ライフサイエンスコーパス: Tat

1 Tat (24 h) caused an Mdm2-dependent loss of NMDAR puncta

2 Tat (4-16 h) potentiated NMDA-evoked whole-cell current

3 Tat also induced [Ca(2+)]i increases and Thr-287 autopho

4 Tat caused a dose-dependent decrease in autophagosome ma

5 Tat colocalized with autophagosome and lysosomal markers

6 Tat exposure also time-dependently increased the mature

7 Tat expression in astrocytes was associated with fewer n

8 Tat functions through master transcriptional regulators

9 Tat had no effect when 3-methyladenine or knockdown of b

10 Tat increased numbers of LC3 puncta and resulted in the

11 Tat interaction with astrocytes has been shown to be imp

12 Tat operates by a cycle in which the receptor complex co

13 Tat precursor proteins possess a conserved twin-arginine

14 Tat transport is mediated by complexes formed from small

15 Tat-activating regulatory DNA-binding protein-43 (TDP-43

16 Tat-Beclin peptides therefore represent a new family of

17 Tat-induced [Ca(2+)]i was attenuated by the NMDAR antago

18 Tat-interactive protein 60 (Tip60) is a MYST histone ace

19 Kinetic analysis of the HIV-1 Tat (transactivator of transcription)-positive transcrip

20 structure of HIV-1 TAR in complex with HIV-1 Tat and human AFF4, CDK9, and CycT1.

21 we explored the synergistic effect of HIV-1 Tat and KSHV oncogene Orf-K1 on angiogenesis.

22 teractive effects of the viral protein HIV-1 Tat and lipopolysaccharide (LPS) on enteric neurons and

23 nsmitted in the presence of HK2 Rec or HIV-1 Tat and Vif.

24 In culture, HIV-1 Tat caused concentration-dependent death of immature OLs

25 revious studies have demonstrated that HIV-1 Tat directly binds to hDAT and some amino-acid mutations

26 aken together, these results show that HIV-1 Tat expression leads to UPR/ER stress in astrocytes, whi

27 HIV-1 Tat hijacks the human superelongation complex (SEC) to p

28 Exposure to HIV-1 Tat in combination with LPS enhanced the expression and

29 Second, HIV-1 Tat interacts with SUPT16H but not SSRP1 protein.

30 These results show that HIV-1 Tat interacts with the TLR4 receptor to enhance the pro-

31 g, we found that infusion of 100 ng of HIV-1 Tat into the lateral ventricle of yellow fluorescent pro

32 HIV-1 Tat is a major culprit for HIV/neuroAIDS.

33 HIV-1 Tat plays an important role in HIV-associated neurocogni

34 HIV-1 Tat protein increases synaptic dopamine (DA) levels by d

35 In this study, we show that the HIV-1 Tat protein interacts with rapid kinetics to engage the

36 The HIV-1 Tat protein is a potent neurotoxin produced during HAND

37 efore, this study analyzed whether the HIV-1 Tat protein is able to activate these two pathways separ

38 The HIV-1 Tat protein is one of the proteins present in HIV that a

39 TLR4 pathway with rapid kinetics, the HIV-1 Tat protein leads to the engagement of both the MyD88 an

40 TLR4 pathway with rapid kinetics, the HIV-1 Tat protein leads to the engagement of both the MyD88 an

41 oter of HIV-1 that is activated by the HIV-1 Tat protein.

42 In D2 MSNs, exposure to HIV-1 Tat reduced dendritic spine density significantly, incre

43 cline-inducible and astrocyte-specific HIV-1 Tat transgenic mice (iTat) and determined the relationsh

44 ant for the ability of ELL2 to promote HIV-1 Tat-mediated proviral transcription.

45 uld still be released and activated by HIV-1 Tat.

46 affinity of the initial hit and displaced a Tat-derived peptide with an IC50 of 40 muM.

47 DCCD interferes with the deep insertion of a Tat signal peptide into the TatBC receptor complex.

48 ssing activity, even allowing transport of a Tat substrate lacking a signal peptide.

