ライフサイエンスコーパス: TFIIH

1 TFIIH consists of a core that includes the DNA helicase

2 TFIIH contains three enzymatic functions and over 30 con

3 TFIIH DNA helicases, XPB and XPD, are also components in

4 TFIIH harbors mutations in two rare genetic disorders, t

5 TFIIH has been implicated in several fundamental cellula

6 TFIIH is a 10-subunit RNA polymerase II basal transcript

7 TFIIH is essential for both RNA polymerase II transcript

8 TFIIH is indispensable for nucleotide excision repair (N

9 TFIIH, whose recruitment to the PIC is known to be facil

10 ven-nineteen lysine-rich leukemia (ELL) as a TFIIH partner.

11 s with only the larger being identified as a TFIIH subunit in T. brucei.

12 merase II and transcript release occurs in a TFIIH-deficient repair extract but not in a reconstitute

13 lly associates with active Pol II genes in a TFIIH-dependent manner and travels across the gene with

14 g into three mechanistic classes that affect TFIIH helicase functions, protein interactions and inter

15 omplexity resulting from mutations affecting TFIIH has been attributed to the nucleotide excision rep

16 al interactions with DNA, RAD23B, CETN2, and TFIIH, whereas functional roles have not yet been assign

17 to a 'cradle' that may position the CTD and TFIIH kinase to stimulate Pol II phosphorylation.

18 However, RNA polymerase II and TFIIH are generally not recruited, and nucleosomes are n

19 TATA-binding protein, RNA polymerase II, and TFIIH are not a component of the TFIIB complex.

20 rast to Sir2, Tup1 prevents TBP, Pol II, and TFIIH recruitment to the HMLalpha1 promoter, thereby abr

21 ion of the cells by TNF-alpha, NF-kappaB and TFIIH are rapidly recruited to the promoter together wit

22 se functional interplay between Mediator and TFIIH in the early stages of PIC development.

23 e role of the Srb8-11 complex, Mediator, and TFIIH, in CTD-dependent basal transcription by either mu

24 anscription, nucleotide excision repair, and TFIIH functional assembly.

25 y upon subsequent association of SWI/SNF and TFIIH with the promoter.

26 at of the general initiation factors TBP and TFIIH, occurs unimpeded to the silent HMRa1 and HMLalpha

27 transcription factors TBP, TFIIA, TFIIB and TFIIH and showed that these factors are essential for in

28 ivergent orthologs of TBP, TFIIA, TFIIB, and TFIIH which, together with the small nuclear RNA-activat

29 he size and complexity of Pol II, TFIID, and TFIIH have precluded their reconstitution from heterolog

30 TFIIE and TFIIH are essential for the promoter opening and escape

31 TBP, TFIIA, TFIIB, Pol II, TFIIF, TFIIE and TFIIH onto promoter DNA using cryo-electron microscopy.

32 o reactions just before this step, TFIIE and TFIIH overcame the requirement for negative superhelicit

33 zed components of the PIC, such as TFIIE and TFIIH, and segments of TFIIA, TFIIB and TFIIF.

34 , preventing stable association of TFIIE and TFIIH, and thus blocks the initiation of mRNA synthesis.

35 equiring negative superhelicity or TFIIE and TFIIH.

36 ive superhelicity or the action of TFIIE and TFIIH.

37 ctors TFIID, TFIIA, TFIIB, TFIIF, TFIIE, and TFIIH.

38 (GTFs; TFIIA, TFIIB, TBP, TFIIE, TFIIF, and TFIIH) and escapes the promoter, but many of the mechani

39 sites of interaction with TFIIE, TFIIF, and TFIIH, serving to define their roles in the transcriptio

40 low intact TFIIE to bind and recruit XPB and TFIIH to form the pre-initiation complex.

41 d for the recruitment of NER factors XPC and TFIIH to UV-induced DNA damage sites.

