ライフサイエンスコーパス: P-TEFb

1 P-TEFb (CDK9/cyclin T) plays a central role in androgen

2 P-TEFb activation classically occurs by a feedback-regul

3 P-TEFb activity is dependent on phosphorylation of Thr18

4 P-TEFb comprises the Cdk9 cyclin-dependent kinase and a

5 P-TEFb, a cellular kinase composed of Cyclin T1 and CDK9

6 P-TEFb-mediated phosphorylation of Spt5, NELF-A and NELF

7 eactivities, confirming that 7SK undergoes a P-TEFb-dependent structural change.

8 inhibitor Hexim1 from the snRNP and activate P-TEFb, thereby uncoupling Tat requirements for kinase a

9 P-TEFb, but it is not sufficient to activate P-TEFb-dependent transcription of the HIV LTR.

10 n inhibitor of the transcriptional activator P-TEFb.

11 suggest that SEC is a major class of active P-TEFb-containing complexes required for transcriptional

12 rol by regulating the availability of active P-TEFb.

13 izing ELL2 in a process that requires active P-TEFb.

14 ition occurs via sequestration of the active P-TEFb kinase complex (CDK 9 and Cyclin T1/T2a/b or K) t

15 ween the inactive P-TEFb pool and the active P-TEFb pool and thereby stimulate proviral reactivation.

16 with AF9 and does not interact with AF9*AF4*P-TEFb complexes.

17 ough the bridging functions of Tat and AFF4, P-TEFb and ELL2 combine to form a bifunctional elongatio

18 re recruited to this proximal promoter after P-TEFb release and were required for its transcriptional

19 ow divergent polymerases are regulated after P-TEFb recruitment with uaRNA levels controlled by the e

20 ity and determine if scaffold binding alters P-TEFb conformation, we determined the structure of a tr

21 These findings reveal cooperativity among P-TEFb, PAF1C, and CDK12 in pausing release and Pol II C

22 ion (ChIP) assays demonstrated that Brd4 and P-TEFb are associated with the basal HTLV-1 LTR, while T

23 We found that BRD4 and P-TEFb, although not present prior to IFN treatment, wer

24 c histone chaperone, independent of BRD4 and P-TEFb.

25 s TFIID for complexes containing ELL/EAF and P-TEFb to facilitate transition of Pol II into the elong

26 even-nineteen lysine-rich leukemia (ELL) and P-TEFb.

27 DSIF (DRB sensitivity-inducing factor)--and P-TEFb (positive elongation factor b), which is the key

28 nteract with 7SK independently of HEXIM1 and P-TEFb.

29 ruitment resolves from RNA polymerase II and P-TEFb, and these factors resolve from Spt6 and Topo I.

30 phosphorylation events during initiation and P-TEFb (positive transcriptional elongation factor b) ev

31 tiviral immunity in insects because NELF and P-TEFb are required to restrict viral replication in adu

32 also recruit RNA polymerase II (RNAPII) and P-TEFb.

33 used by retroviral TAR RNA to engage Tat and P-TEFb.

34 ted with the basal HTLV-1 LTR, while Tax and P-TEFb are associated with the activated template.

35 Stably associated P-TEFb was highly inhibited, but could still be released

36 This interaction attracted P-TEFb, thereby mobilizing downstream transcriptional el

37 unit of positive transcription elongation b (P-TEFb).

38 positive transcription elongation factor b (P-TEFb) activation mechanism that is known to drive adul

39 positive transcription elongation factor b (P-TEFb) and facilitated transcriptional elongation.

40 positive transcription elongation factor b (P-TEFb) complex and influences global RNA polymerase II

41 positive transcription elongation factor b (P-TEFb) complex, as a pivotal regulator of skeletal musc

42 positive transcription elongation factor b (P-TEFb) directly regulates the initial recruitment of PA

43 positive transcription elongation factor b (P-TEFb) exists in two forms in cells as follows: an inac

44 positive transcription elongation factor b (P-TEFb) from its inhibitory 7SK snRNP.