49 ichia coli cells, that, upon expression of a Tat substrate protein, fluorescently labeled TatE-GFP re

50 the ability to interact with TatB and with a Tat substrate but were unable to support the in vivo ass

51 e the substrate receptor complex, and active Tat translocases are formed by the substrate-induced ass

52 structural model for assembly of the active Tat translocase in which substrate binding triggers repl

53 In addition, Tat undergoes a series of reversible post-translational

54 Rs, reverses synapse loss when applied after Tat.

55 that demonstrated sustained spine loss after Tat infusion and transient rescue after ifenprodil admin

56 ned as a therapeutic target for ameliorating Tat-mediated neuroinflammation.SIGNIFICANCE STATEMENT De

57 naive CD4(+) T cells and represses basal and Tat-mediated HIV-1 transcription.

58 subsets of SECs in controlling cellular and Tat-activated HIV transcription, little is known about t

59 es with potential attenuation of cocaine and Tat binding to DAT are of great scientific and clinical

60 h muscle cells on treatment with cocaine and Tat.

61 itment pathway consisting of Med1, Med23 and Tat-SF1, whereas SEC recruits P-TEFb to NELF-A and NELF-

62 s with the autophagy enhancers rapamycin and Tat-Beclin-1 increased ureagenesis and protected against

63 l role in stabilizing basal DA transport and Tat-DAT interaction.

64 itical for regulation of basal DA uptake and Tat-induced inhibition of DA transport.

65 taA activity and affected folding as well as Tat-dependent transport of the enzyme.

66 clade, and the Athila subclade in the Athila/Tat clade.

67 mutation can not only considerably attenuate Tat-induced inhibition of dopamine uptake, but also sign

68 SRI-30827 attenuated Tat-induced inhibition of [(3)H]WIN35,428 binding.

69 H547 mutants attenuated Tat-induced inhibition of DA transport observed in WT hD

70 We found that LRRK2 inhibition attenuates Tat-induced pS935-LRRK2 expression, proinflammatory cyto

71 Analysis of 512 bacterial Tat signal peptides using secondary structure prediction

72 findings are particularly important because Tat protein has recently been detected in the brain of H

73 Tat) and determined the relationship between Tat expression and neurogenesis.

74 ric, multivalent receptor complex that binds Tat substrates, while multiple protomers of TatA assembl

75 s a non-covalent complex with a biotinylated Tat vector, is also efficient but the protein is predomi

76 Importantly, both MK801 and CNQX blocked Tat-induced death of immature OLs, but only MK801 revers

77 protein expression, which were abrogated by Tat heat inactivation, immunodepletion, and cysteine mut

78 but not abrogation of IL-10 and TNF-alpha by Tat-stimulated macrophages from mice deficient in TIRAP/

79 that functional activation of CRISPR/Cas9 by Tat during the course of viral infection excises the des

80 Controlled expression of Cas9 by Tat offers a new strategy for safe implementation of the

81 A virus protein called Tat plays a dual role in HIV infection by regulating the

82 riptional regulatory mechanisms in the cell, Tat precisely controls RNA polymerase II recruitment and

83 In our murine model, cortical Tat injection in LRRK2 knock-out (KO) mice results in si

84 The TAR central loop contacts the CycT1 Tat-TAR recognition motif (TRM) and the second Tat Zn(2+

85 Efficient Tat transduction also enabled the intracellular delivery

86 tion complex (SEC) used by the viral encoded Tat protein to activate HIV transcription.

87 The virally encoded Tat protein hijacks positive transcription elongation fa

88 HIV encodes Tat, a small protein that facilitates viral transcriptio

89 pletion of SUPT16H or SSRP1 protein enhances Tat-mediated HIV-1 LTR (long terminal repeat) promoter a

90 as significantly enhanced in Tat-expressing (Tat+) mice.

91 TAR major groove interacts with the extended Tat ARM.

92 S data were used to help model the extended (Tat Arginine-Rich Motif) ARM, which enters the TAR major

93 autoregulatory viral trans-activating factor Tat is reduced to subthreshold levels.

94 complex member that serves as a cofactor for Tat-mediated transcription.

95 insights into identifying targets on DAT for Tat binding and improving DAT-mediated dysfunction of DA

96 recognition residues in human DAT (hDAT) for Tat-induced inhibition of DA transport and transporter c

97 strocytes has been shown to be important for Tat neurotoxicity and HIV/neuroAIDS.

98 suggesting a miR-223-mediated mechanism for Tat-induced NLRP3 priming.

99 region in the signal peptide is required for Tat-dependent export in Escherichia coli Furthermore, we

100 that transcriptional positive feedback from Tat shifts and expands the regime of LTR bimodality.

