ライフサイエンスコーパス: Tat

1 Tat exposure also time-dependently increased the mature

2 Tat interaction with astrocytes has been shown to be imp

3 Tat precursor proteins possess a conserved twin-arginine

4 Tat-A and Tat-B were significantly more potent than Ixaz

5 Tat-Beclin peptides therefore represent a new family of

6 Tat-TAR inhibition results in loss of RNA polymerase II

7 Tat.AG and HIV-1-CRF02_AG induced the expression of NMT-

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

9 didehydro-cortistatin A (dCA) inhibits HIV-1 Tat activity.

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

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

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

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

14 echanisms involved, we found here that HIV-1 Tat inhibits E2F transcription factor 3 (E2F3), CAMP-res

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

16 HIV-1 Tat is essential for HIV-1 replication and appears to pl

17 HIV-1 Tat is essential for HIV-1 replication and plays an impo

18 ccount for the specificity between the HIV-1 Tat protein and TAR RNA.

19 ndicating that penetrating property of HIV-1 Tat protein attributes to synaptic damage.

20 HIV-1 Tat protein can damage the synaptic membranes contributi

21 HIV-1 Tat protein can penetrate cell membrane freely and secre

22 HIV-1 Tat protein contributes to HIV-neuropathogenesis in seve

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

24 tion of dopaminergic system induced by HIV-1 Tat protein-mediated direct inhibition of the dopamine t

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

26 variations can modulate the ability of HIV-1 Tat to systemically disseminate neuroinflammation.

27 Here we report that the HIV-1 Tat-interacting protein 60 kDa (Tip60) acetyltransferase

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

29 bl cells, which provide readout via an HIV-1 Tat-responsive luciferase gene.

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

31 Human immunodeficiency virus-1 (HIV-1) Tat is degraded in the host cell both by proteasomal and

32 Here, we identified SF3b1 as a Tat-SF1-interacting subunit of the U2 snRNP.

33 a canonical UHM-ULM interface, comprising a Tat-SF1 binding pocket for a ULM tryptophan (SF3b1 Trp(3

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

35 ssing both Gaussia luciferase and hrGFP in a Tat- and Rev-dependent manner was engineered into SupT1-

36 y inhibits SIV Tat binding to TAR, but not a Tat-Rev fusion protein, which activates transcription wh

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

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

39 mic and is triggered by the interaction of a Tat substrate with the Tat receptor complex.

40 nalization via intra-NAc shell infusion of a Tat-GluA2(3Y) peptide.

41 duced recombinant human Smad7 protein with a Tat-tag (Tat-Smad7) that rapidly enters cells.

42 Intravenously injected AAV-Tat or AAV-Exo-Tat mainly infects liver and heart.

43 have generated adeno-associated viruses AAV-Tat and AAV-Exo-Tat viruses.

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

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

46 Rs, reverses synapse loss when applied after Tat.

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

48 Drugs against Tat are unfortunately not clinically available.

49 trating peptide conjugated peptide aldehydes Tat-A and Tat-B showed low micromolar anticancer and ant

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

51 Treatment with Tat-A and Tat-B caused membrane disruption and pore formation in H

52 ptide conjugated peptide aldehydes Tat-A and Tat-B showed low micromolar anticancer and antifungal ac

53 Tat-A and Tat-B were significantly more potent than Ixazomib in in

54 s and necrosis upon treatment with Tat-A and Tat-B.

55 HPASMC with combined exposure to cocaine and Tat (C + T) vs control identified the following top lncR

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

57 h muscle cells on treatment with cocaine and Tat.

58 its Tat proteins(Tat.B), HIV-1-CRF02_AG and Tat.AG significantly increased histone acetyl-transferas

59 HPNs) with methamphetamine and HIV gp120 and Tat increase dynamin-related protein 1 (DRP1)-dependent

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

61 in stabilizing basal dopamine transport and Tat-DAT integration.

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

63 Furthermore, topically applied Tat-Smad7 on K5.TGFbeta1 skin wounds accelerated wound c

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

65 el in regulating endolysosome pH, as well as Tat-mediated HIV-1 LTR transactivation in U87MG cells st

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

67 g cytosolic calcium with BAPTA-AM attenuated Tat endolysosome escape and LTR transactivation.