45 positive transcription elongation factor b (P-TEFb) from the 7SK snRNP in a manner that is dependent

46 positive transcription elongation factor b (P-TEFb) in association with bromodomain-containing prote

47 positive transcription elongation factor b (P-TEFb) in the establishment of latent infection in HPCs

48 -positive transcription elongation factor b (P-TEFb) interaction allowed for localization of the P-TE

49 positive transcription elongation factor b (P-TEFb) involved in the release of "paused" RNA polymera

50 positive transcription elongation factor b (P-TEFb) is a key cellular transcription factor critical

51 positive transcription elongation factor b (P-TEFb) is involved in physiological and pathological ev

52 positive transcription elongation factor b (P-TEFb) is the critical kinase for transcription elongat

53 positive transcription elongation factor b (P-TEFb) kinase was not increased.

54 positive transcription elongation factor b (P-TEFb) of RNA polymerase II (RNAPII).

55 positive transcription elongation factor b (P-TEFb) phosphorylates RNA polymerase II and regulatory

56 positive transcription elongation factor b (P-TEFb) plays a central role in determining the state of

57 Positive transcription elongation factor b (P-TEFb) plays an important role in stimulating RNA polym

58 positive transcription elongation factor b (P-TEFb) promotes transcription elongation through phosph

59 positive transcription elongation factor b (P-TEFb) recruitment are detected immediately after the a

60 positive transcription elongation factor b (P-TEFb) regulates RNA polymerase II elongation.

61 positive transcription elongation factor b (P-TEFb) to phosphorylate and activate this paused polyme

62 Positive transcription elongation factor b (P-TEFb), a complex of Cdk9 and cyclin T1, promotes relea

63 positive transcription elongation factor b (P-TEFb), an essential eukaryotic mRNA transcription fact

64 positive transcription elongation factor b (P-TEFb), and potentiates its transcriptional activity.

65 positive transcription elongation factor b (P-TEFb), comprised of cyclin-dependent kinase 9 (CDK9) a

66 positive transcription elongation factor b (P-TEFb), to target gene promoters, enhancing transcripti

67 positive transcription elongation factor b (P-TEFb), which is composed of CycT1 or CycT2 and CDK9, a

68 positive transcription elongation factor b (P-TEFb), which regulates the transcription elongation of

69 I (Pol II) and positive elongation factor b (P-TEFb), which releases paused Pol II to produce full-le

70 positive transcription elongation factor b (P-TEFb).

71 positive transcription elongation factor b (P-TEFb).

72 positive transcription elongation factor b (P-TEFb).

73 positive transcription elongation factor b (P-TEFb, a complex of CDK9 and cyclin T), we examined whe

74 Because P-TEFb is required for the transition from initiation to

75 Besides P-TEFb, BRD4 binds to acetylated histones through the br

76 Here, we define a novel interaction between P-TEFb and BRD4 involving tri-acetylated cyclin T1 (acK3

77 ntation assay to detect interactions between P-TEFb and its substrate, the C-terminal domain of RNA p

78 on, we investigated the relationship between P-TEFb and histone H1.

79 ns, the second bromodomain and the PID, bind P-TEFb and are required for full transcriptional activat

80 y distinct steps in gene expression: binding P-TEFb and promoting P-TEFb phosphorylation of the C-ter

81 This dual binding activity of PPM1G blocks P-TEFb reassembly onto the snRNP to sustain NF-kappaB-me

82 Both P-TEFb recruitment to the HIV long terminal repeat and e

83 tly increased levels of free P-TEFb and BRD4.P-TEFb and SEC.P-TEFb complexes in cells.

84 thereby constructing an activated Twist/BRD4/P-TEFb/RNA-Pol II complex at the WNT5A promoter and enha

85 ed for release into productive elongation by P-TEFb.