101 entiation, while immunodepletion of Tat from Tat-containing conditioned media or heat inactivation of

102 tor assembly was not required for functional Tat transport of CueO.

103 ing that TatE-GFP associates with functional Tat translocases.

104 Furthermore, Tat-injected LRRK2 KO animals have decreased infiltratio

105 Likewise, in vivo studies in GFAP-Tat tg mice showed increased autophagosome accumulation

106 amino-acid mutations that attenuate the hDAT-Tat binding also significantly decreased dopamine uptake

107 47) of hDAT plays a crucial role in the hDAT-Tat binding and dopamine uptake by hDAT, and that the H5

108 for dopamine uptake and disrupting the hDAT-Tat binding may provide an exciting knowledge basis for

109 Hence, Tat protein may induce autophagosome and lysosome fusion

110 itotoxins that potentiate NMDARs such as HIV Tat may protect from excessive NMDAR activation while al

111 y studied cationic sequence derived from HIV Tat or polyarginine Arg8, and equals that of hydrocarbon

112 Here we sought to determine how HIV Tat dysregulates autophagy in neurons.

113 nly further highlights the importance of HIV Tat protein in HIV/neuroAIDS, but also presents a new st

114 In this study, we have discovered that HIV Tat impairs neurogenesis through the Notch signaling pat

115 HIV-Tat has been demonstrated to be secreted from cells in a

116 tional interaction between PI(4,5)P2 and HIV-Tat was critically required for efficient membrane pore

117 sm of unconventional secretion shared by HIV-Tat and fibroblast growth factor 2.

118 for efficient membrane pore formation by HIV-Tat oligomers.

119 Here, now we demonstrate the effect of HIV-Tat and cocaine on the proliferative TGF-beta signaling

120 Although membrane binding of HIV-Tat did not strictly depend on PI(4,5)P2 but, rather, wa

121 Intriguingly, oligomerization of HIV-Tat on membrane surfaces leads to the formation of membr

122 nd chemically attaching cell penetrating HIV-Tat peptide on the exterior of the capsid.

123 Here we show that HIV-Tat forms membrane-inserted oligomers, a process that is

124 knockdowns of sixteen previously identified Tat interactors and found that a novel E3 ligase, PJA2,

125 o identify additional functionally important Tat cofactors, we performed RNAi knockdowns of sixteen p

126 nctional difference between AFF1 and AFF4 in Tat-transactivation has been traced to a single amino ac

127 translocation was significantly enhanced in Tat-expressing (Tat+) mice.

128 so sufficient for UPR/ER stress induction in Tat-expressing astrocytes and for astrocyte-mediated Tat

129 ophysiological consequences were observed in Tat-exposed D1 MSNs.

130 (v) the crucial role of the TRIF pathway in Tat-induced IL-10 production.

131 d in a reduced rate of colonic propulsion in Tat+ mice treated with LPS.

132 tingly, several different lysine residues in Tat can function as ubiquitin acceptor sites, and variab

133 ant negative alleles of tatC that inactivate Tat function in the presence of wild-type tatC.

134 This includes Tat-induced reductions in D2 MSN dendritic spine density

135 d either by vaccination approaches including Tat as an immunogen in potential candidate vaccines or b

136 Using inducible Tat-expressing transgenic mice, we found that dopamine s

137 at iron(II) supramolecular helicates inhibit Tat-TAR interaction at nanomolar concentrations by bindi

138 uated for their in vitro activity to inhibit Tat-TAR RNA interaction using UV melting studies, electr

139 This mechanism involved Tat-mediated increased expression of DYRK1A and was prev

140 ansactivator of transcription (SIV(mac239Gag/Tat)).

141 ed the export defect of a TorA[KQ]-30aa-MalE Tat reporter protein in which the RR motif was replaced

142 Many Tat systems consist of three essential membrane componen

143 Besides this well-characterized mechanism, Tat appears to modulate cellular transcription, but the

144 significantly alleviated astrocyte-mediated Tat neurotoxicity in vitro and in the brain of Tat-expre

145 ct molecular mechanism of astrocyte-mediated Tat neurotoxicity is not defined.

146 ch in turn contributes to astrocyte-mediated Tat neurotoxicity, and raise the possibility of developi

147 is was tightly coupled to astrocyte-mediated Tat neurotoxicity.

148 tion is indispensable for astrocyte-mediated Tat neurotoxicity.

149 essing astrocytes and for astrocyte-mediated Tat neurotoxicity.

