ライフサイエンスコーパス: transcription from

1 ement, and 3 patients with reduced or absent transcription from 1 allele.

2 during a gammaherpesvirus infection revealed transcription from 28 270 SINE loci, with approximately

3 Transcription from -614/-645 tsp reporter fusions was sp

4 inhibits host transcription while activating transcription from a class of phage promoters.

5 , in TS cells, GATA3 directly regulates Cdx2 transcription from a conserved GATA motif at the intron

6 Transcription from a distal NDC80 promoter directs Set1-

7 ology for the massively parallel analysis of transcription from a high-complexity barcoded template l

8 ry nucleotide ppGpp ("magic spot") regulates transcription from a large subset of Escherichia coli pr

9 y enhances the ability of FOXO1A to activate transcription from a luciferase reporter construct and f

10 owever, we found that PKG potently inhibited transcription from a luciferase reporter driven by the h

11 e cell lines for the ability to activate GFP transcription from a minimal CMV promoter.

12 To investigate poxvirus replication and transcription from a new perspective, we incorporated 5-

13 romoter and decreased both basal and induced transcription from a number of promoters.

14 nscription factors that coordinate divergent transcription from a pair of tightly linked core initiat

15 Transcriptional interference (TI), where transcription from a promoter is inhibited by the activi

16 Here, we show that transcription from a promoter located upstream of mccA d

17 is a DNA-binding protein that can stimulate transcription from a range of sigma(66)-dependent promot

18 ylation, and S-nitrosylation of OxyR induced transcription from a regulon that is distinct from the r

19 gineered bacterial cells in order to control transcription from a simple synthetic gene circuit.

20 e to cellular stress, primarily by increased transcription from a single gene located on chromosome 7

21 taining SigF is sufficient for initiation of transcription from a single sspA promoter.

22 V) controls genome encapsidation and reverse transcription from a single-stranded RNA to a double-str

23 e factor YvrI and coregulator YvrHa activate transcription from a small set of conserved promoters in

24 Both enzymatic activities are essential for transcription from a subset of genes and G(1) progressio

25 ors and showed that each is able to activate transcription from a targeted reporter.

26 gin of replication, and E2 can also regulate transcription from adjacent promoters.

27 ng a gene trap in the Rest gene, eliminating transcription from all coding exons, to remove REST prem

28 ether CyHV-3 expressed genes during latency, transcription from all eight open reading frames (ORFs)

29 tarum (Lpl) appears to be able of initiating transcription from all sources of DNA.

30 TLS was found to repress transcription from all three classes of RNAP III promote

31 Transcription from all three promoters was imaged in liv

32 growth at 37 degrees C a temporal pattern of transcription from all three promoters was observed with

33 h increased silencing of alleles and reduced transcription from alleles positioned peripherally.

34 , and, on the other hand, ETV1 super-induced transcription from an AR binding site on androgen stimul

35 Moreover, whereas p68 robustly coactivated transcription from an estrogen response element, its sum

36 enetically diverse, indicating activation of transcription from an extensive range of proviruses.

37 Transcription from an FNR-dependent promoter with a cons

38 ear factor-kappaB-dependent transcription or transcription from an HIV-1 promoter with inactivated SP

39 locus histone acetylation and activate hGH-N transcription from an inactive locus, we expressed Pit-1

40 in the promoter region of Rv1813c and direct transcription from an initiation site located several hu

41 Surprisingly, Zap1 controls UBI4 by inducing transcription from an intragenic promoter, and the resul

42 PcG proteins are found to occupy and repress transcription from an intronic region containing the mic

43 Transcription from an IRF-3-responsive promoter was part

44 escribe a systematic analysis of pseudogene "transcription" from an RNA-Seq resource of 293 samples,

45 The detection of transcription from areas of the genome not currently ann

46 nt on NK cells and associated with increased transcription from aryl hydrocarbon receptor- and oxidat

47 al was lost and there was no detectable mRNA transcription from ATAK cells.

48 chia coli RNA polymerase, thereby inhibiting transcription from bacterial promoters and phage early p

49 bond breaking in chemical reactions, and DNA transcription from biology.

50 ers and is capable of specific initiation of transcription from both double- and single-stranded DNA.