86 mutant H1.1 that cannot be phosphorylated by P-TEFb also disrupts Tat transactivation in an HIV repor

87 ine the mechanism of scaffold recognition by P-TEFb and reveal an unanticipated intersubunit pocket o

88 CDK7, CDK9 (P-TEFb), and CDK13 are also critical for HIV replication

89 In growing cells, P-TEFb exists in active and inactive forms.

90 In cells, P-TEFb exists in active and inactive forms.

91 In cells, P-TEFb partitions between small active and larger inacti

92 scription elongation activators/coactivators P-TEFb, ELL2, AFF4/1, ENL, and AF9, is recruited by HIV-

93 he positive transcription-elongation complex P-TEFb and thereby prevented phosphorylation of RNA poly

94 ranscription elongation complexes containing P-TEFb, AFF4, ELL2, and ENL or AF9 to the viral promoter

95 results strongly suggest that CTIP2 controls P-TEFb function in physiological and pathological condit

96 trophic cardiomyopathic mice, CTIP2 controls P-TEFb-sensitive pathways involved in the establishment

97 raction of Tax with cyclin T1 can dissociate P-TEFb from the P-TEFb/7SK snRNP/HEXIM1 complex for acti

98 SEC includes ELL, P-TEFb, AFF4, and several other factors.

99 Without Tat, AFF4 can mediate the ELL2-P-TEFb interaction, albeit inefficiently.

100 fore, in addition to its role in elongation, P-TEFb regulates termination by promoting chromatin recr

101 ectively increases transcription elongation, P-TEFb occupancy, and Ser7P-RNAPII levels at these genes

102 rect contacts with HIV Tat, and Tat enhances P-TEFb affinity for AFF4.

103 ent of 3 transcriptional modulators: AF4-ENL-P-TEFb complex (AEP), DOT1L-AF10-ENL complex (referred t

104 s have been identified in higher eukaryotes: P-TEFb and CDK12/CyclinK.

105 the 7SK snRNP to PRG promoters to facilitate P-TEFb recruitment and productive elongation in response

106 the positive transcription elongation factor P-TEFb and prevents phosphorylation of pausing factors.

107 the positive transcription elongation factor P-TEFb is a local explorer that oversamples its environm

108 the human transcriptional elongation factor P-TEFb, a CDK9-cyclin T1 heterodimer that is part of the

109 the positive transcription elongation factor P-TEFb, and then enter productive elongation only under

110 the positive transcription elongation factor P-TEFb, providing evidence that the dysregulated gene ex

111 ed with recruitment of the elongation factor P-TEFb, the co-activator GRIP1, the chromatin remodeling

112 ated by the recruitment of elongation factor P-TEFb.

113 f the assembly of the host elongation factor P-TEFb.

114 nes by dissociating the pause release factor P-TEFb from an inactive complex containing HEXIM1.

115 ription starts when the pause release factor P-TEFb is recruited to initiate productive elongation.

116 oteins to sequester the transcription factor P-TEFb by a mechanism similar to that used by retroviral

117 he positive transcription elongation factor (P-TEFb) component Cyclin T1 (Ccnt1).

118 he positive transcription elongation factor (P-TEFb) is required for the transcription of most genes

119 he positive transcription elongation factor, P-TEFb, and directs the factor to promote productive elo

120 his complex to two major elongation factors, P-TEFb and the PAF complex.

121 by Pol II, which we validated as a bona fide P-TEFb substrate in vivo and in vitro.

122 We also show that Tax competes with Brd4 for P-TEFb binding.

123 dependence on phosphoinositide 3-kinase for P-TEFb recruitment to IL1B paralleled a greater sensitiv

124 nucleoprotein complex is a critical step for P-TEFb to activate transcription elongation.

125 We identify histone H1 as a substrate for P-TEFb involved in cellular and HIV-1 transcription.

126 uses them to enhance the affinity of Tat for P-TEFb, a key SEC component, with different efficiency.

127 Free P-TEFb, which is required for growth, can be recruited t

128 bonucleoprotein (7SK snRNP) and active (free P-TEFb) complexes in cells.

129 In the former, free P-TEFb is a potent transcriptional coactivator.

130 ed, JQ1 transiently increased levels of free P-TEFb and BRD4.P-TEFb and SEC.P-TEFb complexes in cells

131 reactivate HIV, work via the release of free P-TEFb from the 7SK snRNP.

