ライフサイエンスコーパス: transcription factor

1 scovered 30 years ago as a rapidly inducible transcription factor.

2 so pointed to an essential role of the Sox18 transcription factor.

3 r understanding of this complex multifaceted transcription factor.

4 ted protein 1 and is an activator of the YY1 transcription factor.

5 uclear signaling pathway converging on FoxO3 transcription factor.

6 the extracellular ligand Spatzle to the Dif transcription factor.

7 tion, express c-Fos, a component of the AP-1 transcription factor.

8 reading frame of ERG, encoding an ETS family transcription factor.

9 g the root-specific family of SCARECROW-Like transcription factors.

10 chromatin accessibility to lineage-specific transcription factors.

11 ences, DNA template sequences, and conserved transcription factors.

12 binding sites of the FOXA1, FOXA2 and HNF4A transcription factors.

13 tivating the protein kinase A (PKA)-targeted transcription factors.

14 n be achieved by forced expression of master transcription factors.

15 ponse to infection, including genes encoding transcription factors.

16 the expression of additional coactivators or transcription factors.

17 r consensus binding motifs for Nr4a and NFAT transcription factors.

18 ptides and vesicular release components, and transcription factors.

19 eceptor (ADORA2A) promotes hypoxia-inducible transcription factor-1 (HIF-1)-dependent endothelial cel

20 cer associate domain (TEAD) and runt-related transcription factor 2 (RUNX2) transcription factors, re

21 Activating transcription factor 3 (ATF3), an NMD target and a key s

22 fatty acids] and genetic variants in or near transcription factor 7-like 2 (TCF7L2), gastric inhibito

23 B cells expressing the T-bet transcription factor, a marker for ABCs, were generated

24 k motif where two interconnected pathways or transcription factors act in opposite directions on a ta

25 Three transcription factors act on these enhancers to determin

26 We administered lentiviral transcription factor activated luciferase/eGFP reporter

27 Smad transcription factors activated by TGF-beta or by BMP re

28 ng ERK signaling, histone modifications, and transcription factor activity, focusing on the ERK-regul

29 UPR, cleaves Xbp1 mRNA to generate a potent transcription factor adaptive toward ER stress.

30 rough which STAT3 and the Ikaros zinc finger transcription factors Aiolos and Ikaros cooperate to reg

31 cosanoid-forming enzymes as well as relevant transcription factors, allowing us to better understand

32 into "functional subsets" according to their transcription factor and cytokine profiles.

33 previously unrecognized c-di-GMP-responsive transcription factor and provide insights into the molec

34 ndently, and then simultaneously, mutating a transcription factor and the associated promoter it repr

35 The multispecific transcription factor and tumor suppressor FOXO3 is an im

36 are cognate binding sites for the identified transcription factors and are necessary and sufficient f

37 cells expressed reduced levels of B-lineage transcription factors and B cell receptor (BCR)/pre-BCR-

38 me-wide functional screen to interrogate the transcription factors and cofactors in thermogenic gene

39 e the importance of specific combinations of transcription factors and coregulators in the fine tunin

40 Proteome-wide identification of both, transcription factors and coregulators, can profoundly i

41 tification of multiple cell surface markers, transcription factors and cytokine profiles.

42 expression pattern of lung-lineage specific transcription factors and genes, which are involved in a

43 natal day 21 altered expression of genes and transcription factors and levels of proteins involved in

44 ) cell functional subsets are defined by key transcription factors and output of cytokines, such as I

45 underlying redox-regulation of AP-1 Fos/Jun transcription factors and provide structural insight for

46 markers (melan-A, microphthalmia-associated transcription factor, and SRY-related HMG-box gene 10).

47 f p38 and JNK, phosphorylation of downstream transcription factors, and overexpression of IFN-beta mR

48 Transcription factors are essential nuclear proteins tha

49 lterations in the RB-regulated E2F family of transcription factors are infrequent, casting doubt on a

50 lated by NPAS1 and NPAS3 and show that these transcription factors are master regulators of neuropsyc

51 Homeodomain and basic helix-loop-helix transcription factors are required for retinogenesis, as

52 tion, we used the Atonal family of proneural transcription factors as a model.

53 re, we show that transient expression of the transcription factors Ascl1 and Dlx2 (AD) induces the ge

54 We have shown that the transcription factor Atonal homologue 1 (Atoh1) is requi

55 me spacing and directional sliding away from transcription factor barriers.

