ライフサイエンスコーパス: TAT

1 TAT-4BB inhibited LPS-induced calcium changes in a major

2 TAT-CBD3 disrupted CRMP2-NMDAR interaction without chang

3 TAT-conjugated Pirt(N14) peptide (Pirt(N14)) is sufficie

4 TAT-FLAG GAPDH and/or Siah1-directed peptides were used

5 TAT-fused NipR1 attenuated RhoA nitration and barrier di

6 TAT-GILZ also modulated the activation of the survival-c

7 TAT-p27 was also able to provoke greater levels of autop

8 TAT-RasGAP(317-326) is a cell-penetrating peptide-based

9 TAT-RasGAP317-326, a cell-permeable 10-amino acid-long p

10 TAT.ARC protein delivery led to a dose-dependent better

11 TAT.ARC-treated mice showed better performance in the po

12 prothrombin activation fragment 1+2 (F1+2), TAT (thrombin-antithrombin complex), APC, and D-dimer we

13 ighly comparable to data on (225)Ac-PSMA-617 TAT.

14 A TAT peptide containing the Gbetagamma-interacting domain

15 1.35 A TAT cocrystal structures with bisubstrate analogs constr

16 Each eligible OR team member achieving a TAT of 60 minutes or less or an on-time FCS was awarded

17 d cell-permeable GIV-CT peptides by fusing a TAT-peptide transduction domain (TAT-PTD) to the minimal

18 TLR TIR decoy peptide modified to include a TAT sequence (Trans-Activator of Transcription gene in H

19 l data reveals the consistent formation of a TAT triad platform between the two motifs.

20 strated that intratracheal instillation of a TAT-conjugated PKCdelta inhibitory peptide (PKCdelta-TAT

21 By conjugating EEDs to a TAT-PTD/CPP spilt-GFP peptide complementation assay, we

22 n of NET-Thr(30) motif/phosphorylation via a TAT peptide strategy prevents cocaine-induced NET up-reg

23 ilitate the clinical development of (225) Ac TAT for the treatment of soft-tissue metastases.

24 -tubulin Lys40 by tubulin acetyltransferase (TAT) is the only known posttranslational modification in

25 alpha-tubulin by tubulin acetyltransferase (TAT).

26 DAg-L(198-210), containing the 10-amino acid TAT peptide and HDAg-L(198-210), inhibited the interacti

27 tagonist triazole tetraiodothyroacetic acid, TAT, via noncleavable bonding to poly(ethylene glycol) (

28 spiratory panel with a clinically actionable TAT is associated with reduced hospital admissions and,

29 Trans-activating transcriptional activator (TAT), a cell-penetrating peptide, is extensively used fo

30 In addition, TAT-CBD3, but not CBD3 without TAT or TAT-scramble pepti

31 was used as second-line testing (additional TAT, 30 minutes).

32 surface potential on the density of adsorbed TAT.

33 After TAT, grade 3 anemia was observed in 3 of the 14 patients

34 The best PSA response after TAT (a PSA decline >= 50%) was observed in 7 patients, a

35 after (177)Lu-PSMA showed no worsening after TAT.

36 ewly diagnosed grade 1 or 2 xerostomia after TAT was observed in 5 patients.

37 riability in muscle mass and SMD across age, TAT, and race/ethnicity.

38 n of the cardiac L-type calcium channel (AID-TAT) on restoring mitochondrial metabolic activity, and

39 Importantly, AID-TAT was rapidly targeted to the heart, and not retained

40 ice were treated with active or inactive AID-TAT.

41 We also reveal that AID-TAT treatment of precardiomyopathic cTnI-G203S mice, but

42 Utilizing AID-TAT to modulate cardiac metabolic activity may be benefi

43 have elucidated the mode of action allowing TAT-RasGAP(317-326) to kill cells.

44 sitive (Lgr5) and Tyrosine aminotransferase (TAT).

45 is catabolized by tyrosine aminotransferase (TAT).