42 Positive Transcription Elongation Factor b), TFIIH, TFIIF, and FACT (Facilitates Chromatin Transcript

43 esting that a cross-talk might exist between TFIIH and a component of a chromatin remodeler complex i

44 Trypanosoma brucei TFIIH harbours all core complex components and is indisp

45 ally, the CAK module inhibits DNA binding by TFIIH and thereby enhances XPC-dependent specific recrui

46 signaling deficiency, which can be caused by TFIIH impairment as well as by other mechanisms, results

47 bsequent scanning downstream, also driven by TFIIH, which requires displacement of the initial bubble

48 tion initiation process: bubble formation by TFIIH, which fills the Pol II active center with single-

49 strate for SCP1 is RNAP II phosphorylated by TFIIH.

50 ided by the kinetic proofreading provided by TFIIH, form a high-specificity complex at the damage sit

51 apid reinitiation and perhaps also to bypass TFIIH-dependent promoter melting; this open state would

52 as part of the transcription/repair complex TFIIH, cause three distinct phenotypes: cancer-prone xer

53 7, a subunit of the evolutionarily conserved TFIIH complex, is a Ser7 kinase.

54 In contrast, TFIIH CTD kinase has a pronounced preference for RNAPII

55 otential molecular switch that might control TFIIH composition and play a key role in the conversion

56 ion of a new, evolutionarily conserved, core TFIIH subunit is essential for our understanding of TFII

57 and, like strains carrying mutations in core TFIIH subunits, are sensitive to ultraviolet radiation.

58 s19 mutant cells, protein levels of the core TFIIH component Rad3 (XPD homologue) and Ssl2 (XPB homol

59 ty, Tfb5 was found to interact with the core TFIIH subunit Tfb2, but not with other NER proteins.

60 r conferring structural rigidity to the core TFIIH such that the complex is maintained in its functio

61 es an essential helicase subunit of the core TFIIH transcription initiation and DNA repairosome compl

62 he other four essential subunits of the core TFIIH, Tfb1, Tfb2, Ssl1, and Tfb4, and the TFIIK subunit

63 e kinase can be inhibited without disrupting TFIIH.

64 Here we show that the Drosophila TFIIH component Xpd negatively regulates the cell cycle

65 in a mutually exclusive fashion with either TFIIH or the CIA targeting complex.

66 ts in enhanced basal transcription, enhanced TFIIH phosphorylation of the CTD, as well as binding of

67 The basal factor TFIIH can phosphorylate Ser-7 in vitro and is necessary

68 dicated translocase/helicase encoding factor TFIIH.

69 odule of the transcription initiation factor TFIIH.

70 case subunit of transcription and NER factor TFIIH.

71 f the transcription initiation/repair factor TFIIH in this nucleosome.

72 the XPB subunit of the transcription factor TFIIH and initiation of RNA polymerase II mediated trans

73 ve identified the basal transcription factor TFIIH as the potential target for ubiquitination.

74 winding mediated by the transcription factor TFIIH helicase-related subunit XPB/Ssl2.

75 we show that the basal transcription factor TFIIH is constitutively recruited by ER-Y537S, resulting

76 isubunit DNA repair and transcription factor TFIIH maintains an intricate cross-talk with different f

77 Basal transcription factor TFIIH phosphorylates the RNA polymerase II (RNApII) carb

78 bunit of the DNA repair/transcription factor TFIIH result in distinct clinical entities, including th

79 e assembly of the basal transcription factor TFIIH through sequestration of its p44 subunit.

80 ase activity of general transcription factor TFIIH, and subsequent CTD phosphorylation is involved in

81 components of the basal transcription factor TFIIH, and these mutations lead to impaired nucleotide e

82 gest subunit of general transcription factor TFIIH, and to cause degradation of the largest subunit R

83 complemented by the NER/transcription factor TFIIH, but not by purified Mms19 protein.