56 on of gene expression under hypoxia requires transcription factors belonging to group VII ethylene re

57 rosophila, graded expression of the maternal transcription factor Bicoid (Bcd) provides positional in

58 attempted to determine the interplay between transcription factor binding motif evolution and GRN top

59 s by temporal expression pattern, identified transcription factor binding motifs enriched in each clu

60 Finally, by integrating transcription factor binding motifs in a machine learnin

61 on self-organizing maps with sequence-based transcription factor binding prediction led to the ident

62 a simplified integrative energy function for transcription factor binding site prediction.

63 < 1e-05) CpGs are significantly enriched for transcription factor binding sites of EBF1, EP300, and C

64 d a structure-based method for prediction of transcription factor binding sites using an integrative

65 with accessibility of key epithelial and EMT transcription factor binding sites.

66 of this fragment by promoting serum response transcription factor binding to a cryptic cis-element.

67 enriched for histone-tail modifications and transcription factor binding with particular relevance f

68 Finally, analysis of transcription factor-binding site motifs of differential

69 lly through mechanisms other than changes in transcription factor-binding sites that drive patterning

70 Here we found that the transcription factor Blimp-1 (encoded by Prdm1) represse

71 Bromodomain PHD finger transcription factor (BPTF) is the largest subunit of nu

72 PSC-CMs) were transduced with the neurogenic transcription factors Brn2, Ascl1, Myt1l and NeuroD.

73 d metabolic signalling pathways and specific transcription factors, but whether these pathways affect

74 atosis converge in the activation of the AP1 transcription factor c-JUN in the pathologic fibroblasts

75 FPP-mediated induction of the GR target, the transcription factor c-Myc (a biomarker of non-healing w

76 Meanwhile, the myeloid-specific transcription factor C/EBPalpha, usually under the contr

77 rylation and activation of the prosenescence transcription factor C/EBPbeta in primary MEFs undergoin

78 indings demonstrate that during evolution, a transcription factor can act through multiple mechanisms

79 The zinc binuclear cluster transcription factor CLR-1 is necessary for utilization

80 egulatory Factor (MyRF) is one of the master transcription factors controlling myelin formation and d

81 Furthermore, the NAC domain of these transcription factors could directly interact with an NA

82 additional genes involved in regulating this transcription factor critical for immune function.

83 SPI1 encodes PU.1, a transcription factor critical for myeloid cell developme

84 a, where Notch signals are transduced by the transcription factor CSL, called Suppressor of Hairless

85 ers, CpG island shores, binding sites of the transcription factor CTCF and brain eQTLs.

86 How transcription factor dimerization impacts DNA-binding sp

87 ctor 1 (EBF1) and paired box 5, two critical transcription factors directing B cell lineage specifica

88 Analysis of enriched transcription factor DNA-binding sites in the promoters

89 variants, of which at least six (35%) alter transcription factor-DNA binding in neuroblastoma cells.

90 icantly with those bound by the S-phase gene transcription factor E2F1.

91 We find the transcription factor early growth response 3 (EGR3) is i

92 ysosomal exocytosis by overexpression of the transcription factor EB (TFEB) gene was effective in imp

93 Because transcription factor EB (TFEB) has recently emerged as a

94 functions are transcriptionally regulated by transcription factor EB (TFEB) through the induction of

95 aloric restriction, is known to activate the transcription factor EB (TFEB), a master regulator of li

96 ranslocation of the lysosomal stress-sensing transcription factor EB and, eventually, cell death.

97 Here, we identify the zinc finger transcription factor EGR1 as a negative regulator of the

98 A different transcription factor-encoding gene, nkx1-1, is required

99 ly identified by ChIP-seq for islet-specific transcription factors, enhancer regions, and different h

100 In prostate cancer, the gene encoding the transcription factor ERG is recurrently rearranged and p

101 es phosphorylation and activation of the ETS transcription factor ERG, a prerequisite for DLL4 induct

102 es transcription of Sall4, which codes for a transcription factor essential for subsequent spermatoge

103 to disrupt a consensus binding site for the transcription factor ETS within an enhancer region.

104 The E26 transformation-specific transcription factor, ETV4, which is induced by FGF sign

105 ) signaling and then activation of adipocyte transcription factors expressed during development.