46 requires attention to more than the analytic TAT, and will only occur if postanalytic processes (test

47 ting in 566 (82.4%) of 687 cases (analytical TAT, 30 minutes).

48 An increase of F1+2 and TAT levels was observed, that did neither differ between

49 post-LAAC (P=0.038 and P=0.108 for F1+2 and TAT, respectively).

50 F1+2 (prothrombin fragment 1+2) and TAT (thrombin-antithrombin III) were assessed immediatel

51 ychlor inhibited cortisol-stimulated Arg and TAT gene expression.

52 ts of the TAT-Sox2, TAT-Oct4, TAT-Lin28, and TAT-Nanog fusion proteins were 36kD, 40kD, 24kD, and 36k

53 als that SF3B1(HEAT) interacts with PRP5 and TAT-SF1, and maintains its open conformation in U2 snRNP

54 ous, and total adipose tissue (VAT, SAT, and TAT).

55 ma ddPCR assay sensitivity, specificity, and TAT.

56 lays a role in the cross talk between TH and TAT and regulates contractility by influencing NE biosyn

57 FCSs improved from 31% to 64%(P < .001), and TATs of 60 minutes or less increased from 24%to 52%(P <

58 clot elution rate of thrombin-antithrombin (TAT) and fragment F1.2 in the presence and absence of th

59 ned markedly elevated thrombin-antithrombin (TAT) complex levels (indicating uncontrolled thrombin ge

60 -peptide, proinsulin, thrombin-antithrombin (TAT) complex, and a panel of proinflammatory cytokines.

61 the concentration of thrombin-antithrombin (TAT) complexes in plasma.

62 rkers of coagulation (thrombin-antithrombin [TAT]), fibrinolysis (plasmin-antiplasmin [PAP]), and com

63 the territory of the middle cerebral artery, TAT.ARC salvages brain tissue when given during occlusio

64 As TAT was added to the liposome solution the POPC surface

65 r, CRMP2 down-regulation strongly attenuated TAT-CBD3-induced inhibition of reverse NCX.

66 The average TAT was reduced from 7 days (range, 2-14 days) to 2 days

67 The average TATs for the RVP and RPP were 27.9 and 3.0 h, respective

68 However, the cross talk/link between TAT and TH in the heart is unclear.

69 Specific blockage of Cx43 HC function by TAT-Gap19, a Cx43 mimetic peptide, significantly upregul

70 lux into neurons, was strongly suppressed by TAT-CBD3.

71 ectrostatic interaction between the cationic TAT and anionic heparin.

72 However, the positively charged TAT peptide strongly interacts with serum components and

73 A chimeric TAT-gelonin fusion protein was genetically engineered, a

74 generate an equimolar mixture of the codons TAT, TCT, TGT and TTT at that position, encoding a mixtu

75 etion of ADAM10 or delivery of a competitive TAT-Pro-ADAM10709-729 peptide in R6/2 mice prevents N-CA

76 tructures with bisubstrate analogs constrain TAT action to the microtubule lumen and reveal Lys40 eng

77 In contrast, TAT-CBD3 augmented the CRMP2-NCX3 co-immunoprecipitation

78 activity than several other well-known CPPs (TAT, penetratin, Pep-1, and TP10).

79 ilon-caprolactone) (PEG-PCL, PECL) to get DA-TAT-PECL.

80 acid-active tumor targeting nanoplatform DA-TAT-PECL is developed to inhibit the nonspecific interac

81 amines to carboxylic acid; the resulting DA-TAT is conjugated to poly(ethylene glycol)-poly(epsilon-

82 ferential impact of a protein kinase C-delta TAT peptide inhibitor (PKCdelta-i) was also quantified.

83 During glucose deprivation, TAT-p27 inhibited apoptosis, whereas down-regulation of

84 by fusing a TAT-peptide transduction domain (TAT-PTD) to the minimal modular elements of GIV that are

85 at acute myocardial dysfunction by high-dose TAT-HKII peptide administration is a consequence of impa

86 this profile resembles the greatly elevated TAT/PC activity ratios reported in patients with warfari

87 Following extinction, TAT-NET-Thr(30) when given prior to cocaine challenge si

88 f the BD MAX GBS assay but provides a faster TAT, less HoT, and higher throughput.