84 ore form of the general transcription factor TFIIH, containing the helicases XPB, XPD and five 'struc

85 ), a component of human transcription factor TFIIH, in both B lymphocytes and epithelial cells, we hy

86 bunit of the eukaryotic transcription factor TFIIH, is essential for both initiation of transcription

87 General transcription factor TFIIH, previously described as a 10-subunit complex, is

88 integral subunit of the transcription factor TFIIH, which plays a dual role in DNA opening at RNA pol

89 erminal domain (CTD) as transcription factor TFIIH-bound CAK.

90 Ss and the host general transcription factor TFIIH.

91 a subunit of the basal transcription factor TFIIH.

92 activity of the general transcription factor TFIIH.

93 a module of the general transcription factor TFIIH.

94 subunit of the general transcription factor TFIIH.

95 interact with general transcriptional factor TFIIH, a known inducer of ER transactivation.

96 chromatin in complex with the repair factors TFIIH and XPG.

97 F7 interacts with the transcription factors, TFIIH and P-TEFb, resulting in the inhibition of their P

98 pological regions" that function as hubs for TFIIH assembly and more than 35 conserved topological fe

99 the Ssl1-Tfb4 Ring domains are important for TFIIH assembly.

100 of TCR proteins and reveal the mechanism for TFIIH recruitment to DNA damage-stalled RNAPIIo to initi

101 CTD phosphorylation previously reported for TFIIH is also observed with CTDK1 kinase.

102 Consistent with a new role for TFIIH at 3' ends, it was detected within genes and 3'-fl

103 uggest that once the open complex is formed, TFIIH decays into an inactive configuration in the absen

104 Conversely, only four TFIIH subunits have been identified in T. brucei.

105 Tfb6 dissociates from TFIIH as a heterodimer with the Ssl2 subunit, a DNA heli

106 cription and implicate CAK dissociation from TFIIH as essential for kinase activation.

107 Release of excision products from TFIIH requires ATP but not ATP hydrolysis, and release o

108 Excised oligonucleotides released from TFIIH then become bound by the single-stranded binding p

109 Tfb6 does not, however, dissociate Ssl2 from TFIIH in the context of a fully assembled transcription

110 hat removal of the kinase complex TFIIK from TFIIH shifts the TSS in a yeast system upstream to the l

111 Furthermore, TFIIH and recombinant Cdk7-CycH-Mat1 as well as recombin

112 The general transcription factor II H (TFIIH) is a major actor of both nucleotide excision repa

113 with the general transcription factor II H (TFIIH) it activates RNA polymerase II by hyperphosphoryl

114 NA repair factor, transcription factor II H (TFIIH) that catalyzes the unwinding of a damaged DNA dup

115 As a component of transcription factor II H (TFIIH), XPD is involved in DNA unwinding during nucleoti

116 K subunits Tfb3, Kin28, and Ccl1 of the holo TFIIH were not much affected by Mms19.

117 phorylation of the CTD of RNA pol II by holo-TFIIH in vitro.

118 bunit of the basal transcription factor holo-TFIIH and its trimeric sub-complex TFIIK.

119 it Med4 in an assay, including purified holo-TFIIH, and either Mediator or recombinant Med4 alone.

120 standing discrepancy between yeast and human TFIIH complexes.

121 olecular structures of trypanosome and human TFIIH.

122 cryo-electron microscopy structure of human TFIIH at 4.4 A resolution.

