ライフサイエンスコーパス: RNA pol II

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 R enzymes AAG and APE1, Elongator and active RNA pol II.

6 ensed chromatin regions together with active RNA pol II for the first time using super-resolution mic

7 ent of African Sleeping Sickness, deploys an RNA pol II that contains a non-canonical CTD to accompli

8 as inhibited after gene activation, Adr1 and RNA pol II remained at promoters, and RNA pol II remaine

9 uppressed by defects in the Paf1 complex and RNA pol II.

10 gested that S. cerevisiae growth control and RNA pol II transcription might be coupled by using the R

11 w that HIV-1 Tat protein stimulated DSIF and RNA pol II phosphorylation by P-TEFb during elongation.

12 Both the expression of RNase H1 and RNA pol II inhibition recovered the ability to phosphory

13 that an intimate association between MLL and RNA pol II occurs at MLL target genes in vivo that is re

14 ed Mediator contained some kinase module and RNA pol II, Mediator purified through F-Med26 contained

15 r1 and RNA pol II remained at promoters, and RNA pol II remained in the ORF with associated nascent t

16 assess the relative contributions of RT and RNA pol II to HIV-1 mutagenesis, a system was establishe

17 te the relative contribution of HIV-1 RT and RNA pol II to viral mutagenesis.

18 We have applied the method to arrest RNA pol II elongation complexes on a DNA template contai

19 triplex structure and isolation of arrested RNA pol II elongation complexes should be generalizable

20 However, the fusion proteins as well as RNA pol II were recruited to heat shock puffs during hea

21 in activated Th cells by promoter-associated RNA pol II.

22 , such as Fas/APO1, have low levels of bound RNA pol II but undergo damage-induced activation through

23 BRCA1-RNA pol II complexes showed evidence of a multiply phosp

24 show that the non-canonical CTD of T. brucei RNA pol II is important for normal protein-coding gene e

25 episome, suggesting that it is controlled by RNA pol II.

26 longation factors, which block elongation by RNA pol II shortly after the initiation of transcription

27 s a strong block to transcript elongation by RNA pol II.

28 ted by the quality of pre-mRNAs generated by RNA pol II.

29 er and terminator and triggers initiation by RNA pol II.

30 nd in the DHFR gene, which is transcribed by RNA pol II.

31 ls of template uracilation, transcription by RNA pol II was completely blocked.

32 ein-coding gene expression, likely directing RNA pol II to the TSSs within the genome.

33 at functioned in concert with the CTD during RNA pol II transcription.

34 tion complex and travels with the elongating RNA pol II, whereas TFIIH is released from the elongatio

35 important for the progression of elongation RNA pol II on the egr1 gene.

36 First, RNA pol II transcription in poliovirus-infected cell ext

37 C sites but not with intervening or flanking RNA pol II transcribed genes.

38 GlcNAc-transferase activity is essential for RNA pol II promoter recruitment and that pol II goes thr

39 tion completes the set of human homologs for RNA pol II subunits defined in yeast and should provide

40 icing may have uncoupled the requirement for RNA pol II-mediated mRNA production.

41 I (IIO), in preference to hypophosphorylated RNA pol II (IIA) expected at promoters.

42 asic transcription factor RNA polymerase II (RNA pol II) and the coactivator p300 on the endogenous M

43 transcriptionally active RNA polymerase II (RNA pol II) at super-resolution is still lacking.

44 a general coactivator of RNA polymerase II (RNA pol II) bridging enhancer-bound transcriptional fact

45 e that phosphorylates the RNA polymerase II (RNA pol II) C-terminal domain (CTD) within a transcripti

46 homogeneous population of RNA polymerase II (RNA pol II) elongation complexes arrested at a DNA damag

47 epair factor TFIIH to the RNA polymerase II (RNA pol II) initiation complex to facilitate promoter cl

48 The RNA polymerase II (RNA pol II) interacted with the Ifng gene promoter in an

49 A unique feature of RNA polymerase II (RNA pol II) is its long C-terminal extension, called the

50 r level, AT7519 inhibited RNA polymerase II (RNA pol II) phosphorylation, a CDK9, 7 substrate, associ

51 ly and the recruitment of RNA polymerase II (RNA pol II) to the promoter.

52 In eukaryotic cells, RNA polymerase II (RNA pol II) transcription and pre-mRNA processing are co

53 such functions coupled to RNA polymerase II (RNA pol II) transcription, perhaps by affecting the comp

54 anscription initiation by RNA polymerase II (RNA pol II) via direct interaction with the basal transc

55 -PK promoter occupancy by RNA polymerase II (RNA pol II), acetylated histone H3 (Ac-H3), and acetylat

56 -terminal domain (CTD) of RNA polymerase II (RNA pol II), as well as negative elongation factors, whi

57 scription Factors (GTFs), RNA polymerase II (RNA pol II), co-activators, co-repressors, and more.