51 Allele-specific expression (ASE) quantifies transcription from both haplotypes using individuals het

52 with STAT3, RORgammat, and Runx1 to enhance transcription from both il17a and il17f promoters.

53 Taf1 depletion in vivo and instead repressed transcription from both promoter types.

54 ranscription from HSP1 and h-mtTFA-dependent transcription from both promoters is enhanced and a high

55 ing 105 glutamines, it potentiates activated transcription from both TATA-containing and TATA-lacking

56 Although PKG was able to inhibit transcription from both the CTNNB1 and TCF reporters, th

57 of truncated RNAs resulting from convergent transcription from both the promoters that are capable o

58 Although all of these pathways modulate transcription from chromatin in vivo, the mechanisms by

59 remodeling activity is required for optimal transcription from chromatin.

60 that bind DNA but show defects in activating transcription from class I, class II or both types of pr

61 Conversely, transcription from cloned promoters can interfere with p

62 mpact of AT-rich DNA on host fitness reduced transcription from constitutive, but not activator-depen

63 regulator complex cooperate to enhance basal transcription from core promoters containing both a TATA

64 complex is crucial for suppressing aberrant transcription from cryptic start sites within intragenic

65 plays key roles in repressing aberrant gene transcription from cryptic transcription initiation site

66 out the integrated output of FoxO1-dependent transcription from different neuronal populations and mu

67 ted deacetylase bodies, whereas E2 activates transcription from distal enhancers.

68 ions, due to either reduced H3K4me3 or ncRNA transcription from distal or antisense promoters.

69 strate that ZFP809 is able to potently block transcription from DNA constructs of human T-cell lympho

70 erase II is the central eukaryotic enzyme in transcription from DNA to RNA.

71 eotic gene network, preferentially activates transcription from DPE- versus TATA-dependent promoters.

72 -day- and activity-dependent upregulation of transcription from E-box-containing clock gene promoters

73 he enhanced E2R showed greater repression of transcription from E2-responsive reporter plasmids in ma

74 h X chromosomes in XX animals and halves the transcription from each.

75 Decreasing transcription from early promoter A3 is sufficient to ma

76 n of c-Fos promotes the progression of viral transcription from early to late stages and accelerates

77 monstrate that TAL effectors can drive plant transcription from EBEs on either strand and in both dir

78 K27ac, but has surprisingly minor effects on transcription from either enhancers or promoters.

79 A-dependent promoters in vitro and activates transcription from ExsA-dependent promoters both in vitr

80 the release of musclin-encoding gene (Ostn) transcription from forkhead box O1 transcription factor

81 ce function to prevent translation-uncoupled transcription from generating R-loops, which would block

82 ification for DNase-seq, analysis of nascent transcription from Global-Run On (GRO-seq) data, and cha

83 This allows us to uncouple transcription from histone modifications at the centrome

84 id (PPE) protein Rv1168c (PPE17) can augment transcription from HIV-1 LTR in monocyte/macrophage cell

85 that bind the host RNAP and inhibit in vitro transcription from host promoters, but not from middle o

86 Transcription from HPV chromatin requires AP-1-dependent

87 transcription template, h-mtTFA-independent transcription from HSP1 and h-mtTFA-dependent transcript

88 However, transcription from HSP2 has been reported only once in a

89 Transcription from HSP2 is also observed when HeLa cell

90 Here, we document transcription from HSP2 using an in vitro system of defi

91 e located on both sides of the start site of transcription from HSP2, suggesting that TFAM binding in

92 IE gene transcription from HSV-1 genomes associated with high le

93 s attributed to an intrinsic weakness of Id2 transcription from Id2 C57BL/6 allele, leading to an ove

94 erence, both inhibitors convergently induced transcription from identical sites, as we found TINATs t

95 tail (Gn-T) blocked RIG-I- and TBK1-directed transcription from IFN-stimulated response elements (ISR

96 d each AP-1 complex is capable of activating transcription from in vitro-reconstituted HPV chromatin

97 ed several stochastic rounds of human Pol II transcription from individual DNA templates, observed at

98 s of CDK8 protect beta-catenin/TCF-dependent transcription from inhibition by E2F1.

99 cription termination, thus preventing lncRNA transcription from invading and repressing the downstrea

100 both derepression and an uncoupling of lctO transcription from its growth phase pattern.

