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 on in vitro in HIV-1 latency cell lines in a P-TEFb (CDK9/cyclin T1)-dependent manner.

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

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

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

11 n inhibitor of the transcriptional activator P-TEFb.

12 timulate myogenic transcription after active P-TEFb function is shut off.

13 Fb that allows transfer of the kinase active P-TEFb from Hsp90 to 7SK snRNP for its suppression.

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

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

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

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

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

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

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

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

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

27 y an intermediate complex between HEXIM1 and P-TEFb that allows transfer of the kinase active P-TEFb

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

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

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

31 , and elongation (e.g., DSIF, NELF, PAF, and P-TEFb).

32 We propose Paf1C and P-TEFb act antagonistically to regulate the timing of th

33 pected, NELF and DSIF increased pausing, and P-TEFb promoted pause release.

34 cally, interfering with the axis of RBM7 and P-TEFb provokes cellular hypersensitivity to DNA-damage-

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

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

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

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

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

40 positive transcription elongation factor b (P-TEFb) activity, a key factor in promoting transcriptio

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

58 Positive Transcription Elongation Factor b (P-TEFb) phosphorylates Ser2 residues of the C-terminal d

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

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

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

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

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

64 positive transcription elongation factor b (P-TEFb) via its release from the inhibitory 7SK small nu

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

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

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

68 positive transcription elongation factor b (P-TEFb), composed of CDK9 and cyclin T, stimulates trans

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

85 We propose that the control of BRD4-P-TEFb recruitment is a novel temporal checkpoint in the

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

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

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

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

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

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

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

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

94 nent of the transcription elongation complex P-TEFb - bound to the MYCN-amplicon superenhancer, and i

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

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

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

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

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

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

101 5-AzadC-induced DNA damage enhanced P-TEFb occupancy via a mechanism that involved activatio

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

111 of positive transcription elongation factor P-TEFb.

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

113 the positive transcription elongation factor P-TEFb.

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

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

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

117 uitment of BRD4 and the pause release factor P-TEFb, followed by productive elongation of circadian t

118 The general transcription factor P-TEFb, a master regulator of RNA polymerase (Pol) II el

119 and phosphorylation of transcription factor P-TEFb.

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

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

122 he positive transcription elongation factor (P-TEFb), instating a large proliferative response.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

138 Hence, P-TEFb activity is a key limiting determinant of whether

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

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

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

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 action with other SEC components and impairs P-TEFb-mediated C-terminal domain phosphorylation of RNA

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

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

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

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

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

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

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

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

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

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

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

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

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

158 hen resulted in enhanced occupancy of NF-kB, P-TEFb, and serine 2 phosphorylated RNA Polymerase II on

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

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

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

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

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

164 Down-regulation of HEXIM1 locks P-TEFb in the Hsp90 complex, keeping it in the active st

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

166 ormally associated with adult megakaryocytic P-TEFb activation.

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

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

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

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

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

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

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

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

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

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

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

178 osphorylation directs the kinase activity of P-TEFb and alters its specificity from Ser5 to Ser2.

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 embryos lacking the CDK9 kinase component of P-TEFb exhibit a surfeit of NC progenitors and their der

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

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

185 In the nucleus, more than half of P-TEFb are sequestered in the inactive-state 7SK snRNP c

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

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

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

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

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

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

192 y is determined and indicate modification of P-TEFb levels could be utilised to drive regeneration of

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

194 of the Saccharomyces cerevisiae ortholog of P-TEFb.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

214 7SK RNA and the kinase inhibitor Hexim1 once P-TEFb has been released from the 7SK snRNP.

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

216 and increases in H3K9ac+ and phosphorylated P-TEFb in CD4 + T cells compared to placebo (p<=0.02).

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

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

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

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

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

222 omotes elongation of HIV-1 RNA by recruiting P-TEFb to the HIV-1 long terminal repeat (LTR), and we s

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

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

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

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

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

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

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

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

231 transcription elongation factor b releases (P-TEFb) paused complex after phosphorylating DSIF that l

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 Surprisingly, P-TEFb exhibits Ser5 phosphorylation activity in vitro.

241 1 that is used by AR to initiate and sustain P-TEFb activity, which may be exploited to drive AR in C

242 Cdk9/cyclin T1 (P-TEFb) catalyzes inhibitory phosphorylation of PP1 and

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

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

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

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

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

250 last differentiation into myotubes, and that P-TEFb and its two positive complexes are eliminated in

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

252 Recently, we demonstrated that P-TEFb also controls the expression of EMT regulators to

253 We show here that P-TEFb surprisingly inhibits the myoblast differentiatio

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

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

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 op region in AFF4-CHD as a substrate for the P-TEFb kinase cyclin-dependent kinase 9, which triggers

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 models of latency have higher levels of the P-TEFb subunit cyclin T1 than primary cells, which may e

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

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

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

271 Cit1810 is needed for interaction with the P-TEFb (positive transcription elongation factor b) kina

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

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

274 Several stimuli can affect this P-TEFb equilibrium.

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

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

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

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 The mechanism garnering Ser2 specificity to P-TEFb remains elusive and hinders understanding of the

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

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

284 In turn, P-TEFb relocates to chromatin to induce transcription of

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

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

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

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

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

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

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

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

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

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

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

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

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