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 Transcription from a distal NDC80 promoter directs Set1-

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

23 e deleterious effects of strong constitutive transcription from acr promoters.

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

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

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

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

28 Transcription from all three promoters was imaged in liv

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

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

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

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

33 Transcription from an FNR-dependent promoter with a cons

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

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

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

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

38 cription interference occurs when the act of transcription from an upstream promoter suppresses utili

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

40 pite inducing accumulation of HIF-1alpha and transcription from another HRE-containing promoter.

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

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

43 he cellular fitness by inhibiting intragenic transcription from AT-rich target regions, preventing th

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

45 milies to deconvolve the effect of pervasive transcription from autonomous LINE-1 activity.

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

47 sponse to BDNF-TrkB signaling, and activates transcription from BDNF promoter IV by recruiting CBP.

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

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

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

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

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

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

54 pt spacing, with interleaved and overlapping transcription from both strands, resulting in a minuscul

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

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

57 agents, could characterize residual HBV-RNA transcription from cccDNA and assist drug development an

58 agents, could characterize residual HBV RNA transcription from cccDNA, and assist new drug developme

59 A(Cnp1) chromatin assembly, Hap2 facilitates transcription from centromere DNA.

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

61 c modification that directly stimulates gene transcription from chromatin.

62 remodeling activity is required for optimal transcription from chromatin.

63 We quantified transcription from cis-regulatory elements without the i

64 Conversely, transcription from cloned promoters can interfere with p

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

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

67 and creation of new spliced exons activated transcription from cryptic promoters.

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

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

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

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

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

73 designed in silico and produced by in vitro transcription from DNA templates.

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

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

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

77 Decreasing transcription from early promoter A3 is sufficient to ma

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

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

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

81 equired during interphase to prevent ongoing transcription from eliciting a DNA damage response.

82 er control of Sox2 expression that uncouples transcription from enhancer proximity.

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

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

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

86 Transcription from H1-bound chromatin is elicited by the

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

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

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

90 Transcription from HPV chromatin requires AP-1-dependent

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

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

93 Transcription from HSP2 is also observed when HeLa cell

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

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

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

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

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

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

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

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

102 e DLP; each VP1 achieves many rounds of mRNA transcription from its associated genome segment.

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

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

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

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

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

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

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

110 MvaT and MvaU leads to increased intragenic transcription from loci directly controlled by these pro

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

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

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

114 ARMS2 transcription from minigene vectors carrying different a

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

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

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

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

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

120 vel tool to infer allele-specific effects on transcription from MPRA data.

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

122 Inhibiting exon splicing reduced transcription from nearby promoters, and creation of new

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

124 tion in cis, implying that the vPIC mediates transcription from newly replicated DNA.

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

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

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

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

129 By blocking transcription from normally cryptic promoters, Kmg restr

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

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

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

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

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

135 X-chromosome inactivation (XCI) silences transcription from one X chromosome in female mammals, o

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

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

138 5 hexamer, has no effect on ExsA-independent transcription from P(exsC).

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

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

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

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

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

144 Transcription from P3, which is indirectly activated by

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

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

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

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

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

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

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

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

153 iated HC-PFC synchrony, suggesting that Bdnf transcription from promoter IV plays a key role in HC-PF

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

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

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

157 ral bZIP transcription factor that initiates transcription from promoters of viral lytic genes.

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

159 loyed by sigma(70) family factors to enhance transcription from promoters with weak sigma4/-35 elemen

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

161 Transcription from R. sphaeroides rRNA promoters was une

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

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

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

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

166 and analyze multiple features of readthrough transcription from RNA-seq and other next-generation seq

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

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

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

170 lymerase-sigma(X) holoenzyme to help promote transcription from sigma(X)-targeted promoters.

171 combined readout of protein-DNA contact and transcription from single-cell samples.

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

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

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

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

176 on elongation machinery that enforces active transcription from target loci.

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

178 Transcription from the -271 tsp was severely downregulat

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

219 Transcription from the HSP70 promoter was assessed relat

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 ak expression is mediated by both infrequent transcription from the inverted transgene in recombinant

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

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

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

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

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

231 of pUS28 at the time of infection represses transcription from the major immediate early promoter (M

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

253 terial RNA polymerase engaged in reiterative transcription from the pyrG promoter, which contains eig

254 tributions, which reflects mRNAs obtained by transcription from the repressor-bound and repressor-fre

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 It activates transcription from the rrn promoter by both the housekee

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

279 Approaches that force HIV transcription from these cells, making them susceptible

280 YAP modulates transcription from these elements predominantly by regul

281 Transcription from these promoters is silenced by the hi

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

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

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

285 onsense mutation that completely dissociated transcription from translation.

286 uring which chromatin condensation decouples transcription from translation.

287 Transcription from two different start sites in the let-

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

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

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

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

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

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

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

295 FG-4592 also failed to activate transcription from Zp in a reporter assay despite induci

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

297 Likewise, HIF-1alpha failed to activate transcription from Zp when p53 was knocked out by CRISPR

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.