150 the NF-kappaB pathway, miR-891a-5p mediates Tat and K1 synergistic induction of angiogenesis.

151 CueO is thus the first example for a natural Tat substrate of such incomplete folding state.

152 The absence of Tat reduces HIV transcription and protein production to

153 which causes them to enhance the affinity of Tat for P-TEFb, a key SEC component, with different effi

154 t neurotoxicity in vitro and in the brain of Tat-expressing mice.

155 yD88 and TRIF pathways, (ii) the capacity of Tat to induce TIRAP/MAL degradation, (iii) the crucial r

156 op engages the CycT1 TRM and compact core of Tat, while the TAR major groove interacts with the exten

157 haracterization of the stimulatory effect of Tat on P-TEFb catalytic efficiency.

158 imately suppressed the synergistic effect of Tat- and K1-induced angiogenesis.

159 The synergistic effects of Tat and LPS resulted in a reduced rate of colonic propul

160 or fully reverse the detrimental effects of Tat, glutamate receptors could be a potential therapeuti

161 ed that soluble Tat or ectopic expression of Tat enhanced K1-induced cell proliferation, microtubule

162 that a chronic very low-level expression of Tat is associated with astrocyte activation, inflammator

163 icing and, like 1C8, decreased expression of Tat, Gag and Env.

164 erate bimodality by stochastic extinction of Tat.

165 IL-6, IL-1beta and TNF-alpha in the ilea of Tat+ mice and by enteric glia.

166 PC differentiation, while immunodepletion of Tat from Tat-containing conditioned media or heat inacti

167 ortantly, we demonstrated that inhibition of Tat- or GFAP-induced UPR/ER stress by the chemical chape

168 contributes to the productive interaction of Tat precursor proteins with the TatBC receptor complex.

169 he necessary recognition, the interaction of Tat signal peptides with the receptor complex plays a cr

170 ur current understanding of the mechanism of Tat transport in light of these new structural data.

171 ether, our data unravel a novel mechanism of Tat-mediated neuronal toxicity through dysregulation of

172 rs as common probes to sense the presence of Tat.

173 sing the HIV gene to confirm the presence of Tat.

174 ggest that a chronic low-level production of Tat may contribute to progressive neurological damage in

175 le of the MyD88 pathway in the production of Tat-induced TNF-alpha and IL-10, (iv) a reduction but no

176 at these mutations lower the release rate of Tat, as predicted.

177 Herein, we demonstrate a novel role of Tat in priming and activating NLR family pyrin domain co

178 vely, these findings suggest a novel role of Tat in priming and activating the NLRP3 inflammasome.

179 in itself were present in the supernatant of Tat-expressing astrocytes.

180 ne-associated proteins in the supernatant of Tat-expressing astrocytes.

181 re oligodendrocytes can be direct targets of Tat.

182 omotor behavior was unaffected by 2 weeks of Tat induction.

183 Effect of SRI-30827 on Tat-induced inhibition of [(3)H]WIN35,428 binding was al

184 tern blotting showed that recombinant Tat or Tat-containing conditioned media activated Hes1 transcri

185 ion between the HIV-1 transactivator protein Tat and TAR (transactivation responsive region) RNA, pla

186 The HIV-1 transactivator protein Tat is implicated in the neuronal damage that contribute

187 direct exposure to the HIV-related proteins Tat or gp120 induces TREM-1 expression in macrophages an

188 reviously shown that HIV-1-secreted proteins Tat and Nef regulate the KSHV life cycle and synergize w

189 ed media or heat inactivation of recombinant Tat abrogated those effects.

190 itioned media from astrocytes or recombinant Tat protein inhibited NPC proliferation and migration an

191 and Western blotting showed that recombinant Tat or Tat-containing conditioned media activated Hes1 t

192 d in vivo, and LAMP2A overexpression reduces Tat-induced neurotoxicity.

193 e discuss the functions of HIV-1 regulatory (Tat and Rev) and accessory (Vif, Vpr, Vpu, and Nef) prot

194 e t-butyl ester (DAPT) significantly rescued Tat-impaired NPC differentiation in vitro and neurogenes

195 ath of immature OLs, but only MK801 reversed Tat effects on myelin-like membranes.

196 ilies of membrane proteins that are dual Sec-Tat-targeted.

197 t-TAR recognition motif (TRM) and the second Tat Zn(2+)-binding loop.