132 tin, also leads to the rapid release of free P-TEFb from the 7SK snRNP.

133 e inhibitors lead to a rapid release of free P-TEFb, followed by its reassembly into the 7SK snRNP.

134 Mechanistically, dissociation of HEXIM1 from P-TEFb and subsequent activation of P-TEFb are required

135 cells dissociates HEXIM1 and 7SK snRNA from P-TEFb, but it is not sufficient to activate P-TEFb-depe

136 (eleven-nineteen lysine-rich leukemia gene)/P-TEFb (positive transcription elongation factor)-contai

137 ndings suggest a crucial role for the HEXIM1/P-TEFb pathway in the regulation of satellite cell-media

138 n inhibits the ability of Tax to disrupt HMW P-TEFb complexes.

139 Little is known about how P-TEFb activity and expression are regulated in resting

140 ase from the snRNP are becoming clearer, how P-TEFb remains in the 7SK-unbound state to sustain trans

141 To determine how P-TEFb may connect chromatin remodeling to transcription

142 proximately 100 putative substrates of human P-TEFb, which were enriched for proteins implicated in t

143 mediate association of P-TEFb with AF9, (ii) P-TEFb, through direct interactions, provides the link f

144 Importantly, P-TEFb directs H1 phosphorylation in response to wild-ty

145 nduces significant conformational changes in P-TEFb.

146 sis factor alpha because of a restriction in P-TEFb levels, which can be overcome by activation of th

147 phosphatase 1alpha (PP1alpha), resulting in P-TEFb mobilization and CDK9-mediated AR S81 phosphoryla

148 SK snRNA and recruits as well as inactivates P-TEFb in the 7SK snRNP.

149 P2 copurifies and interacts with an inactive P-TEFb complex containing the 7SK snRNA and HEXIM1.

150 reassembles at the promoter with an inactive P-TEFb:7SK snRNP complex and later transfers P-TEFb to T

151 at HNRNPL may partake in delivering inactive P-TEFb to Aire.

152 the rapid dissociation of the large inactive P-TEFb:7SK RNP (small nuclear RNA 7SK ribonucleoprotein)

153 The inactive P-TEFb complex associates with CTIP2 at the MYH7 gene pr

154 t can shift the balance between the inactive P-TEFb pool and the active P-TEFb pool and thereby stimu

155 es of other transcription factors, including P-TEFb, TFIIH, and CIITA, ensuring an orderly progressio

156 All these stimuli increase P-TEFb-dependent transcription.

157 tein neither binds to 7SK snRNA nor inhibits P-TEFb.

158 ified an alternative pathway of irreversible P-TEFb activation in megakaryopoiesis that is mediated b

159 ly by PJA2 requires that Tat first binds its P-TEFb cofactor.

160 th the RNA polymerase II (Pol II) CTD kinase P-TEFb.

161 Other known P-TEFb-releasing agents, including histone deacetylase i

162 a distinct ELL-containing complex that lacks P-TEFb and other components of SEC named the "little elo

163 horylation of CDK9 at the T-loop, liberating P-TEFb from the inactive 7SK snRNP, and inducing the for

164 n (ChIP) experiments reveal that Ssu72, like P-TEFb and AFF4, is recruited by Tat to the integrated H

165 at the HIV long terminal repeat and limiting P-TEFb levels contribute to transcriptional silencing le

166 ters and were found to be responsive to many P-TEFb-releasing compounds.

167 ormally associated with adult megakaryocytic P-TEFb activation.

168 e specificity of the Drosophila melanogaster P-TEFb (DmP-TEFb) in vitro.

169 es (SECs) containing ELL/EAF family members, P-TEFb, and other proteins, but the mechanism of their r

170 CDK9 dephosphorylation mobilizes P-TEFb from an inhibitory 7SK ribonucleoprotein complex,

171 ent the first experimental system to monitor P-TEFb activation in living cells.

172 nally, we identified 5'-azacytidine as a new P-TEFb-releasing agent.