101 , we showed that SMU.1349 could also repress transcription from its own promoter by binding to the in

102 ermobacter thermautotrophicus in addition to transcription from its own promoter.

103 In vitro, this complex initiates transcription from late phiKZ promoters in rifampicin-re

104 rinostat has been demonstrated to induce HIV transcription from latently infected cells when administ

105 tly, HMBA has also been shown to trigger HIV transcription from latently infected cells, via a CDK9/H

106 tant, multicopy expression of csrA repressed transcription from LEE1, grlRA, LEE2, LEE5, escD, and LE

107 Here we evaluate transcription from light-strand (LSP) and heavy-strand (

108 tifaceted enhancer element, able to activate transcription from long distances independently of orien

109 opposite orientation from LSP explaining why transcription from LSP requires DNA bending, whereas tra

110 monstrated Isw2 is required to repress ncRNA transcription from many of these NFRs.

111 ARMS2 transcription from minigene vectors carrying different a

112 We found that ICBP90 is essential for MIF transcription from monocytes/macrophages, B and T lympho

113 We show that gp67 has little to no effect on transcription from most promoters but is a potent inhibi

114 port that Pol III can, like Pol II, initiate transcription from most tested Pol II core promoters whe

115 Infected cell polypeptide 4 (ICP4) activates transcription from most viral promoters.

116 her T4 motA(Am)or asiA(Am) and for impairing transcription from MotA/AsiA-activated middle promoters

117 occurs by a variety of mechanisms, including transcription from multiple promoters by two sigma facto

118 Further, an active transcription from multiple rRNA operons in chromosome i

119 RTA activates transcription from nearly 40 early and delayed-early vir

120 mutation or rapid subunit depletion reduces transcription from nearly all genes, measured by newly s

121 nduced MALT1 protease activity and increased transcription from NFAT or NF-kappaB response element re

122 ize is negatively regulated to repress ncRNA transcription from NFRs.

123 riguingly, a significant fraction of Pol III transcription from non-coding regions is not subjected t

124 (but not during latency), there is extensive transcription from noncoding regions, including both int

125 By blocking transcription from normally cryptic promoters, Kmg restr

126 coactivator Mastermind (MAM) to up-regulate transcription from Notch target genes.

127 ts with coregulators to repress and activate transcription from Notch target genes.

128 inds Su(H) (the fly CSL ortholog) to repress transcription from Notch targets.

129 rt-lived DNA binding protein that stimulates transcription from numerous genes involved in cell cycle

130 show that hybrid formation prevents further transcription from occurring, implying a regulatory role

131 X chromosome inactivation (XCI) silences transcription from one of the two X chromosomes in femal

132 ovel role for esBAF in suppressing pervasive transcription from open chromatin regions in ESCs.

133 levels, supporting the view that overlapping transcription from opposite strands may play a regulator

134 site in the CTX Phi prophage, both represses transcription from P(A) and coactivates transcription fr

135 5 hexamer, has no effect on ExsA-independent transcription from P(exsC).

136 (RM) transcription or bind O(R)3 and repress transcription from P(RM) is <2-fold.

137 verexpression of HLP in trans also represses transcription from P(SMU.1348).

138 ue of Escherichia coli HU protein, represses transcription from P(SMU.1348).

139 s of P2 and P3, it is widely considered that transcription from P2 and P3 only occurs in a strictly A

140 ion with LPS or IFN-gamma leads to increased transcription from P3 in inflammatory M1 macrophages.

141 Transcription from P3, which is indirectly activated by

142 tion of NELF from Pol II, thereby transiting transcription from pausing to elongation.

143 s and phage early promoters and coactivating transcription from phage middle promoters.

144 mutants exhibit increased open chromatin and transcription from piRNA clusters and transposons, resul

145 Robust activation of wound-induced transcription from ple and Ddc requires Toll pathway com

146 to a solely Pol III-dependent initiation of transcription from Pol II promoters.

147 which bound within the PR1 region to repress transcription from PR1-2 and PR1-3.

148 However, primary transcription from pre-formed RNPs deposited by infectin

149 ting cells, methods to differentiate nascent transcription from preexisting mRNAs are desired.