198 vaccinated with vectors that express SIVGag/Tat.

199 Our results showed that soluble Tat or ectopic expression of Tat enhanced K1-induced cel

200 in a membrane-enriched fraction, suggesting Tat increases autophagic degradation.

201 twin-arginine protein translocation system (Tat) transports folded proteins across the bacterial cyt

202 Thus, it may be interesting to target Tat as a pathogenic factor early after HIV-1 infection.

203 Therapies targeting Tat-mediated autophagy alterations may decrease neurodeg

204 A tetramethylrhodamine-Tat conjugate is effectively translocated into the secre

205 we showed that neurotoxic factors other than Tat protein itself were present in the supernatant of Ta

206 We conclude that Tat signal peptides play roles in substrate targeting an

207 We confirmed that Tat expression and infection of pseudotyped HIV.GFP led

208 In addition, we demonstrated that Tat-induced lysosomal exocytosis was astrocyte-specific

209 tes with TAU RNA, further demonstrating that Tat interferes with host RNA metabolism in the absence o

210 In addition, we found that Tat associates with TAU RNA, further demonstrating that

211 l, and neuronal cell cultures and found that Tat promotes TAU 3R up-regulation through increased leve

212 We found that Tat-induced lysosomal exocytosis was tightly coupled to

213 We report here that Tat uses unexpected regulatory mechanisms to reprogram t

214 Here, we tested the hypothesis that Tat-induced loss and ifenprodil-mediated rescue of synap

215 py and activates NF-kB, we hypothesized that Tat could prime the NLRP3 inflammasome.

216 ring RNAs (siRNAs), we demonstrated (i) that Tat was able to activate both the MyD88 and TRIF pathway

217 We previously reported that Tat-dependent protein translocation into membrane vesicl

218 iquitin chain assembly by PJA2 requires that Tat first binds its P-TEFb cofactor.

219 Mechanistic studies revealed that Tat promoted K1-induced angiogenesis by enhancing NF-kap

220 is in vivo Together, these results show that Tat adversely affects NPCs and neurogenesis through Notc

221 In this study, we showed that Tat expression or GFAP expression led to formation of GF

222 Furthermore, co-IP studies showed that Tat interacts with lysosomal-associated membrane protein

223 Mechanistically, we showed that Tat synergized with K1 to induce the expression of miR-8

224 o NPC-derived neurosphere assays showed that Tat-containing conditioned media from astrocytes or reco

225 We have recently shown that Tat expression leads to increased glial fibrillary acidi

226 We have shown that that Tat induces GFAP expression in astrocytes and that GFAP

227 , these results show for the first time that Tat promotes lysosomal exocytosis in astrocytes and caus

228 The Tat machinery catalyzes the transport of folded proteins

229 The Tat protein export system translocates folded proteins a

230 The Tat system in Escherichia coli is composed of TatA, TatB

231 The Tat system may need to transport flexibly folded protein

232 The Tat system of Escherichia coli is made up of TatA, TatB,

233 The Tat translocation site is formed by substrate-triggered

234 The Tat transporter is assembled from multiple copies of the

235 The Tat-Beclin-1 (TB1) peptide has been reported as an autop

236 r results clearly indicate that, besides the Tat motif, the h-region of the Tat signal peptides is an

237 ation to define the interactions between the Tat proteins of Escherichia coli at molecular-level reso

238 These results highlight that both the Tat substrate and ubiquitin modification have plastic si

239 utlined various strategies for detecting the Tat protein, which helps transcribe the virus and enhanc

240 However, the Tat positive-feedback loop that controls HIV's fate deci

241 he leaky tetracycline promoter system in the Tat-transgenic mouse to show that a chronic very low-lev

242 Interestingly, the Tat-Beclin-2 (TB2) peptide, derived from the human Becli

243 ing the first molecular-level glimpse of the Tat machinery.

244 an absolute requirement for operation of the Tat pathway by screening for dominant negative alleles o

245 By detection of the Tat protein, virus transmission can be detected in high-

246 es capable of neutralizing the effect of the Tat protein.

247 , besides the Tat motif, the h-region of the Tat signal peptides is another important binding determi

248 includes positive feedback activation of the Tat transactivator, it lacks ultrasensitivity.

249 with TatE being a regular constituent of the Tat translocase in E. coli.

250 n signal peptide-independent assembly of the Tat translocase.

251 res the relatively low hydrophobicity of the Tat-dependent transmembrane domain.