89 Here we use dimeric fluorescence TAT as a model CPP to explore the broader consequences o

90 4-390] versus 78 [19-240] ng/mL, P=0.002 for TAT).

91 Conclusion: Our first clinical data for TAT using (225)Ac-PSMA-I&T showed a promising antitumor

92 versus 183% [95% CI, 118%-248%] increase for TAT, P=0.048), with all patients in both groups progress

93 e obtained the dissociation constants Kd for TAT binding to POPC and POPG liposomes and the maximum n

94 elucidate the mechanistic underpinnings for TAT activity and its preference for microtubules with sl

95 Functionally, TAT.ARC treatment inhibited DAXX-ASK1-JNK signaling in t

96 Further, TAT-p27 enhanced autophagy and repressed cardiomyocytes

97 GABA type A (GABAA) receptor subunit gamma2 (TAT-GABAgamma2) and muscimol, a GABAA receptor agonist.

98 neoplastic lesions by (111)In-anti-gammaH2AX-TAT (defined as >5% injected dose per gram of tissue) wa

99 2.5-fold increase in (111)In-anti-gammaH2AX-TAT accumulation in the mammary fat pads of mice aged 76

100 Conclusion: (111)In-anti-gammaH2AX-TAT allows monitoring of DNA damage after (177)Lu-DOTATA

101 e SPECT imaging agent (111)In-anti-gammaH2AX-TAT allows visualization of the DNA damage repair marker

102 o investigate whether (111)In-anti-gammaH2AX-TAT detects the DDR during mammary oncogenesis in BALB-n

103 DDR imaging using (111)In-anti-gammaH2AX-TAT identified mammary tumors significantly earlier than

104 Conclusion: (111)In-anti-gammaH2AX-TAT imaging allows non-invasive detection of DNA damage

105 Conclusion: (111)In-anti-gammaH2AX-TAT imaging allows noninvasive detection of DNA damage r

106 e that show uptake of (111)In-anti-gammaH2AX-TAT in the pancreas survive for a significantly shorter

107 e that show uptake of (111)In-anti-gammaH2AX-TAT in the pancreas survive significantly shorter than m

108 (111)In-anti-gammaH2AX-TAT localises preferentially in high-grade PanIN lesions

109 (111)In-anti-gammaH2AX-TAT localizes preferentially in high-grade PanIN lesions

110 (111)In-anti-gammaH2AX-TAT or a control probe was administered intravenously to

111 mice with physiologic (111)In-anti-gammaH2AX-TAT uptake.

112 ce with physiological (111)In-anti-gammaH2AX-TAT uptake.

113 KPC mice imaged with (111)In-anti-gammaH2AX-TAT was evaluated.

114 d and coinjected with (111)In-anti-gammaH2AX-TAT, (111)In-IgG-TAT control, or vehicle.

115 SPECT imaging agent, (111)In-anti-gammaH2AX-TAT, allows visualisation of the DNA damage repair marke

116 Uptake of (111)In-anti-gammaH2AX-TAT, but not (111)In-IgG-TAT or (18)F-FDG, within the pa

117 Uptake of (111)In-anti-gammaH2AX-TAT, but not (111)In-IgG-TAT or (18)F-FDG, within the pa

118 ed with (18)F-FDG and (111)In-anti-gammaH2AX-TAT.

119 ng SPECT imaging with (111)In-anti-gammaH2AX-TAT.

120 ed with (18)F-FDG and (111)In-anti-gammaH2AX-TAT.

121 ator phenotype, with markedly elevated TCT-->TAT and TCG-->TTG mutations and overall mutation frequen

122 High TAT was related to a higher odds of low SMD (OR: 9.62; 9

123 netrating peptide (CPP) conjugate of the HIV TAT protein that is fused to an aminoterminal sequence o

124 rans-Activator of Transcription gene in HIV; TAT-4BB) affected LPS-induced intracellular calcium flux

125 In comparison I, TATs for 61,157 urine cultures were extracted for two pe

126 with (111)In-anti-gammaH2AX-TAT, (111)In-IgG-TAT control, or vehicle.