58 e transcribed by cellular RNA polymerase II (RNA pol II), ICP4 must interact with components of the p

59 gene delivery systems for RNA polymerase II (RNA pol II)-based promoters have been developed and are

60 d template containing the RNA polymerase II (RNA pol II)-dependent adenovirus major late promoter.

61 d functional complex with RNA polymerase II (RNA pol II).

62 e two largest subunits of RNA polymerase II (RNA pol II).

63 onal machinery, including RNA polymerase II (RNA pol II).

64 Loss of function Mll results in defects in RNA pol II distribution.

65 e screened 102 candidate factors involved in RNA pol II cleavage and termination, elongation, splicin

66 K9 inhibition and the resultant reduction in RNA pol II phosphorylation, which leads to the downregul

67 everal approaches to show a role for WRNp in RNA pol II transcription, possibly as a transcriptional

68 ecific effects on gene regulation, including RNA pol II elongation, histone deacetylation, and activa

69 rho termination factor from E. coli induces RNA pol II to release at all of these pause sites.

70 y E2f1 and Foxo1 transcription by inhibiting RNA pol II binding and E2F1 binding at the Foxo1 locus,

71 ional activity assay, where F-Med26 Mediator/RNA pol II was the most active.

72 purified through F-Med26 contained the most RNA pol II and the least kinase module as demonstrated b

73 f1 in tRNA gene-mediated silencing of nearby RNA pol II transcription.

74 irects 3' end formation of nonpolyadenylated RNA pol II transcripts, such as snoRNAs.

75 erestingly, localization studies of numerous RNA pol II transcription and pre-mRNA processing factors

76 red after the phosphorylation of serine 5 of RNA pol II C-terminal domain (CTD) has occurred, but bef

77 y enhances the phosphorylation of the CTD of RNA pol II by holo-TFIIH in vitro.

78 s demonstrate a critical role for the CTD of RNA pol II LS in the intranuclear targeting of splicing

79 In mammalian cells, truncation of the CTD of RNA pol II LS prevents the targeting of the splicing mac

80 regulatory carboxy-terminal domain (CTD) of RNA pol II disrupts transcriptional silencing, indicatin

81 In WT mES cells, the elongating form of RNA pol II accumulates near Vezf1 binding sites within t

82 The initiation competent form of RNA pol II and general transcription factors appeared in

83 rs, whereas the elongation competent form of RNA pol II was detected even later.

84 of Set2 with the hyperphosphorylated form of RNA pol II.

85 ollowing chemical or genetic inactivation of RNA pol II.

86 GSK-3beta activation was independent of RNA pol II dephosphorylation confirmed by alpha-amanitin

87 endogenous CDKN1C mediates an inhibition of RNA pol II CTD phosphorylation in HeLa cells upon treatm

88 II inihibitor, showing potent inhibition of RNA pol II phosphorylation without corresponding effects

89 ciation can dramatically reduce the level of RNA pol II CTD phosphorylation at both Ser-2 and Ser-5 o

90 R3 transcription, as predicted by a model of RNA pol II engagement with DPE-containing Drosophila pro

91 at domain in the catalytic subunit (p220) of RNA pol II, and the complex was highly functional in tra

92 he clearance of promoter-proximal pausing of RNA pol II on the HIV-1 long terminal repeat at differen

93 Phosphorylation of RNA pol II CTD by TFIIH is thought to play an important

94 k7, SNS-032 inhibited the phosphorylation of RNA pol II in all four lines and blocked RNA synthesis.

95 sed H3K9me3 and H3K27me3, and a reduction of RNA pol II occupancy on viral genes.

96 , we find that CDKN1C-mediated repression of RNA pol II phosphorylation is E2F1-dependent, suggesting

97 function, occurs exclusively as a result of RNA pol II-mediated transcription.

98 e showed that two of the largest subunits of RNA pol II coprecipitated with the N-terminal 315-residu

99 cyclin A2 as a key transcriptional target of RNA pol II during HU-induced centriole overduplication.

100 We infer that the lack of ubiquitylation of RNA pol II LS in Cockayne's syndrome cells does not caus

101 ol II LS), suggesting that ubiquitylation of RNA pol II LS may be necessary for TCR in eukaryotes.

102 nctional Rsp5, there is no ubiquitylation of RNA pol II LS.

103 This control on RNA pol II-dependent transcription rate is obtained by c

104 Collectively, our results show that ongoing RNA pol II transcription is required for centriole overd

105 h could have been introduced by either RT or RNA pol II, whereas the other eleven mutations were only

106 during which growth is inhibited and overall RNA pol II transcription is reported to be inhibited.

107 fraction colocalized with the phosphorylated RNA pol II decreased with the inhibition of transcriptio

108 actions: one colocalized with phosphorylated RNA pol II and the other as nascent aggregates.