150 tions to this correlation were the result of transcription from previously unidentified, unmethylated

151 Transcription from promoter PR1-2 was dependent on the a

152 ibed, a large fraction of which is divergent transcription from promoters and enhancers that is tight

153 nteracted with RNA polymerase and stimulated transcription from promoters dependent on sigma(G) but n

154 This facilitates transcription from promoters dependent on stationary pha

155 f NFAT and NFkappaB correlated with enhanced transcription from promoters responsive to these transcr

156 ess effective reverse transcription and mRNA transcription from proviral DNA and was associated with

157 hat the removal of this insert shifts F gene transcription from readthrough M-F mRNA to monocistronic

158 e SUV39 histone methyltransferases represses transcription from repetitive DNA sequences and ensures

159 ous Myc expression, we observe a decrease in transcription from retroviral vectors during morphogenes

160 The use of rhamnose-inducible transcription from rhaBp allows regulation of the insert

161 BLIMP1 strongly induced transcription from Rp as well as Zp, with there being th

162 ) epithelial and B-cell lines and activating transcription from Rp.

163 ading MED19, shifting the balance of defence transcription from SA-responsive defence to JA/ET-signal

164 t quantitative information about dynamics of transcription from single-cell sequencing data, as well

165 ation, the amino acid response (AAR) induces transcription from specific genes through a collection o

166 To initiate transcription from specific promoters, the bacterial RNA

167 also serves as an essential co-activator of transcription from T4 middle promoters.

168 gene promoter, and increased Nrf2-dependent transcription from target gene promoters.

169 With one exception, transcription from tested T4 early promoters is either u

170 Transcription from the -271 tsp was severely downregulat

171 onal reporter fusions were used to show that transcription from the -305 tsp was induced in all cells

172 lso been recently found to enhance antisense transcription from the 3' end of the GAL10 coding sequen

173 iptional interference and prevent downstream transcription from the 3' long terminal repeat.

174 anscription did not interfere with antisense transcription from the 3' LTR and vice versa, even with

175 Antisense transcription from the 3' LTR regulates expression of a

176 the 5' LTR does not interfere with antisense transcription from the 3' LTR, allowing viral genes enco

177 xpression of a single gene, hbz, while sense transcription from the 5' LTR controls expression of all

178 We found that sense transcription from the 5' LTR does not interfere with an

179 The observation that repression of transcription from the adeno-associated virus serotype 2

180 e Sp1/Sp3 site decreases DNA replication and transcription from the adjacent ORF62 and ORF63 promoter

181 Activator-dependent transcription from the aer promoter was reconstituted in

182 ion assays revealed that AgrA alone promoted transcription from the agr P2 promoter, with SarA enhanc

183 chanism of gene regulation due to convergent transcription from the antagonistic prgX/prgQ operon in

184 promoters, pR and pL, and activates its own transcription from the auto-regulated pRM promoter.

185 the ava4025-vnfDGKEN operon, each repressed transcription from the ava4025-vnfDGKEN promoter and a m

186 In the presence of ample tryptophan, transcription from the Bacillus subtilis trp operon prom

187 presses host general transcription, inhibits transcription from the beta interferon promoter, and pro

188 We simultaneously followed transcription from the beta-actin alleles in real time a

189 In support, we observed increased transcription from the c-di-GMP-regulated pel promoter.

190 that originates downstream and converges on transcription from the canonical promoter.

191 fection assays demonstrate that Fli-1 drives transcription from the CCL5 promoter in a dose-dependent

192 , another Ets family member, and Fli-1 drive transcription from the CCL5 promoter, although Fli-1 tra

193 myces cerevisiae that detects alterations in transcription from the centromere-proximal rDNA gene of

194 the toxboxes required for the activation of transcription from the cholera toxin promoter PctxAB hav

195 y I, when superinfected, initially supported transcription from the common EBNA promoters Wp and Cp (

196 regulatory element effectively uncouples PIN transcription from the CRF-mediated cytokinin regulation

197 ns and simultaneously led to enhanced RNAPII transcription from the decondensed model chromatin.

198 ly regulated genes, H3K27me3 did not prevent transcription from the dehydration stress-responding gen

199 sses transcription from P(A) and coactivates transcription from the divergent P(R).

200 two YqjI binding sites cooperate to control transcription from the divergent promoters.