106 performed after model parameterisation with transcription factor expression values predicted that hu

107 proliferation and intracellular cytokine and transcription factor expression were assessed by means o

108 ate lymphoid cells (ILC2) share cytokine and transcription factor expression with CD4(+) Th2 cells, b

109 AP1-motifs, which bind JUN and FOS transcription factor families, were observed in MED25-oc

110 itative binding specificity models across 27 transcription factor families.

111 Members of the MiT transcription factor family are pivotal regulators of se

112 Here, we show that two Arabidopsis thaliana transcription factors, FAR1 RELATED SEQUENCE 7 (FRS7) an

113 periments on cells depleted for the Forkhead transcription factors, Fkh1 and Fkh2, previously associa

114 cation respirome in strains deficient in the transcription factors FnrP, Nnr and NarR was explored an

115 andidate haematopoietic stem-cell-specifying transcription factors for their capacity to promote mult

116 ive regulators of the light response, mainly transcription factors, for degradation.

117 reas reduced expression of the Treg cell key transcription factor forkhead box p3 (Foxp3) was observe

118 remature induction of effector genes and the transcription factors forkhead box protein O1 (Foxo1) an

119 The forkhead box transcription factor FOXC1 plays a critical role in embr

120 Here we report that a Fox family transcription factor, Foxc1, is obligate for appreciable

121 els promote the expression of the promitotic transcription factor FOXM1 (Forkhead box protein M1).

122 The oncogenic transcription factor FoxM1 plays a vital role in cell cy

123 f certain ALKBH5 target genes, including the transcription factor FOXM1.

124 nodes in the metabolic network, the forkhead transcription factor FOXO has been shown to interact wit

125 bal gene expression profiling identified the transcription factor FoxO1 as a SIRT1 target involved in

126 suppress the induction of expression of the transcription factor Foxp3 in T cells, trans-presentatio

127 The vp1 gene is positively regulated by a transcription factor from the Rgg family and its cognate

128 ntification and characterization of 175 bHLH transcription factors from apple (Malus x domestica).

129 in vitro Furthermore, SRC-2 coactivated the transcription factors GATA-binding protein 4 (GATA-4) an

130 Cytokines and transcription factor gene methylation were assessed.

131 In this study, an R2R3-MYB transcription factor gene, designated CaMYB31, was isola

132 olarity pathway, Shh/BMP signalling, and the transcription factors Grhl2/3, Pax3, Cdx2 and Zic2.

133 The transcription factor hepatocyte nuclear factor-1beta (HN

134 tors of gene expression, including other AP2 transcription factors, histone-modifying enzymes, and re

135 es suggested that Vpr degrades helicase-like transcription factor (HLTF) DNA helicase in a proteasome

136 Here we show that an HD-Zip transcription factor homologous to the LATE MERISTEM IDE

137 of structural variants, as they affect more transcription factor hubs in the tissue-specific network

138 ery endothelial cells (PAECs), expression of transcription factor hypoxia inducible factor-1alpha (HI

139 fied the prooncogenic basic helix-loop-helix transcription factor ID1 as an IRE1alpha RNase target.

140 cer located upstream of HLX (which encodes a transcription factor implicated in sprouting angiogenesi

141 roach for identification of master regulator transcription factor in a genome.

142 e find no evidence of a direct role for this transcription factor in development of this region in a

143 ification of a natural allele of a C2H2-type transcription factor in rice that confers non-race-speci

144 xperiments revealed a critical role for FOXO transcription factors in mediating these proliferative v

145 ection promoted the expression of osteogenic transcription factors in normal jaw bone MSCs.

146 e.g., top ten) in the GRN all center at some transcription factors in the context of epithelial cell

147 the present work we examine three dimers of transcription factors in the NFkappaB family: p50p50, p5

148 tly targeted Smad4, Hif1a, and Rora, all key transcription factors in the Th17 cell gene-expression p

149 oteasome activity and the expression of FOXO transcription factors in three wild-type (WT) and three

150 recruitment of DNA-binding nuclear receptors/transcription factors in trans to hot spot enhancers ser

151 in parallel, regulate the activity of stress transcription factors, including signal transducer and a

152 The inappropriate activation of transcription factors, including STATs, is known to prom

153 levels of SOX5, SOX6, and SOX21 (SOX5/6/21) transcription factors increase in stem cells of the subv

154 Thus, two enhancers integrate combinatorial transcription factor input, feedback and redundancy to g

155 ptual framework for how different classes of transcription factors interact to select and activate re

156 We found that the TCR-signal-induced transcription factor Irf4 is essential for the different

157 y hyperresponsiveness, and expression of the transcription factors IRF4 and NFAT1.