123 The function of human TFIIH-associated Cdk7 in RNA polymerase II (Pol II) tran

124 We demonstrate that the human TFIIH complex proteins XPB (ERCC3) and XPD (ERCC2) play

125 present the complete structure of the human TFIIH core complex, determined by phase-plate cryo-elect

126 Conserved from yeast to humans, TFIIH is essential for RNA polymerase II transcription a

127 indicates that the data can be explained if TFIIH integrates inputs from multiple signals, regulatin

128 ymerase II general transcription factor IIH (TFIIH) by affinity purification, by peptide sequence ana

129 General transcription factor IIH (TFIIH) consists of nine subunits: cyclin-dependent kinas

130 Transcription factor IIH (TFIIH) is a heterodecameric protein complex critical for

131 Transcription factor IIH (TFIIH) is a multiprotein complex involved in both transc

132 Transcription factor IIH (TFIIH) is essential for both transcription and nucleotid

133 The general transcription factor IIH (TFIIH) is held at promoters prior to promoter escape and

134 Human transcription factor IIH (TFIIH) is part of the general transcriptional machinery

135 a component of the transcription factor IIH (TFIIH) transcription complex and plays essential roles i

136 complex, including transcription factor IIH (TFIIH), is recruited are largely unknown.

137 is a component of transcription factor IIH (TFIIH), which functions in transcription initiation and

138 n overlap with the transcription factor IIH (TFIIH)-dependent serine 5 phosphorylation events during

139 and repair factor, Transcription Factor IIH (TFIIH).

140 e basal transcription/DNA repair factor IIH (TFIIH).

141 xpected to cause framework defects impacting TFIIH integrity.

142 elements typically having severe defects in TFIIH subunit association.

143 nating a network of interactions involved in TFIIH assembly and regulation of its activities.

144 anscription and DNA repair, and mutations in TFIIH can result in human disease.

145 g entity that enhances damage recognition in TFIIH.

146 anscription pre-initiation complex including TFIIH.

147 1 N-terminal extension (NTE) domain inhibits TFIIH function without affecting subunit association.

148 CIA targeting complex before assembling into TFIIH.

149 assembly and prevents XPD incorporation into TFIIH.

150 n ATP hydrolysis-dependent process involving TFIIH creates access to the junction, allowing incision.

151 ranscriptional program, possibly through its TFIIH-associated kinase function.

152 add up to a molecular mass of about 500 kDa, TFIIH is also essential for nucleotide excision repair.

153 complementation group B [XPB]), the largest TFIIH subunit, with the same cells functionally compleme

154 of the +1 nucleosome, the combination of low TFIIH occupancy and high occupancy of the transcription

155 In yeast and metazoans, TFIIH is composed of a core of seven conserved subunits

156 In XPB cells carrying mutant TFIIH, loop formation failed and the serum response was

157 the DNA helicase subunit XPD/Rad3 in native TFIIH and is required for the integrity and function of

158 fied and biochemically characterized a novel TFIIH-associated protein complex in T. brucei (Med-T) co

159 In the absence of TFIIH the trimeric complex phosphorylates the T-loop of

160 clude that the recruitment and activation of TFIIH represents a rate-limiting step for the emergence

161 In transcription, the helicase activity of TFIIH functions to melt promoter DNA; however, the in vi

162 We find that the kinase activity of TFIIH is critical for the phosphorylation of TFIIB serin

163 the in vitro basal transcription activity of TFIIH itself and impeding the efficient recruitment of t

164 suggesting that the E3 Ub ligase activity of TFIIH mediates the transcriptional response to DNA damag

165 he Ssl2 and DNA-dependent ATPase activity of TFIIH suggests that Ssl2 has a processivity of approxima

166 d the nucleotide excision repair activity of TFIIH.

167 ility to compensate for a limiting amount of TFIIH activity in extracts.

168 nly partial insight into the architecture of TFIIH and its interactions within transcription pre-init

169 he structure uncovers the molecular basis of TFIIH assembly, revealing how the recruitment of XPB by

170 Our understanding of the biochemistry of TFIIH has greatly benefited from studies focused on dise

171 ift analyses of PICs and characterization of TFIIH preparations carrying mutant XPB translocase subun

172 As a component of TFIIH, Cdk7 phosphorylates serines 5 and 7 of the carbox

173 his picture, the key catalytic components of TFIIH, the Ssl2 ATPase/helicase and the Kin28 protein ki

174 eincision complex (PInC) further composed of TFIIH, XPA, RPA, XPG, and ERCC1-XPF.