127 1)In-anti-gammaH2AX-TAT, but not (111)In-IgG-TAT or (18)F-FDG, within the pancreas correlated positiv

128 1)In-anti-gammaH2AX-TAT, but not (111)In-IgG-TAT or (18)F-FDG, within the pancreas was positively cor

129 MALDI-TOF MS significantly improved TAT for organism ID.

130 son II results, MALDI significantly improved TAT to organism ID compared to CONV (21.3 to 18 h).

131 In summary, TLA significantly improved TAT to organism ID, AST report, and preliminary negative

132 - SD; p = 0.005; T2-weighted MRI) smaller in TAT.ARC-treated mice (1 mug intraventricularly during MC

133 and tolyfluanid attenuated cortisol-induced TAT expression.

134 Szyk et al. now provide insight into TAT's mechanism of action and its unique time-stamping a

135 optimization methods that reduced the in-lab TAT for GAS NAAT.

136 regression established that the total in-lab TAT was significantly reduced by direct specimen submiss

137 ither by the previously described PDZ ligand TAT-GESV or by the ExF motif-bearing region of NOS1AP, e

138 the confined intraluminal location of Lys40, TAT efficiently scans the microtubule bidirectionally an

139 Before FIP implementation, the mean TAT varied between 77 and 83 minutes, with only 18%to 26

140 Moreover, TAT-Kalpha2 peptide protected the mice, that were challe

141 In the presence of an intact GEF motif, TAT-GIV-CT peptides enhanced diverse processes in which

142 One of them is the use of stable and native TAT-MeCP2 fusion proteins to replenish its levels in neu

143 istration of TAT-NET-Thr(30) peptide but not TAT-NET-T30A (mutant peptide) completely blocked cocaine

144 digm, mice receiving TAT-NET-Thr(30) but not TAT-NET-T30A on postconditioning test day exhibited sign

145 molecular weights of the TAT-Sox2, TAT-Oct4, TAT-Lin28, and TAT-Nanog fusion proteins were 36kD, 40kD

146 s further clarify the mechanism of action of TAT-CBD3 and identify a novel regulatory checkpoint for

147 sensitizing and antimetastatic activities of TAT-RasGAP317-326.

148 26 sequence for the anticancer activities of TAT-RasGAP317-326.

149 portantly, intraperitoneal administration of TAT-C1aB in mice following transient middle cerebral art

150 served, when compared with administration of TAT-gelonin alone.

151 Therapeutic administration of TAT-GILZ induced inflammation resolution, decreased cyto

152 In vivo administration of TAT-NET-Thr(30) peptide but not TAT-NET-T30A (mutant pep

153 Furthermore, topical application of TAT-GIV-CT peptides enhanced the complex, multireceptor-

154 ce-selective method, to study the binding of TAT to anionic 1-palmitoyl-2-oleoyl-sn-glycero-3-phospho

155 t by simply changing the relative content of TAT/CGC triplets in the switches, we can rationally tune

156 ignificantly augmented (58-fold) delivery of TAT-gelonin to the tumor target was observed, when compa

157 Finally, intra-striatal delivery of TAT-GluN1C1 did not affect acute responses to cocaine bu

158 Delayed delivery of TAT.ARC may present a promising target for stroke therap

159 , cardiac NE, beta-AR, and downregulation of TAT and plasma levels of NE.

160 the efficacy of TAT-CD degrees was assessed in a postinfection treatment

161 d to inhibit the nonspecific interactions of TAT in the bloodstream.

162 lipopolysaccharide and bacteremia but not of TAT and PAP.

163 s and thus to accelerate the optimization of TAT.

164 TH, whereas knockdown and overexpression of TAT demonstrated that TAT inhibited TH.

165 n-induced apoptosis, even in the presence of TAT-p27.