158 The p53 transcription factor is a critical barrier to pancreatic

159 Unexpectedly, the transcription factor is an ortholog of the stomatal regu

160 This 'master regulator' transcription factor is at the top of the hierarchy of t

161 Several Kruppel-like transcription factors (KLF), including KLF15, are induce

162 Induction of the transcription factor Klf4 in differentiated SMCs is esse

163 ll types including a network centered on the transcription factor KLF4.

164 ion defects that are mimicked by loss of the transcription factor KLF4.

165 that the differentiation-dependent cellular transcription factors KLF4 and BLIMP1 induce lytic EBV r

166 ion by increasing expression of two cellular transcription factors (KLF4 and BLIMP1) which cooperativ

167 lly, we found that overactivation of one key transcription factor, Klf4, which is associated with the

168 The aryl hydrocarbon receptor (AhR), a transcription factor known for mediating xenobiotic toxi

169 ver-enriched, endoplasmic reticulum-tethered transcription factor known to regulate the hepatic acute

170 The transcription factor Kruppel-like factor 2 (KLF2) is a c

171 natal anemia (Nan) mutation in the EKLF/KLF1 transcription factor leads to ectopic expression of prot

172 -fructose diet in mice and that loss of this transcription factor leads to hepatic inflammation and e

173 Thus, binding site affinity and transcription factor levels are finely tuned to regulate

174 nge from changes in protein conformation and transcription factor localization to chromosome reorgani

175 The transcription factor Meis1 drives myeloid leukemogenesis

176 caused by mutations in the gene encoding the transcription factor Methyl CpG Binding Protein 2 (MECP2

177 ooperate to bind components of the available transcription factor milieu.

178 contained the gene microphthalmia-associated transcription factor Mitf that has previously been assoc

179 Among them, microphthalmia-associated transcription factor (MITF) and paired-box 3 (PAX3) are

180 cing expression of microphthalmia-associated transcription factor (MITF), and subsequent reductions i

181 The transcription factors Msn2 and Msn4 (multicopy suppresso

182 se A (PKA) to accelerate aging by inhibiting transcription factors Msn2/4.

183 e the Arabidopsis thaliana SG2-type R2R3-MYB transcription factor MYB15 as a regulator of defense-ind

184 NAc-modified proteins at the promoter of the transcription factor MYBL1, which was also characterized

185 le pathways is necessary to activate all the transcription factors necessary for gene transcription a

186 ortex reveals enrichment of mRNAs related to transcription factors, neurogenesis, the cell cycle, and

187 andidate genes, including cell type-specific transcription factors, neurotransmitter-synthesizing enz

188 nuated activation of ERK/MAPK and the master transcription factor NF-kappaB in response to FGF and IL

189 um oscillations and the up-regulation of the transcription factor NFATc1.

190 owed that Tnc expression is repressed by the transcription factor Nkx2-1, a well-established suppress

191 rotein-protein interaction (PPI) between the transcription factor Nrf2 and its negative regulator, Ke

192 The basic leucine zipper transcription factor nuclear factor (erythroid-derived 2

193 ort that the myeloid differentiation-related transcription factor nuclear factor I-A (NFI-A) controls

194 tion potently inhibited the pro-inflammatory transcription factor nuclear factor kappaB (NF-kappaB),

195 By mapping changes in enhancer landscape and transcription factor occupancy (using ChIP-seq), we show

196 investigate the function of the pluripotency transcription factor OCT4 during human embryogenesis.

197 FOXM1 is a transcription factor of the Forkhead family that is requ

198 by the expression of GRF1 and possibly other transcription factors of the GRF family.