175 ion and play a key role in the conversion of TFIIH from a factor active in transcription to a factor

176 The dependence of TFIIH-CAK on sequence-specific MITF and c-MYC constitute

177 C2-targeted genes are specifically devoid of TFIIH, known to phosphorylate RNA polymerase II (RNAPII)

178 Significantly, the promoter is devoid of TFIIH.

179 ns nor does it provoke the disassociation of TFIIH from gene promoters.

180 n TC-NER is modulated by the distribution of TFIIH and Spt4/Spt5 in transcribed chromatin and Rad26 m

181 Our meta-analysis revealed downregulation of TFIIH subunits in preeclamptic placentas.

182 insight into the conformational dynamics of TFIIH and the regulation of its activity.

183 ansactivation of GTF2H1 as a core element of TFIIH.

184 suggesting that the specific enhancement of TFIIH kinase activity results in Kin28 being the primary

185 an ssl2 mutant, encoding an altered form of TFIIH, as a suppressor of the cold-sensitive growth defe

186 ontinuous ATP hydrolysis and the function of TFIIH in promoter escape.

187 in maintaining the integrity and function of TFIIH.

188 s required for the integrity and function of TFIIH.

189 lead us to conclude that other functions of TFIIH, rather than the kinase activity, are critical for

190 hiodystrophy, highlighting the importance of TFIIH for cellular physiology.

191 etailed time courses show that the levels of TFIIH at the promoter fluctuate in parallel with NF-kapp

192 the RNAP II CTD by the CDK7 kinase module of TFIIH.

193 has been isolated as a breakdown product of TFIIH.

194 and is required for efficient recruitment of TFIIH to a promoter.

195 hances XPC-dependent specific recruitment of TFIIH.

196 preeclampsia and delineate the relevance of TFIIH, providing etiologic clues which could eventually

197 To investigate the role of TFIIH during HIV reactivation in vivo, we developed a po

198 This review aims to depict the structure of TFIIH and to dissect the roles of its subunits in differ

199 in-dependent activating kinase subcomplex of TFIIH).

200 and how the core and kinase subcomplexes of TFIIH are connected.

201 ysically interacts with the Dmp52 subunit of TFIIH and co-localizes with TFIIH in the chromatin.

202 co-factor that can assist the XPB subunit of TFIIH during transcription initiation and the transition

203 The p8 subunit of TFIIH maintains the basal levels of the complex by inter

204 The Cdk7 subunit of TFIIH phosphorylates RNA polymerase II (Pol II) during i

205 roteasomal degradation of the XPB subunit of TFIIH, and concurrently suppresses acute HIV infection i

206 s in ERCC2, which encodes the XPD subunit of TFIIH, but not in XP cells with ERCC2 mutations.

207 As the kinase subunit of TFIIH, Cdk7 participates in basal transcription by phosp

208 XPB, a subunit of TFIIH, contains an ATP-dependent helicase activity that

209 vivo function of the Cdk7 kinase subunit of TFIIH, which has been hypothesized to be involved in RNA

210 t cell proteins that bind the p62 subunit of TFIIH.

211 OmegaXaV motif in NSs and the p62 subunit of TFIIH.

212 ed in the degradation of Rad25, a subunit of TFIIH.

213 rm a complex with cdk and cyclin subunits of TFIIH.

214 This revises our understanding of TFIIH and prompts investigation into the core subunits f

215 ubunit is essential for our understanding of TFIIH function in transcription, DNA repair and human di

216 e counterbalancing forces of two proteins on TFIIH--the FUSE binding protein (FBP) and the FBP-intera

217 pite the absence of multiple Mediator and/or TFIIH interactions with polymerase.

218 is important for association with many other TFIIH subunits.