166 lyze brain tissue and study the transport of TAT-MeCP2 variants across an in vitro model of the blood

167 33a overexpression prevented upregulation of TAT and suppression of TH in the heart after streptozoto

168 een 77 and 83 minutes, with only 18%to 26%of TATs being 60 minutes or less; on-time FCSs averaged 29%

169 Effectively communicating the importance of TATs and on-time FCSs and publishing individual results

170 and POPG liposomes and the maximum number of TATs that can bind to a given liposome surface.

171 Inclusion of (Arg)9 or TAT(57-57) CPPs further modified the translation readout

172 Parnate, an enzymatic inhibitor of LSD1, or TAT-SNAG, a cell-permeable peptide corresponding to the

173 and TseL, despite lacking a classical Sec or TAT secretion signal, were able to reach the periplasm w

174 ition, TAT-CBD3, but not CBD3 without TAT or TAT-scramble peptide, inhibited increases in cytosolic C

175 c cell-permeable peptide derived from ORF45, TAT-10F10, which is composed of the ORF45 56 to 76 amino

176 Outcomeswere TAT, whichwas defined as "wheels out" to "wheels in," an

177 TLA further improved overall TAT to ID (18 to 16.5 h) and AST (42.3 to 40.7 h) result

178 4 versus 2.0 h) but showed a shorter overall TAT for all 60 samples (3.98 versus 7.18 h) due to an in

179 BG-P-TAT demonstrated significant suppression of neuroblastom

180 BG-P-TAT is a dual-targeting agent, targeting the NET functio

181 In conclusion, BG-P-TAT represents a potential lead candidate for the treatm

182 In this work, the novel compound BG-P-TAT was synthesized and evaluated in the neuroblastoma S

183 CPP sequence (Transportan > R8 > Penetratin~TAT > Xentry).

184 pplication of a NF-kappaB inhibitory peptide TAT-NBD or GAP43(S41A) (dominant-negative GAP43) or knoc

185 dification with the cell penetrating peptide TAT facilitates brain-specific delivery that is restrict

186 oparticles with the cell-penetrating peptide TAT increases their biophysical association with cell su

187 abeled dimer of the cell-penetrating peptide TAT, dfTAT, penetrates live cells by escaping from endos

188 ide linker (pp), a cell penetrating peptide (TAT), and a model drug (doxorubicin).

189 1 association with a cell-permeable peptide (TAT-GluN1C1) left individual D1R and NMDAR-dependent sig

190 The resulting peptide (TAT-C1aB) suppressed enhanced whole-cell K(+) currents p

191 th trans-activator of transcription peptide (TAT)-GILZ, a cell-permeable GILZ fusion protein, shorten

192 Furthermore, a peptide, TAT-HDAg-L(198-210), containing the 10-amino acid TAT pe

193 aptic currents, whereas the control peptide, TAT-myc, had no effect.

194 We saved 13 minutes per TAT, for an estimated savings of $177 000.We estimate an

195 ugated PKCdelta inhibitory peptide (PKCdelta-TAT) is lung protective in a rat model of sepsis-induced

196 epatocellular and endothelial damage, plasma TAT concentration, and hepatic platelet accumulation wer

197 t affect APAP-induced liver injury or plasma TAT levels.

198 Prolonged TATs and late FCSs occur frequently at academic medical

199 at ectopic delivery of a p27 fusion protein (TAT-p27) was sufficient to induce autophagy in neonatal

200 cell-penetrating motif of the HIV-1 protein, TAT-CBD3, but not CBD3 without TAT, attenuated N-methyl-

201 forms a BSL that is sandwiched between PRP5, TAT-SF1 and SF3B1(HEAT).