199 lved in neural differentiation, and that the transcription factor OLIG2 is a central node in the affe

200 Although most transcription factors operate as monomers or dimers, a f

201 olished in null mutants of the pH-responsive transcription factor PacC, and PacC proteolytic processi

202 rrelated with the expression of multiple ETS transcription factors, particularly in SDHD promoter wil

203 volving established cancer-related signaling/transcription factor pathways (for example, Wnt, TGF-bet

204 Here we describe a parasite-specific transcription factor PfAP2-I, belonging to the Apicomple

205 e, the phosphate starvation (PHO) responsive transcription factors Pho4 and Pho2 are required for gen

206 sed auxin biosynthesis, mediated by the bHLH transcription factor PHYTOCHROME-INTERACTING FACTOR 4 (P

207 Regulatory networks that include the Gata2 transcription factor play central roles in hematopoietic

208 BACH2, a B-cell-specific transcription factor, plays a critical role in oxidative

209 Zbtb16-encoded transcription factor PLZF directs the differentiation of

210 rtly by intercellular communication, and the transcription factor PqsR is a necessary component in th

211 We now show that the homeodomain-containing transcription factor Prep1 is a repressor of adipogenic

212 the major ER stress-associated proapoptotic transcription factor, protected fibroblasts from 5-aza o

213 e, it was recently shown that Tbrain, a Tbox transcription factor protein, has evolved a changed pref

214 ent RNA polymerase and intermediate and late transcription factors provided evidence for a temporal c

215 At the 1q24 locus, we hypothesized that the transcription factor PRRX1 could be a strong candidate g

216 We demonstrated that the bHLH transcription factor R1 and hexokinase HEX9 might act as

217 Pioneer transcription factors recognise and bind their target se

218 ding between nucleosome-forming histones and transcription factors regulates zebrafish genome activat

219 Additionally, transcription factors regulating lignin biosynthesis wer

220 Several transcription factors regulating pancreas lineage specif

221 fate establishment and has implications for transcription factor-related hematologic dysfunctions.

222 CarH activity as a transcription factor relies on the modulation of its oli

223 ecies Arabidopsis thaliana, the AP2-type AP2 transcription factor represents a major A-function prote

224 enes and reduces the DNA occupancy of YY1, a transcription factor required for OL maturation.

225 ific predicted basic helix-loop-helix (bHLH) transcription factor required for tapetal differentiatio

226 rage proteins, oil biosynthesis enzymes, and transcription factors, reside in genomic regions devoid

227 runt-related transcription factor 2 (RUNX2) transcription factors, respectively.

228 f TH17 cells by antagonizing the function of transcription factor RORgammat and promoted polarization

229 lls by directly repressing the expression of transcription factor Slug, a key regulator of EMT.

230 The high-mobility group box transcription factor SOX4 is the most highly expressed S

231 decreased levels of the chondrogenic master transcription factor sox9 and its downstream target, col

232 Instead, a second Wg-responsive transcription factor, SoxNeuro (SoxN), cooperates with S

233 ling, as manifested by downregulation of the transcription factor Sp1.

234 otein kinases required for activation of the transcription factor Spo0A.

235 ransition, it is antagonized by the MADS box transcription factor SQUAMOSA (SQUA).

236 endothelin receptor type B [EDNRB]), and the transcription factors SRY-box 10 (SOX10) and zinc finger

237 The hybrid transcription factor SS18:SSX alters SWItch/Sucrose Non-

238 We have found that in mice the transcription factor STAT3 protects these cells from dea

239 (HvMPK3) and MAPK substrate 1 (HvMKS1), and transcription factors such as HvERF1/5, HvNAC42, HvWRKY2

240 independent control over distinct groups of transcription factors, synergy between multiple pathways

241 , and TH17) defined by expression of the key transcription factors T-bet, GATA3, and RORgammat, respe

242 reduced expression of Th1 and Th2 associated transcription factors, Tbet and GATA3, and reduced produ

243 r hERG channels) and TBX20 (encoding for the transcription factor Tbx20) variants found by next-gener

244 ical DC (cDC) is controlled by the E protein transcription factor TCF4 (E2-2).

245 Comprehensive transcription factor (TF) annotation discovered 978 TFs

246 The transcription factor (TF) basic/Helix-Loop-Helix (bHLH)

247 Transcription factor (TF) binding of cis-elements is oft

248 Plants have significantly more transcription factor (TF) families than animals and fung

249 on and disease, yet its functional impact on transcription factor (TF) occupancy and enhancer activit

250 g the investigation of the rules that govern transcription factor (TF) occupancy.