219 Unlike other TFIIH subunits, Tfb5 is not essential for cell survival.

220 binant CDK8 subcomplex identifies predicted (TFIIH and RNA polymerase II C-terminal domain [Pol II CT

221 long with Cockayne syndrome group B protein, TFIIH, and other BER proteins.

222 Here, we characterize the first protistan TFIIH which was purified in its transcriptionally active

223 uence transcription by oppositely regulating TFIIH at the promoter site.

224 rmed on premelted (bubble) templates require TFIIH for effective transcript elongation to +20.

225 CTD phosphorylation by the serine 5-specific TFIIH complex, or its kinase module TFIIK, is indeed suf

226 tion sites of these promoters and stimulates TFIIH binding in an MBII-dependent manner.

227 CDK7 associates with the 10-subunit TFIIH complex and regulates transcription by phosphoryla

228 The seven-subunit TFIIH core complex formed by XPB, XPD, p62, p52, p44, p3

229 have prepared homogeneous human ten-subunit TFIIH and its seven-subunit core (Core7) without the CAK

230 ructure analysis of purified Med-T and Med-T/TFIIH complexes by electron microscopy revealed that Med

231 f Rad14p facilitates the recruitment of TBP, TFIIH, and RNA polymerase II to the GAL1 promoter.

232 her transcription factors, including P-TEFb, TFIIH, and CIITA, ensuring an orderly progression in tra

233 that govern Pol II initiation (e.g., TFIID, TFIIH, and Mediator), pausing, and elongation (e.g., DSI

234 neral transcription factors including TFIIF, TFIIH and Mediator.

235 TFIIA, TFIIB, TFIID (or TBP), TFIIE, TFIIF, TFIIH and TFIIK were positioned within promoters and exc

236 contains TFIIA, TFIIB, TFIID, TFIIE, TFIIF, TFIIH, RNAPII, and Mediator.

237 We further demonstrate that TFIIH restricts CDK7 kinase function to the RNAPII CTD,

238 Furthermore, we provide evidence that TFIIH associates with the elongation complex much longer

239 these disorders and underline the fact that TFIIH can be considered a promising target for therapeut

240 We propose that TFIIH primes the CTD and promotes recruitment of P-TEFb/

241 These observations suggest that TFIIH phosphorylation of the CTD causes Mediator dissoci

242 G and CSB in TCR initiation and suggest that TFIIH-dependent remodeling of stalled RNAPII without rel

243 The TFIIH core complex is sufficient for its repair function

244 The TFIIH general transcription factor facilitates transcrip

245 The TFIIH-associated kinase Cdk7/Kin28 hyperphosphorylates t

246 way through its interaction with CSA and the TFIIH complex.

247 This inactivation is not caused by the TFIIH kinase activity, the loss of transcription factors

248 hosphorylation of Serine 118 (Ser118) by the TFIIH kinase, cyclin-dependent kinase (CDK)7.

249 d by three kinetic proofreading steps by the TFIIH transcription/repair factor.

250 TP-independent despite a requirement for the TFIIH DNA translocase subunit Ssl2.

251 ides with the end of the requirement for the TFIIH helicase for efficient transcript elongation.

252 Taken together, our results implicate the TFIIH kinase in placing bivalent Ser5 and Ser7 marks ear

253 Mutations in the TFIIH subunits XPB, XPD, and p8 lead to severe premature

254 F results in consecutive loss of CDK7 in the TFIIH-CAK subcomplex.

255 During transcription initiation, the TFIIH-kinase Kin28/Cdk7 marks RNA polymerase II (Pol II)

256 Depletion of Kin28, the TFIIH subunit that phosphorylates the CTD, does not affe

257 Moreover, the TFIIH factor, XPD, occupies a central role in triggering

258 To define their functions, we mutated the TFIIH-associated kinase Mcs6 and P-TEFb homologs Cdk9 an

259 also regulates transcription as part of the TFIIH basal transcription factor, is an attractive targe

260 NA repair, but only one other subunit of the TFIIH complex, the 5'-3' helicase XPD, has been identifi

261 ng an adequate cellular concentration of the TFIIH component Rad3 and suggest that Mms19 has distinct

262 re reveals the molecular architecture of the TFIIH core complex, the detailed structures of its const

263 lexes, combined with the localization of the TFIIH helicases XPD and XPB, support a DNA translocation

264 ates from the enhancer upon depletion of the TFIIH kinase.