173 plementation assay could be used to find new P-TEFb-releasing agents, compare different classes of ag

174 Notably, P-TEFb association with both in vitro-reconstituted and

175 Notably, P-TEFb complexes associated with short BRD4 contain HEXI

176 irs SMAD recruitment and the accumulation of P-TEFb-associated RNA polymerase II (RNAPII) C-terminal

177 IM1 from P-TEFb and subsequent activation of P-TEFb are required for satellite cell proliferation and

178 uired for full transcriptional activation of P-TEFb response genes.

179 cantly represses the Cdk9 kinase activity of P-TEFb.

180 akaryocytic upregulation of calpain 2 and of P-TEFb-dependent cytoskeletal remodeling factors.

181 nd AFF4 independently mediate association of P-TEFb with AF9, (ii) P-TEFb, through direct interaction

182 However, examination of P-TEFb complexes by gel-filtration chromatography showed

183 Prior to stimulation, a fraction of P-TEFb is recruited to promoter-proximal regions in a ca

184 Both genetic and chemical inhibition of P-TEFb in mitosis lead to delays in the progression of c

185 a role in modulating the available level of P-TEFb upon transcriptional down-regulation by sequester

186 ting primary CD4(+) T cells, where levels of P-TEFb are vanishingly low, the most potent HDACi, suber

187 ist, bryostatin 1, which increased levels of P-TEFb, then SAHA once again reactivated HIV.

188 NA, implicating the PID in the liberation of P-TEFb from the 7SK small nuclear ribonucleoprotein comp

189 However, the mechanism of P-TEFb recruitment and regulation of NELF/DSIF during tr

190 Although mechanisms of P-TEFb release from the snRNP are becoming clearer, how

191 onal repressor CTIP2 is a major modulator of P-TEFb activity.

192 of the Saccharomyces cerevisiae ortholog of P-TEFb.

193 CDK9, as part of P-TEFb and the super elongation complex (SEC), is by far

194 bitor showed that IFN-induced recruitment of P-TEFb and NELF/DSIF was under the control of BRD4.

195 inding and subsequent further recruitment of P-TEFb, generating a positive feedback loop that sustain

196 was largely independent of the reduction of P-TEFb (positive transcription elongation factor b) leve

197 omplex containing the recognition regions of P-TEFb and AFF4.

198 rest, this repression involves regulation of P-TEFb recruitment and promoter-proximal Pol II pausing.

199 This release of P-TEFb correlated directly with activation of human HIV

200 In this study, the release of P-TEFb from the 7SK snRNP led to increased synthesis of

201 T cells, thus limiting the sequestration of P-TEFb in the 7SK RNP complex, indicating that this mech

202 y, we show that CTIP2 inhibits large sets of P-TEFb- and 7SK snRNA-sensitive genes.

203 fficulties in determining the specificity of P-TEFb toward the various heptad repeat motifs within th

204 by PKC represents a major regulatory step of P-TEFb activity in cells.

205 and 39 have evolved orthogonal strengths of P-TEFb binding versus RNAPII phosphorylation, suggesting

206 ntacts, mainly with the cyclin T1 subunit of P-TEFb, but also with the T-loop of the Cdk9 subunit.

207 Tax interacts with the cyclin T1 subunit of P-TEFb, forming a distinct Tax/P-TEFb LMW complex.

208 sociation of Cyclin T1 (CCNT1), a subunit of P-TEFb, with the Tat-LTR axis.

209 e been shown to bind the cyclin T subunit of P-TEFb.

210 a structure complementary to the surface of P-TEFb and makes extensive contacts, mainly with the cyc

211 se II (RNAPII), but is distinct from that of P-TEFb (dCDK9 + dCyclin T).

212 Thus, our visualization of P-TEFb activation by fluorescent complementation assay c

213 " developmental program that is dependent on P-TEFb kinase activation and cytoskeletal remodeling.

214 n inhibitory effect of Fushi tarazu (Ftz) on P-TEFb recruitment and the regulation of RNA polymerase

215 rization of the stimulatory effect of Tat on P-TEFb catalytic efficiency.

216 7SK RNA and the kinase inhibitor Hexim1 once P-TEFb has been released from the 7SK snRNP.