252 7SK snRNP, and inducing the formation of the Tat-SEC complex at the viral promoter.

253 wnstream of the MyD88 and TRIF pathways, the Tat protein activated the protein kinase C (PKC) betaII

254 ry and single-cell imaging, we find that the Tat circuit exhibits a transient activation threshold.

255 y, computational analysis indicates that the Tat circuit's noncooperative "nonlatching" feedback arch

256 des that is involved in their binding to the Tat translocase, but some facets of this interaction rem

257 in T1 (CCNT1), a subunit of P-TEFb, with the Tat-LTR axis.

258 reasing the cellular level/activity of these Tat-friendly SECs, we could potently activate latent HIV

259 ed conformation by thetwinargininetransport (Tat) pathway.

260 of TatB that restored transport activity to Tat signal peptides with inactivating twin arginine subs

261 rther, the polyubiquitin chain conjugated to Tat by PJA2 can itself be assembled through variable ubi

262 of NLRP3 expression in microglia exposed to Tat compared with control.

263 aseline amplitudes after 24 h of exposure to Tat.

264 n rat hippocampal cultures after exposure to Tat.

265 e that the mechanism of handover from Sec to Tat pathway requires the relatively low hydrophobicity o

266 neurons (MSNs) are selectively vulnerable to Tat exposure compared with D1 receptor-expressing MSNs.

267 iption both through the viral transactivator Tat and via Tat-independent mechanisms.

268 V-1 protein transactivator of transcription (Tat) and its cognate transactivation response element (T

269 and the HIV transactivator of transcription (Tat) as well as the cyclin-dependent kinases CDK13 and C

270 ry protein trans-activator of transcription (Tat) continues to be expressed in virally suppressed pat

271 V-1 protein transactivator of transcription (Tat) disrupts synaptic connections both in vitro and in

272 upon HIV-1 transactivator of transcription (Tat) exposure.

273 s of HIV-1 trans-activator of transcription (Tat) in dopamine subtype 1 (D1) and dopamine subtype 2 (

274 HIV protein transactivator of transcription (Tat) initially potentiates NMDARs that then adapt to the

275 ch as HIV-1 Transactivator of Transcription (Tat) protein can activate microglia is thus of paramount

276 cause HIV-1 Transactivator of Transcription (Tat) protein continues to be present despite antiretrovi

277 hat the HIV transactivator of transcription (Tat) protein manipulates the intrinsic toggling of HIV's

278 g the HIV-1 transactivator of transcription (Tat) protein.

279 e and HIV-1 transactivator of transcription (Tat) protein.

280 ral protein transactivator of transcription (Tat) that potentiate NMDAR function.

281 spiny neurons (MSNs) by breeding transgenic Tat-expressing mice to Drd1a-tdTomato- or Drd2-eGFP-repo

282 co-translational Sec and post-translational Tat pathways for integration.

283 The twin-arginine translocase (Tat) transports folded proteins across the bacterial cyt

284 The twin arginine translocase (Tat) transports folded proteins of widely varying size a

285 The twin-arginine translocation (Tat) pathway transports folded proteins across bacterial

286 nsported by the twin-arginine translocation (Tat) pathway, which transports folded proteins, a requir

287 able N-terminal twin-arginine translocation (Tat) peptide to transport across membrane and bind to ba

288 The twin-arginine translocation (Tat) system, found in prokaryotes, chloroplasts, and som

289 Twin-arginine translocation (Tat) systems mediate the transmembrane translocation of

290 Twin-arginine translocation (Tat) systems transport folded proteins across cellular m

291 The twin-arginine protein translocation (Tat) system mediates transport of folded proteins across

292 that a novel E3 ligase, PJA2, ubiquitinates Tat in a non-degradative manner and specifically regulat

293 ons identified two cell penetrating vectors, Tat and C105Y, which readily translocate into mast cells

294 through the viral transactivator Tat and via Tat-independent mechanisms.

295 The viral Tat protein recruits human super elongation complexes (S

296 The viral Tat protein utilizes Cyclin T1 to activate proviral tran

297 upporting HIV-1 transactivation by the viral Tat protein, the AFF4-SEC is more important for HSP70 in

298 In vitro Tat transport proved that the cofactor assembly was not

299 play a predominant role in cooperating with Tat to reverse latency.

300 The pretreatment of human monocytes with Tat protein for 10 to 30 min suffices to irreversibly en