68 Y88F/H547A mutant attenuated Tat-induced inhibition of dopamine uptake observed in wi

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

70 resident two-pore channels (TPCs) attenuated Tat endolysosome escape and LTR transactivation.

71 ates that at least 23 proteins are authentic Tat substrates, and they are functionally categorized in

72 we expressed Tat proteins of HIV-1 clade B (Tat-B) or C (Tat-C) or their position 57 variants in HeL

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

74 Because Tat disrupts intracellular calcium homeostasis, we inves

75 iscover steric restriction points that block Tat-mediated recruitment of the host SEC to HIV-1 TAR.

76 In the brain, Tat can be taken up by CNS cells via receptor-mediated e

77 lpha in human monocytes and macrophages, but Tat.B and HIV-1-subtype-B had no effect.

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

79 ocusing in particular on the roles played by Tat signal peptides in protein targeting and translocati

80 Transactivation by Tat-B was significantly reduced by R57S substitution, wh

81 Tat proteins of HIV-1 clade B (Tat-B) or C (Tat-C) or their position 57 variants in HeLa cells.

82 that in the globally dominant HIV-1 clade C, Tat displays a naturally occurring polymorphism, R57S, i

83 ed from HIV-1 infected or transfected cells, Tat can be up-taken into cells by receptor-mediated endo

84 Secreted from infected or transfected cells, Tat has the extraordinary ability to cross the plasma me

85 reporter TZM-bl cells resulted in decreased Tat-dependent HIV-1 long-terminal repeat (LTR) promoter

86 tion (CHIPDeltaU-box), was unable to degrade Tat protein.

87 regulate basal dopamine uptake but diminish Tat-induced inhibition of dopamine uptake by changing do

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

89 The virally encoded Tat protein hijacks positive transcription elongation fa

90 and its internalization into endolysosomes, Tat must be released in order for it to activate the HIV

91 ze that acidifying endolysosomes may enhance Tat degradation in endolysosomes and restrict LTR transa

92 led to higher virion production and enhanced Tat-mediated HIV-1 LTR promoter transactivation, along w

93 Exo-Tat loses this penetrating property.

94 Intravenously injected AAV-Tat or AAV-Exo-Tat mainly infects liver and heart.

95 adeno-associated viruses AAV-Tat and AAV-Exo-Tat viruses.

96 Wild-type Tat, but not Exo-Tat, reduces the expression level of synaptic marker syn

97 Short-term expression of Tat or Exo-Tat doesn't change the expression levels of neuronal cyt

98 ave recently engineered an exosomal Tat (Exo-Tat) which can activate latent HIV-1 in resting CD4+ T l

99 s enhanced cellular degradation of exogenous Tat.

100 malarial drug chloroquine prevents exogenous Tat degradation and enhances the amount of Tat available

101 acilitate HIV-1 viral replication, exogenous Tat has to escape the degradation by endolysosomes.

102 We have recently engineered an exosomal Tat (Exo-Tat) which can activate latent HIV-1 in resting

103 (TAR), Tat, and Nef RNAs but do not express Tat and Nef proteins.

104 at transactivation assay, where we expressed Tat proteins of HIV-1 clade B (Tat-B) or C (Tat-C) or th

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

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

107 tion elongation and pre-mRNA splicing factor Tat-SF1 associates with the U2 small nuclear ribonucleop

108 molecules to block multiple sites in DAT for Tat binding.

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

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

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

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

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

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

115 HIV Tat is a well-known RNA binding protein secreted by HIV.

116 An interaction between HIV Tat and LINC00313 contributed to the dissociation of PRC

117 s, and this interaction was disrupted by HIV Tat, suggesting that LINC00313 may mediate transcription

118 this suppressive effect was relieved by HIV Tat.

119 ring KSHV lytic reactivation, as a novel HIV Tat-interacting lncRNA that potentially mediates HIV-KSH

120 cells to express GFP under regulation of HIV Tat and Rev.

121 the impact and underlying mechanisms of HIV Tat in KSHV-infected endothelial cells undergoing viral

122 e pathways was absent in the presence of HIV Tat.

123 The HIV-1 secreted protein HIV Tat has been found to synergize with KSHV lytic proteins

124 ion through recruitment of PRC2 and that HIV Tat alleviates repression through disruption of this ass

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

126 56 to 76 amino acid (aa) region and the HIV Tat protein transduction domain, and this peptide marked

127 during KSHV reactivation, interacts with HIV Tat to promote endothelial cell motility.