201 onstant by a negative feedback loop in which transcription from the dksA promoter is inhibited by Dks

202 In the absence of trans translation, transcription from the dnaA promoter and an origin-proxi

203 at a switch in forward and reverse noncoding transcription from the Drosophila melanogaster vestigial

204 g that both E. coli NrdR and CT406 repressed transcription from the E. coli nrdH and C. trachomatis n

205 gdorferi, lp17, can negatively regulate ospC transcription from the endogenous gene on the circular p

206 In cells transfected with WT p53, transcription from the ER promoter was increased 8-fold.

207 control ET-1 bioavailability is the rate of transcription from the ET-1 gene (edn1).

208 vation of HepG2 hepatoma cells also enhanced transcription from the FOXA2 and FOXA3 genes.

209 Transcription from the gene-internal tRNA promoter requi

210 In the absence of transcription from the H3-H4 promoter, "proto-HLBs" (con

211 Also, knockdown of DDX5 enhanced transcription from the HBV minichromosome.

212 The level of transcription from the HBV promoters depends on both the

213 ), which specifically binds to and represses transcription from the hermaphrodite X chromosomes.

214 Tat-AFF1 affinity in vivo and Tat-dependent transcription from the HIV promoter.

215 nbiased screen for genes that could activate transcription from the HIV-1 LTR in an NF-kappaB-indepen

216 uated the expression of E6 RNA and inhibited transcription from the HPV early promoter, revealing a n

217 It was also observed that transcription from the hrtB promoter is reduced in a dtx

218 Transcription from the HSP70 promoter was assessed relat

219 -3 and NF-kappaB activation are required for transcription from the IFN-beta promoter.

220 a repressive Egr3/Nab1 complex that silences transcription from the ifngr1 promoter.

221 e silencing of sense and antisense germ-line transcription from the IgH D cluster and thereby influen

222 eins impart a profound deficiency to reverse transcription from the initial stages of cDNA synthesis,

223 1 through selective binding and promotion of transcription from the insulin response element site.

224 e altered motifs that led to increased viral transcription from the intact genome also greatly augmen

225 In addition, Fur repression of transcription from the irr promoter in vitro was relieve

226 Quantitative analysis of transcription from the LEE1 promoter further revealed th

227 ription template, a condition that activates transcription from the light-strand promoter (LSP) in vi

228 is necessary but not sufficient to increase transcription from the LTR.

229 in is a bifunctional regulator that inhibits transcription from the major class of bacterial promoter

230 in Escherichia coli, sigma(70), and inhibits transcription from the major class of sigma(70)-dependen

231 h the remaining HCMV-encoded GPCR results in transcription from the major immediate early promoter, t

232 frame (ORF) (UL83Stop) resulted in decreased transcription from the major immediate-early promoter in

233 atxA control region to demonstrate that atxA transcription from the major start site P1 is dependent

234 ystem, ALR-1 enhances MEC-3/UNC-86-dependent transcription from the mec-3 promoter, showing that ALR-

235 Transcription from the middle promoter, P(m), requires t

236 printing, DNase I footprinting, and in vitro transcription from the mitochondrial light-strand promot

237 ilarly impaired capability for activation of transcription from the Msx1 and Bmp4 promoters.

238 We demonstrate that transcription from the NFAT2 promoter is significantly s

239 t association that correlated with increased transcription from the noncoding first exon 1C.

240 We have shown that OmpR directly activates transcription from the omrA and omrB promoters, allowing

241 hexamer is dispensable for ExsA-independent transcription from the P(exsC) promoter and that deletio

242 y regulate fim gene expression by repressing transcription from the P(fimY) promoter, independent of

243 quitination of p53 and that p53-induced HDMX transcription from the P2 promoter can play a key role i

244 he ability of p68 to stimulate p53-dependent transcription from the p21 promoter, suggesting that Del

245 mE-dependent regulator, which stimulate gadE transcription from the P3 and P2 promoters.

246 SRSF2 did not affect transcription from the P97 promoter that controls viral

247 and also decreased HNF4alpha stimulation of transcription from the PEPCK-C gene promoter.