251 The jasmonic acid (JA)-responsive AP2/ERF transcription factor (TF), ORCA3, and its regulator, CrM

252 Cis-regulatory modules contain multiple transcription factor (TF)-binding sites and integrate th

253 criptional dysregulation induced by aberrant transcription factors (TF) is a key feature of cancer, b

254 Transcription factors (TFs) are proteins that bind to sp

255 Five transcription factors (TFs) belonging to three distinct

256 Genome-wide transcription factors (TFs) binding data has been extens

257 ith the adipogenic cocktail, which activates transcription factors (TFs) glucocorticoid receptor (GR)

258 nisms that affect the binding specificity of transcription factors (TFs) is critical for understandin

259 Characterizing the binding specificities of transcription factors (TFs) is crucial to the study of g

260 Here, we describe a screen for transcription factors (TFs) that regulate the Aux/IAA ge

261 In the 25 related transcription factors (TFs), our analysis of The Cancer

262 PRDM16 is a transcription factor that activates brown fat-specific g

263 Nuclear Factor Y (NF-Y) is a heterotrimeric transcription factor that binds CCAAT elements.

264 tumor suppressor p53 is a well-characterized transcription factor that can bind gene promoters and re

265 3 tumour suppressor protein is a short-lived transcription factor that can inhibit the growth, or sti

266 TonEBP/NFAT5 is an osmo-sensitive transcription factor that controls expression of genes c

267 of compounds that bind and inhibit ToxT, the transcription factor that directly regulates the two pri

268 As a result, forkhead box O1 (FoxO1), a transcription factor that is negatively regulated by Akt

269 ing framework, we identify EOR-1 as a unique transcription factor that may regulate chromatin dynamic

270 ifferentiation 1 (Id1) is a helix-loop-helix transcription factor that plays an important role in cel

271 YTOCHROME INTERACTING FACTOR 4 (PIF4), a key transcription factor that promotes hypocotyl growth.

272 phosphorylate ICE1, a basic-helix-loop-helix transcription factor that regulates the expression of CB

273 Response gene to complement 32 (RGC32) is a transcription factor that regulates the expression of mu

274 expression of farnesoid X receptor alpha, a transcription factor that upregulates HBV transcription.

275 ing a regression approach, we identified key transcription factors that appear to drive these transcr

276 creted proteins controlled by a group of MYB transcription factors that are required for sperm releas

277 sion profiles at the tipping point indicates transcription factors that drive the state transition to

278 litating fibrotic diseases, but the critical transcription factors that maintain AT2 cell identity ar

279 and promoters, which is mediated by pioneer transcription factors that recruit activating chromatin

280 iral proteins EBNA3A, EBNA3B, and EBNA3C are transcription factors that regulate a multitude of cellu

281 istinguishing features such as gene sets and transcription factors that show different activities amo

282 vestigated whether variation in binding of a transcription factor, the vitamin D receptor (VDR), whos

283 DELLA proteins associate with transcription factors to control plant growth in respons

284 ergy metabolism by directly interacting with transcription factors to modulate gene expression.

285 se (MMP2/MMP9) expression and microphthalmia transcription factor upregulation.

286 r SmgGDS interacts with the RNA polymerase I transcription factor upstream binding factor (UBF).

287 RCD1) is one such hub, interacting with many transcription factors via their flexible IDRs.

288 The GATA2 transcription factor was identified as an upstream regul

289 3), an NMD target and a key stress-inducible transcription factor, was stabilized in a p38alpha- and

290 with non-sex-specific terminal selector-type transcription factors, whereas the sex specificity of dm

291 YTOCHROME INTERACTING FACTOR (PIF) family of transcription factors which have been shown to be involv

292 ion of the SAM pointed domain-containing ETS transcription factor, which contributes to goblet cell h

293 is agrees with the estimated number of human transcription factors, which is approximately 1400.

294 EGR1 is an early growth response zinc finger transcription factor with broad actions, including in di

295 the most ancient family of nuclear receptor transcription factors with important roles in human meta

296 min A, acts as a ligand for nuclear receptor transcription factors with more than 500 known target ge

297 ulation of two basic helix-loop-helix (bHLH) transcription factors with predicted effector binding el

298 s) and could facilitate localization of some transcription factors within regulatory CGIs, where DNA

299 this study, we describe the dual role of the transcription factor Xylanase promoter binding protein 1

300 swap-minus (dsm) mutations are functional as transcription factors yet are defective in replication o