202 he aim of this work was to characterize PSMA-TAT-nonresponding lesions by targeted next-generation se

203 ings encourage future studies combining PSMA-TAT and DNA damage-repair-targeting agents such as poly(

204 Conclusion: Patients with resistance to PSMA-TAT despite PSMA positivity frequently harbor mutations

205 acity of five CPP sequences (Penetratin, R8, TAT, Transportan, Xentry) and cyclic derivatives in diff

206 Median (range) TAT for plasma ddPCR was 3 (1-7) days.

207 Tissue genotyping median (range) TAT was 12 (1-54) days for patients with newly diagnosed

208 free tubulin and its modest catalytic rate, TAT can function as a slow clock for microtubule lifetim

209 In the cocaine CPP paradigm, mice receiving TAT-NET-Thr(30) but not TAT-NET-T30A on postconditioning

210 ath domain of the p75 neurotrophin receptor (TAT-Pep5) and in mice lacking the extracellular neurotro

211 to measure endogenous MeCP2 and recombinant TAT-MeCP2 fusion protein levels in a 96-well plate forma

212 the intravenous injection of the recombinant TAT-Cre protein alters the amplitude of the preovulatory

213 ide (Abeta1-6A2V), linked to the HIV-related TAT protein, which is widely used for brain delivery and

214 significant decreases in microbiology report TATs.

215 he thylakoid membrane and lumen by the SEC1, TAT, or SRP/ALB3 translocases.

216 adhesion molecule-1, E-selectin, P-selectin, TAT (thrombin/antithrombin complex), tumor necrosis fact

217 sted CPSs, also better than the much smaller TAT peptide, the original cell-penetrating peptide from

218 The molecular weights of the TAT-Sox2, TAT-Oct4, TAT-Lin28, and TAT-Nanog fusion proteins were

219 rpart on beta-arrestin-2 or using a specific TAT-P1 peptide to block the interaction between beta-arr

220 pression in CATH.a neuronal cells suppressed TAT with concomitant upregulation of TH, whereas knockdo

221 ontractility of diabetic hearts by targeting TAT, regulating NE biosynthesis, and consequently, beta-

222 porter assay confirmed that miR-133a targets TAT.

223 CRMP2 interacts with NCX and NMDAR and that TAT-CBD3 protects against glutamate-induced Ca(2+) dysre

224 at rest and after metabolic stress, and that TAT-p27 inhibits apoptosis by promoting autophagy in glu

225 ingle-molecule measurements demonstrate that TAT catalytic activity, not constrained luminal diffusio

226 and overexpression of TAT demonstrated that TAT inhibited TH.

227 Mechanistically, we found that TAT-Kalpha2 peptide destabilized the viral membranes, de

228 We found that TAT-STEP, a peptide that renders STEP enzymatically inac

229 ing with an anti-NCX3 antibody revealed that TAT-CBD3 induced NCX3 internalization, suggesting that b

230 says with diverse tubulin polymers show that TAT is stimulated by microtubule interprotofilament cont

231 This work shows that TAT-RasGAP(317-326) kills cells via a form of necrosis t

232 These results suggest that TAT-Kalpha2 peptide is a potential antiviral agent for c

233 The TAT for nevi decreased from 2 days to 1 day, for melanom

234 nged from 1.2 to 3.5 min per sample, and the TAT was 1 to 2.3 h.

235 4 (BMP4), EGF, or PDGF was unaffected by the TAT-SNX9 peptide.

236 ce of amino acids in the protein, called the TAT peptide, enables the TAT protein to penetrate cell m

237 maleic anhydride (DA) is used to convert the TAT's amines to carboxylic acid; the resulting DA-TAT is

238 protein, called the TAT peptide, enables the TAT protein to penetrate cell membranes.

239 six polyethylene glycol (PEG) units from the TAT-PTD-cargo significantly enhanced cytoplasmic deliver

240 eshielding and exposure of the TAT; (iv) the TAT-mediated cell internalization; (v) the TAT-induced e

241 ctures formed in the absence of ligands, the TAT triad interface occludes ligand binding at the 3' qu

242 ing activity, warning against the use of the TAT carrier in the design of AD therapeutics.