217 ivation by histone deacetylase inhibitors or P-TEFb activation but are susceptible to reactivation by

218 the core 7SK snRNP component MePCE promoted P-TEFb release and consequent upregulation of a cohort o

219 ene expression: binding P-TEFb and promoting P-TEFb phosphorylation of the C-terminal domain in RNAPI

220 We then used recombinant P-TEFb, HEXIM1, LARP7 and MEPCE to reconstruct a functio

221 been shown to bind 7SK directly and recruit P-TEFb to TAR.

222 the reprogramming factor KLF4 helps recruit P-TEFb to pluripotency promoters.

223 BRD4 regulates the Adipoq gene by recruiting P-TEFb onto acetylated histones in the transcribed regio

224 Upon stimulation, Brd4 recruits P-TEFb to Spt5/DSIF via a recruitment pathway consisting

225 ed1, Med23 and Tat-SF1, whereas SEC recruits P-TEFb to NELF-A and NELF-E via Paf1c and Med26, respect

226 The HIV-1 Tat protein selectively recruits P-TEFb as part of a super elongation complex (SEC) organ

227 BRD4 depletion reduced P-TEFb recruitment and histone acetylation on the transc

228 elongation factors, mechanisms that regulate P-TEFb involving the 7SK small nuclear ribonucleoprotein

229 ), a cellular RNA binding protein, regulates P-TEFb expression.

230 ents that activate these proteins or release P-TEFb from the inactive 7SK small nuclear ribonucleopro

231 eroylanilide hydroxamic acid, which releases P-TEFb from the 7SK small nuclear ribonucleoprotein, the

232 During viral replication, P-TEFb is recruited via interactions of its cyclin T1 su

233 Many of these genes require P-TEFb for expression and exhibit pausing-associated chr

234 ChIP with sequencing revealed P-TEFb-sensitive poised RNA polymerase II at this proxim

235 ly, compounds that enhance the levels of SEC-P-TEFb also potently stimulated HSV reactivation from la

236 d by transcriptional elongation, and the SEC-P-TEFb complex is specifically required to drive the lev

237 evels of free P-TEFb and BRD4.P-TEFb and SEC.P-TEFb complexes in cells.

238 ter-proximal regions to facilitate "on-site" P-TEFb activation and Pol II elongation.

239 development by modulating a lineage-specific P-TEFb activation mechanism, revealing potential strateg

240 1 that is used by AR to initiate and sustain P-TEFb activity, which may be exploited to drive AR in C

241 ture of a quaternary complex containing Tat, P-TEFb, and the SEC scaffold, AFF4.

242 tion motif and increases the affinity of Tat-P-TEFb for TAR 30-fold.

243 unds that would specifically inhibit the Tat.P-TEFb complex and block HIV replication.

244 we describe the crystal structure of the Tat.P-TEFb complex containing HIV-1 Tat, human Cdk9 (also kn

245 We found that Ssu72 is essential for Tat:P-TEFb-mediated phosphorylation of the S5P-CTD in vitro.

246 a transition step in which preassembled Tat:P-TEFb complexes switch to TAR.

247 It is unknown how the Tat:P-TEFb complex transitions to TAR to activate the P-TEFb

248 T1 subunit of P-TEFb, forming a distinct Tax/P-TEFb LMW complex.

249 722) lacking a previously defined C-terminal P-TEFb-interacting domain (PID).

250 , which are mediated by the carboxy-terminal P-TEFb binding domain.

251 show that P-TEFb interacts with H1 and that P-TEFb inhibition by RNAi, flavopiridol, or dominant neg

252 Additionally, we demonstrate that P-TEFb-mediated Ser2 phosphorylation of Pol II is dispen

253 Here, we show that P-TEFb artificially recruited to the nascent transcript

254 ary cell model of HIV-1 latency to show that P-TEFb availability in resting memory CD4(+) T cells is

255 We show that P-TEFb interacts with H1 and that P-TEFb inhibition by R

256 The P-TEFb equilibrium determines the state of cellular acti

257 The P-TEFb-dependent transition into productive elongation w

258 b complex transitions to TAR to activate the P-TEFb kinase.