248 ls, IsoNAM and resveratrol failed to repress transcription from the PEPCK-C gene promoter; overexpres

249 ents examining the direct effects of PrgX on transcription from the prgQ promoter, as well as quantit

250 -repressed P(SMU.1348) resulted in increased transcription from the promoter, suggesting a role for C

251 sites, and ectopic cpxR expression activated transcription from the promoters for the RND efflux syst

252 inhibits its ability to bind to and activate transcription from the promoters of its gluconeogenic ta

253 Furthermore, RUNX3 protein represses transcription from the proximal promoter in T cells.

254 he native transcriptional regulator SoxR and transcription from the PsoxS promoter allows cell respon

255 ranscription from the RpoN promoter prevents transcription from the RpoD promoter, and the RpoN-depen

256 However, transcription from the RpoN promoter prevents transcript

257 characterize RcsB acetylation, we monitored transcription from the rprA promoter, which requires Rcs

258 he remodeler is necessary for high levels of transcription from the same promoter, and we propose tha

259 Moreover, Osr2 expression repressed the transcription from the Sema3a and Sema3d promoters in co

260 cells is sufficient to cause derepression of transcription from the SERPINB2 promoter.

261 The bEBP formed by HrpR and HrpS activates transcription from the sigma(54)-dependent hrpL promoter

262 mediates dosage compensation by upregulating transcription from the single male X chromosome approxim

263 ombination with changes in activation of SHH transcription from the Slk ZRS allele.

264 aiR binding and SaiR-dependent repression of transcription from the spxA2 promoter in vitro.

265 enes required for virion production initiate transcription from the strong P(A) promoter, which is du

266 active, sustained the latency III program of transcription from the superinfecting-virus genomes, fai

267 Here we show that variable transcription from the synthetic tetO promoter in S. cer

268 scription assay that SMU.1349 could activate transcription from the TnSmu2 operon promoter.

269 e insufficient to address the role of lncRNA transcription from the transcript which has impeded anal

270 the regulatory genes patS, hetN, and patA on transcription from the tsps were determined.

271 ssociate with A:T-rich sequences and promote transcription from the Twist promoter.

272 erences in their ability to adversely affect transcription from the two reporters.

273 revious studies suggested that Tax activates transcription from the viral long terminal repeat (LTR)

274 might alleviate this restriction by inducing transcription from the viral LTR.

275 is also important for efficient induction of transcription from the viral major immediate-early promo

276 a membrane-mediated activity that represses transcription from the viral promoter remains unexplored

277 like the full-length E2 protein, to repress transcription from the viral promoter that directs the e

278 long the C. elegans X chromosome to equalize transcription from the X between males and hermaphrodite

279 Transcription from the XMRV U3 region was stimulated up

280 allow SWI/SNF remodeling factor-independent transcription from the yeast HO promoter in vivo.

281 We also demonstrate that YtgR repressed transcription from the ytg promoter in a heterologous in

282 we show that a sequence located between, and transcription from, the divergently transcribed H3-H4 ge

283 YAP modulates transcription from these elements predominantly by regul

284 Transcription from these promoters is silenced by the hi

285 lete loss of methylation and derepression of transcription from this promoter in oocytes derived from

286 We also found that Msx1 by itself represses transcription from this proximal Bmp4 promoter, and that

287 Housekeeping sigmas direct transcription from thousands of promoters, whereas most

288 r with a sense that just about every step in transcription-from transcription initiation through to e

289 Transcription from two different start sites in the let-

290 Because of transcription from two distinct promoters, the p63 gene

291 We further show that transcription from two intragenic antisense promoters st

292 We also demonstrate calcium-dependent transcription from two regions of the IL-33 gene that co

293 also crucial for the inhibition of spurious transcription from within coding regions.

294 We found 1520 human genes that initiate transcription from within TE-derived promoter sequences.

295 -level antisense and, at lower levels, sense transcription from within the downstream D cluster, with

296 istone H3K4 methylation is connected to gene transcription from yeast to humans, but its mechanistic

297 ctive form of TbetaRI induced 15- to 25-fold transcription from Zp in gastric carcinoma AGS cells.

298 cing elements act synergistically to repress transcription from Zp, thereby tightly controlling BZLF1

299 some EBV-positive (EBV(+)) B-cell lines and transcription from Zp, with all Z(+) cells in oral hairy

300 20 to 30% of TGF-beta-mediated activation of transcription from Zp.