128 n LINC00313 overexpression combined with HIV Tat treatment.

129 ncoding RNA (lncRNA) that interacts with HIV Tat.

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

131 treated with and without cocaine and/or HIV-Tat.

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

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

134 The contribution of astrocytes in Tat-mediated amyloidosis remains an enigma.

135 the HIF-1alpha/lncRNABACE1-AS/BACE1 axis in Tat-mediated induction of astrocytic amyloidosis, which

136 tory role of HIF-1alpha in BACE1-AS/BACE1 in Tat-mediated amyloidosis.

137 e investigated the involvement of calcium in Tat endolysosome escape and subsequent LTR transactivati

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

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

140 at calcium released from TPCs is involved in Tat endolysosome escape and subsequent LTR transactivati

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

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

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

144 uctural and functional details of individual Tat subunits have been reported previously, the sequence

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

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

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

148 Mechanistically, ZL0580 inhibits Tat transactivation in microglia by disrupting binding o

149 Compared to HIV-1-subtype-B and its Tat proteins(Tat.B), HIV-1-CRF02_AG and Tat.AG significa

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

151 essing astrocytes and for astrocyte-mediated Tat neurotoxicity.

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

153 In addition, mutating Tat renders M28 bacteria more sensitive to oxidative str

154 nhibition or E2F3 overexpression neutralizes Tat's effects and restores normal distribution of the sy

155 ral transactivation and replication, but not Tat.B- or HIV-1-subtype-B-mediated effects.

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

157 s Tat degradation and enhances the amount of Tat available to activate HIV-1 LTR, we hypothesize that

158 vation in microglia by disrupting binding of Tat to CDK9, a process key to HIV transcription elongati

159 We report here that disruption of Tat increases the sensitivity of Brucella melitensis M28

160 ted previously, the sequence and dynamics of Tat translocase assembly remain to be determined.

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

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

163 Short-term expression of Tat or Exo-Tat doesn't change the expression levels of n

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

165 erate bimodality by stochastic extinction of Tat.

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

167 Subcutaneous injection of Tat-Smad7 attenuated infiltration of F4/80(+) and CD11b(

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 P-expressing plasmid decreased the levels of Tat protein in a dose-dependent manner, without affectin

171 e stress caused by H(2)O(2) Further, loss of Tat significantly attenuates B. melitensis infection in

172 Based on the intrinsic disordered nature of Tat protein, we focused our attention on host cell E3 ub

173 consistent with a functional partnership of Tat-SF1 and SF3b1.

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

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

176 Additionally, the rate of Tat protein degradation as measured by cycloheximide (CH

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 transactivation, along with stabilization of Tat protein.

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

181 reduced by R57S substitution, while that of Tat-C was enhanced by the reciprocal S57R substitution.

182 Co-transfection of Tat with a CHIP-expressing plasmid decreased the levels

183 Furthermore, CHIP promoted ubiquitination of Tat by both WT as well as Lys-48-ubiquitin, which has on

184 rise recent advances in our understanding of Tat transport, focusing in particular on the roles playe

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

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

187 examined the effect of this polymorphism on Tat uptake and its consequences for cellular gene transa

188 K channels, because the effects of ML-SA1 on Tat-mediated HIV-1 LTR transactivation were blocked usin

189 mic of TAR's cognate protein binding partner Tat, is able to restore a native-like conformation by pr

190 -1 and casein-kinase-(CK)-II-alpha prevented Tat.AG- and HIV-1-CRF02_AG-mediated viral transactivatio

191 endent degradation of its regulatory protein Tat.

192 The HIV-1 transactivation protein (Tat) binds the HIV mRNA transactivation responsive eleme

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

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

195 ong (env) and short (TAR) RNAs and proteins (Tat, Pr55, and p24) in T-cells and macrophages using bot

196 ared to HIV-1-subtype-B and its Tat proteins(Tat.B), HIV-1-CRF02_AG and Tat.AG significantly increase

197 Importantly, we found that SF3b1 regulates Tat-SF1 levels and that these two factors influence expr

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

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

200 l viral lineages at the Mamu-A*01-restricted Tat-SL8 epitope.

