IV and back to Pol III.
281                              CsMAF1 binds to Pol III to restrict transcription; however, exactly how
282 ion cryo-EM structure of yeast Maf1 bound to Pol III, establishing that Maf1 sequesters Pol III eleme
283 ose that in yeast, GTP depletion may lead to Pol III stalling.
284 creases CsMAF1 affinity to CsC34, leading to Pol III derepression, and that Ser 45, found only in pla
285 overed a subset of transcripts vulnerable to Pol III hypofunction, including a global reduction in tR
286 en tissues and insufficient amounts of total Pol III in vivo.
287 enesis, the fraction of actively transcribed Pol III genes increases reaching a plateau during immort
288 ndensin onto RNA polymerase III-transcribed (Pol III) genes and highly transcribed Pol II genes; cond
289                            We found that two Pol III elements within the promoter region influence AN
290  that can effectively compete with wild-type Pol III alpha and form initiation complexes, but cannot
291 ically with tRNA and snoRNA genes undergoing Pol III transcription.
292                                         When Pol III genes are hypo-methylated, MYC amplifies their t
293 eading frames not previously associated with Pol III transcription, suggesting the existence of a sma
294  Pol IV has a unique ability to coexist with Pol III on the same beta clamp and to positively dissoci
295 tion and chromatin looping concurrently with Pol III recruitment.
296 sites in the yeast genome that interact with Pol III transcription complexes.
297 ol II transcription robustly interferes with Pol III function at specific tRNA genes.
298                  Simultaneous knockdown with Pol III abolished these regulatory events.
299          Simultaneous knockdown of MAF1 with Pol III or BRF1 (subunit of TFIIIB) diminished the activ
300  the mechanism used by Pol IV to switch with Pol III* is distinct from those used by the other Pols.
301 erences in how Pol IV and Pol II switch with Pol III*.

 
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