259 of the Pol II C-terminal domain (CTD) by the P-TEFb complex, CDK-9/cyclin T.

260 ith cyclin T1 can dissociate P-TEFb from the P-TEFb/7SK snRNP/HEXIM1 complex for activation of the vi

261 One key regulator of such programs is the P-TEFb kinase, which phosphorylates RNA polymerase II (P

262 rogating recruitment to the chromatin of the P-TEFb component CDK9 in a BRD2-4-dependent manner.

263 AFF4 meanders over the surface of the P-TEFb cyclin T1 (CycT1) subunit but makes no stable con

264 low for specific and rapid inhibition of the P-TEFb kinase CDK9, which is implicated in polymerase pa

265 nascent TAR RNA and the CycT1 subunit of the P-TEFb kinase in a SEC.

266 interaction allowed for localization of the P-TEFb phosphorylation site as well as characterization

267 , the effects of JQ1 and HMBA or SAHA on the P-TEFb equilibrium were cooperative.

268 s transcription elongation by recruiting the P-TEFb (positive transcription elongation factor-b) (Cyc

269 Transcripts sensitive to the P-TEFb inhibitor flavopiridol were reduced by Hnrnpl kno

270 interactions of both JMJD6 and Brd4 with the P-TEFb complex permit its activation and pause release o

271 This P-TEFb equilibrium determines the state of growth and pr

272 Several stimuli can affect this P-TEFb equilibrium.

273 wever, no good method exists to analyze this P-TEFb equilibrium in living cells.

274 Thus, P-TEFb regulates its own equilibrium in cells, most like

275 xim proteins associated with 7SK RNA bind to P-TEFb and reversibly inhibit its activity.

276 mes this limitation by bringing more ELL2 to P-TEFb and stabilizing ELL2 in a process that requires a

277 ecreasing the binding of 7SK snRNP/HEXIM1 to P-TEFb.

278 ex, but mechanisms targeting phosphatases to P-TEFb are unclear.

279 es while maintaining their responsiveness to P-TEFb and suggest that Mediator overcomes a Gdown1-medi

280 er with differential promoter sensitivity to P-TEFb, is central to quantitative regulation of this im

281 P-TEFb:7SK snRNP complex and later transfers P-TEFb to TAR on the nascent transcript, displacing the

282 This triggers P-TEFb-mediated transitioning of RNAPII to the serine 2-

283 uced/poised IE gene, was more dependent upon P-TEFb than was the case for the TNF gene.

284 ducible transcription factors, which utilize P-TEFb to phosphorylate RNA polymerase II (Pol II) in re

285 d the release of active low-molecular-weight P-TEFb complexes.

286 gammaH2AX accumulation decreases when P-TEFb is inhibited, confirming that DDR signalling resu

287 evious observations in dividing cells, where P-TEFb can be regulated by its sequestration in the 7SK

288 each other and with elongating RNAPII, while P-TEFb was not among the interactors.

289 qually available for all nuclear sites while P-TEFb reaches its targets in a position-dependent manne

290 tial for 7SK RNA stability and assembly with P-TEFb.

291 containing AFF2 and AFF3 in association with P-TEFb, ENL/MLLT1, and AF9/MLLT3.

292 d step requires the association of BRD4 with P-TEFb.

293 Compared with P-TEFb, dCDK12 amounts are lower at the 5' end and highe

294 s induced to form an inhibitory complex with P-TEFb, the kinase that initiates transcription elongati

295 Consistent with P-TEFb controlling release from pausing, treatment with

296 -SL4 is poised to make ternary contacts with P-TEFb and HEXIM or Tat.

297 by demonstration of HNRNPL interactions with P-TEFb components (CDK9, CCNT2, HEXIM1, and the small 7S

298 D4, a BET family protein that interacts with P-TEFb.

299 1 and, via the loop 2 of the 7SK snRNA, with P-TEFb.

300 Without P-TEFb, Gdown1 led to the production of stably paused po