201 L-SA1 acidified endolysosomes and restricted Tat-mediated HIV-1 LTR transactivation.

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

203 We quantified the secreted Tat proteins and measured their uptake by TZM-bl cells,

204 dCA specifically inhibits SIV Tat binding to TAR, but not a Tat-Rev fusion protein, wh

205 based assays, that dCA directly binds to SIV Tat's basic domain.

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

207 ombinant human Smad7 protein with a Tat-tag (Tat-Smad7) that rapidly enters cells.

208 HIV trans-activation response element (TAR), Tat, and Nef RNAs but do not express Tat and Nef protein

209 structural details are used to model the TAR-Tat-super-elongation complex (SEC) that is essential for

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

211 Injection of TB1 (Tat-Beclin1) activated mitophagy, attenuated mitochondri

212 t E2F3 up-regulates CREB expression and that Tat interferes with this up-regulation.

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

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

215 aptic protein synaptophysin, confirming that Tat alters these factors, leading to neurite retraction

216 or persistent infection, we demonstrate that Tat is required for full virulence of B. melitensis M28.

217 We demonstrated that Tat-SF1 preferentially and directly binds the SF3b1 subu

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

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

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

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

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

223 m resolution crystal structure revealed that Tat-SF1 contains a U2AF homology motif (UHM) protein-pro

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

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

226 The Tat inhibitor didehydro-cortistatin A suppresses SIV rep

227 The Tat machinery catalyzes the transport of folded proteins

228 The Tat machinery comprises membrane proteins from the TatA

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

230 The Tat translocation site is formed by substrate-triggered

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

232 direct effects of viral proteins such as the Tat protein.

233 mutations in parallel viral lineages at the Tat-SL8 epitope highlights the challenge posed by viral

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

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

236 We next compared the Tat-SF1-binding affinities for each of the five known SF

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

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

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

240 er and underlying interactions mediating the Tat-SF1-U2 snRNP association remain unknown.

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

242 However, the roles of the Tat system and related substrates in Brucella remain unc

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

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

245 Assembly of the Tat translocon is dynamic and is triggered by the intera

246 nd within this series blocked binding of the Tat-ARM peptide to TAR in solution assays, whereas its l

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

248 7SK snRNP, and inducing the formation of the Tat-SEC complex at the viral promoter.

249 association depends on the integrity of the Tat-SF1 UHM.

250 ults define a new molecular interface of the Tat-SF1-U2 snRNP complex for gene regulation.

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

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

253 Collectively, our work establishes that the Tat pathway plays a critical role in Brucella virulence.

254 A key prediction is that the Tat transactivation domain makes modest contacts with th

255 Targeting of substrates to the Tat system is mediated by the presence of an N-terminal

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

257 the interaction of a Tat substrate with the Tat receptor complex.

258 nd low-affinity SF3b1 ULM complexes with the Tat-SF1 UHM at 1.9 angstrom and 2.1 angstrom resolutions

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

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 n human primary astrocytes (HPAs) exposed to Tat.

264 Finally, we exposed microglia to Tat variants and found that R57 is required for maximal

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 protein binding partner, the transactivator Tat.

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

269 We also used a transcellular Tat transactivation assay, where we expressed Tat protei

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

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

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

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

276 HIV-1 transactivator of transcription (Tat) protein has been shown to induce the production of

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

278 The viral trans-activator of transcription (Tat) protein uses an archetypal arginine-rich motif (ARM

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 translocation (Tat) pathway transports folded proteins across bacterial

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

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

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

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

289 The twin-arginine protein transport (Tat pathway) is found in prokaryotes and plant organelle

290 Wild-type Tat, but not Exo-Tat, reduces the expression level of sy

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

292 M/H547A) mutations on basal dopamine uptake, Tat-induced inhibition of DAT function, and dynamic tran

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

294 eterminants of TAR recognition by: (i) viral Tat proteins, (ii) an innovative lab-evolved TAR-binding

295 However, the underlying mechanisms whereby Tat escapes endolysosomes remain unclear.

296 ht to identify the E3 ligase associated with Tat degradation.

297 but the specific molecules that engage with Tat from these pathways are not known.

298 of autosis during the late phase of I/R with Tat-Beclin 1 exacerbated injury.

299 Treatment with Tat-A and Tat-B caused membrane disruption and pore form

300 f apoptosis and necrosis upon treatment with Tat-A and Tat-B.

301 A short treatment with Tat-Smad7 was also sufficient to reduce TGF-beta and NF-