265 KR, NSs also promotes the degradation of the TFIIH subunit p62.

266 We also revealed that the recruitment of the TFIIH subunit TTDA, involved in trichothiodystrophy grou

267 Mutation of CSB, CSA, or the TFIIH helicases XPB and XPD can also cause defective TCR

268 at UVSSA is the key factor that recruits the TFIIH complex in a manner that is stimulated by CSB and

269 Set1 association depends upon the TFIIH-associated kinase that phosphorylates the Pol II C

270 ted that the ATM protein interacted with the TFIIH basal transcription factor and the XPG protein of

271 VFV NSs protein is able to interact with the TFIIH subunit p62 inside infected cells and promotes its

272 ested the function of these regions in three TFIIH core module subunits, i.e., Ssl1, Tfb4, and Tfb2,

273 which induces c-MYC pulse regulation through TFIIH, and experimental depletion of MITF results in con

274 ressor (FIR) regulates transcription through TFIIH, these components have been speculated to be the m

275 hydrolysis, suggesting that it is coupled to TFIIH's established promoter melting activity.

276 TFIIE-p62 interactions that link core-PIC to TFIIH.

277 from studies focused on diseases related to TFIIH mutations.

278 Accordingly, characterization of trypanosome TFIIH did not identify a kinase component.

279 uent between the two structures, trypanosome TFIIH lacked the knob-like CAK moiety and exhibited extr

280 YC promoter when far upstream element is via TFIIH helicase activity early in the transcription cycle

281 We find that under conditions when TFIIH is not normally required for transcription, Mediat

282 th TFIIH occurs largely in the nucleus where TFIIH functions.

283 g that of the tfb1-101 mutant cells in which TFIIH activity is compromised but not eliminated.

284 the cytoplasm, whereas its association with TFIIH occurs largely in the nucleus where TFIIH function

285 FBP1 collaborates with TFIIH and additional transcription factors for optimal t

286 opurifies from yeast whole-cell extract with TFIIH, the largest general transcription factor required

287 Via interactions with TFIIH and FBP-interacting repressor (FIR), FBP modulates

288 Dmp52 subunit of TFIIH and co-localizes with TFIIH in the chromatin.

289 stablished a dynamically remodeled loop with TFIIH at the P2 promoter.

290 Together with TFIIH subunits cyclin H and Mat1, Cdk7 kinase is also fo

291 nregulating the XPD helicase activity within TFIIH.

292 han 35 conserved topological features within TFIIH, illuminating a network of interactions involved i

293 erase II (pol II) requires a helicase within TFIIH to generate the unpaired template strand.

294 the small molecule triptolide (TPL), an XPB/TFIIH inhibitor, to block transcriptional initiation and

295 lesion verification mechanism involving XPC, TFIIH, and XPA for efficient NER.

296 tide excision repair factors (RPA, XPA, XPC, TFIIH, XPG, and XPF-ERCC1), core DNA damage checkpoint p

297 , in addition to damaged DNA, RPA, XPA, XPC, TFIIH, XPG, XPF-ERCC1, ATR-ATRIP, TopBP1, and EXO1 const

298 he molecular architecture of human and yeast TFIIH by an integrative approach using chemical crosslin

299 Structures of complete 10-subunit yeast TFIIH and of a nested set of subcomplexes, containing 5,

300 Here we show that yeast TFIIH contains an Ssl2-dependent double-stranded DNA tra