109 molecular switch for transcription of poised RNA pol II.

110 ed using either ACTB (beta-actin) or POLR2A (RNA pol II large subunit), but not when RNA levels are n

111 ated with a large fraction of the processive RNA pol II activity present in undamaged cells, and the

112 Preferential interaction with processive RNA pol II in undamaged cells places BRCA1 in position t

113 interacts with both CDK7 and CDK9 (putative RNA pol II CTD kinases) and that CDKN1C blocks their abi

114 ty of Snt1 and the Set3C complex, recruiting RNA pol II and interfering with Rap1 binding to activate

115 provide direct evidence of a 9-fold reduced RNA pol II binding capacity for the -63C allele.

116 itment to the promoter, resulting in reduced RNA pol II loading.

117 se gaps were enriched with phosphorylated S5 RNA pol II, and were sensitive to the cellular transcrip

118 tion confirmed by alpha-amanitin, a specific RNA pol II inihibitor, showing potent inhibition of RNA

119 ted by alpha-amanitin, a potent and specific RNA pol II inhibitor.

120 Isolation of stable RNA pol II elongation complexes arrested at DNA damage s

121 We developed a stepwise RNA pol II walking approach and used Western blotting to

122 We have used a stepwise RNA pol II walking approach and Western blotting to dete

123 itro transcription assay markedly stimulates RNA pol II-dependent transcription carried out by nuclea

124 tylation of RNA polymerase II large subunit (RNA pol II LS), suggesting that ubiquitylation of RNA po

125 ivity by n-3 PUFA correlated with suppressed RNA pol II, Ac-H3, and Ac-H4 occupancy on the L-PK promo

126 Surprisingly, RNA pol II-mediated RNA synthesis in 24 hr-treated cells

127 orylation may be a prerequisite for targeted RNA pol II degradation.

128 ous observations, these results suggest that RNA pol II may terminate by a mechanism closely related

129 ions among ERalpha, its coactivators and the RNA pol II machinery are all required for ERalpha- media

130 sphorylation-driven interactions between the RNA pol II CTD and the WW domain of Ess1/Pin1, we sugges

131 We further show that deletion of the RNA pol II C-terminal domain (CTD) kinase Ctk1, or parti

132 data all point to OGA as a component of the RNA pol II elongation machinery regulating elongation ge

133 to support a model in which the entry of the RNA pol II gene expression machinery into newly forming

134 to the carboxyl-terminal domain (CTD) of the RNA pol II large subunit.

135 endent on the carboxy-terminal domain of the RNA pol II largest subunit.

136 CR, demonstrating that ubiquitylation of the RNA pol II LS is not required for TCR.

137 rved post-translational modifications on the RNA pol II C-terminal domain (CTD) and the chromatin tem

138 Following exposure to UV radiation, the RNA pol II elongation complex is blocked at sites of UV-

139 ched at a DSB were the phosphatase Sit4, the RNA pol II degradation factor Def1, the mRNA export prot

140 The RNA pol-II promoters are also unconventional and charact

141 atin landscape is a central function of this RNA pol II-distinguishing domain.

142 ntly reduced expression of genes adjacent to RNA pol-II promoters, where glutamine mimics abnormally

143 ubiquitin-protein ligase that ubiquitylates RNA pol II LS in cells exposed to DNA-damaging agents.

144 Unlike RNA pol II-dependent promoter repression, overexpressing

145 ber of the Paf1 complex that associates with RNA pol II and regulates transcription elongation.

146 s demonstrate that DSIF/NELF associates with RNA pol II complexes during early transcription elongati

147 Here we report that p16INK4A associates with RNA pol II CTD and TFIIH.

148 op1-lacZ fusion protein was colocalized with RNA pol II in some but not all of the nonpuff, interband

149 polymerase II (pol II) and colocalizes with RNA pol II at a subset of actively transcribed target in

150 enhancer-bound transcriptional factors with RNA pol II.

151 The head and middle modules interact with RNA pol II, and the tail module interacts with transcrip

152 We demonstrated that interaction with RNA pol II is a conserved feature of BRCA1 proteins from

153 The yeast Paf1 complex interacts with RNA pol II and mediates histone modifications during elo

154 t blocks gene activation by interfering with RNA pol II, activator and coactivator recruitment, and e

155 NA and needs to gain access to Ig loci, with RNA pol II transcription possibly providing both aspects

156 ctivity and fidelity were also observed with RNA pol II using uracil base excision repair (UBER)-defi

157 of genes, showing considerable overlap with RNA pol II, SPT5, TRIM28-KAP1-TIF1beta, and O-GlcNAc its

158 mechanistically linked to transcription with RNA pol II serving as a platform to recruit RNA processi

159 o interact functionally with the other yeast RNA pol II subunits in vivo.