243 chanisms of binding and translocation of the TAT peptide into the cell, investigators have used phosp

244 Acute systemic administration of the TAT-4BB reversed M3G-induced tactile allodynia in a dose

245 The molecular weights of the TAT-Sox2, TAT-Oct4, TAT-Lin28, and TAT-Nanog fusion prot

246 mediated PEG deshielding and exposure of the TAT; (iv) the TAT-mediated cell internalization; (v) the

247 efficacy studies also revealed that only the TAT-gelonin/T84.66-Hep complex yielded a significant inh

248 -amino acid peptide from CRMP2, fused to the TAT cell-penetrating motif of the HIV-1 protein, TAT-CBD

249 with Abeta1-6A2VTAT(D) was likely due to the TAT intrinsic attitude to increase Abeta production, avi

250 ion of the Poisson-Boltzmann equation to the TAT liposome SHG data, was shown to be in good agreement

251 tor insertion in the cell membrane using the TAT-GABAgamma2 peptide in the dorsal mPFC, but not the v

252 nting the nuclear import of pSMAD3 using the TAT-SNX9 peptide inhibited profibrotic TGF-beta activity

253 ption of the TROY/RKIP interaction using the TAT-TROY (234-371 aa) protein reduced the glioma develop

254 e TAT-mediated cell internalization; (v) the TAT-induced endosomal escape; (vi) the inhibition of P-g

255 oprotein mediated drug efflux; and (vii) the TAT-medicated nuclear translocation.

256 Furthermore, while the TAT-SNX9 peptide prevented TGF-beta's profibrotic activi

257 ment with the Kalpha2 peptide fused with the TAT peptide significantly inhibited IAV replication and

258 remendous promise in targeted alpha therapy (TAT) applications due to its attractive half-life and it

259 225) Ac chelation in targeted alpha therapy (TAT).

260 Targeted alpha-therapy (TAT) appears to be an ideal therapeutic technique for el

261 inical data for PSMA-targeted alpha-therapy (TAT) using (225)Ac-PSMA imaging and therapy (I&T).

262 en (PSMA)-targeting alpha-radiation therapy (TAT) is an emerging treatment modality for metastatic ca

263 Thus, TAT-GIV peptides provide a novel and versatile tool to m

264 and their effect on in-lab turnaround time (TAT) at a tertiary care microbiology lab.

265 ecimen containers, and long turnaround time (TAT) hindered access to quality laboratory services.

266 However, improving the turnaround time (TAT) of a test requires attention to more than the analy

267 e specimen can increase the turnaround time (TAT) significantly.

268 nds-on time (HoT) and total turnaround time (TAT) varied considerably depending on the sample number

269 Test turnaround time (TAT) was measured in business days from blood sampling u

270 thm with a short analytical turnaround time (TAT), and prospectively validated the algorithm.

271 first results (TFR), total turnaround time (TAT), number of return visits to load additional specime

272 cular assay with a 3-h test-turnaround-time (TAT).

273 Operating room (OR) turnaround times (TATs) and on-time first-case starts (FCSs) are commonly

274 technologies, we compared turnaround times (TATs) for positive and negative urine cultures before an

275 ulness of EVD with DD, and turnaround times (TATs).

276 ulness of EVD with DD, and turnaround times (TATs).

277 ding age, stage, site, total adipose tissue (TAT), race/ethnicity, neutrophil-lymphocyte ratio, smoki

278 mparison I results, median pre- and post-TLA TATs to organism IDs (18.5 to 16.9 h), AST results (41.8

279 P(2) in cells renders them more resistant to TAT-RasGAP(317-326), while reducing the ability of cells

280 revented NCX3 internalization in response to TAT-CBD3 exposure.

281 When mixing together, TAT-gelonin and T84.66-Hep could associate tightly and a

282 A transactivator of transcription (TAT) peptide strategy was utilized to test the involveme

283 e effect of transactivator of transcription (TAT) protein transduction of the apoptosis repressor wit

284 e expressed transactivator of transcription (TAT)-fused proteins, Sox2, Oct4, Lin28, and Nanog in Sf9

285 of various transactivator of transcription (TAT)-MeCP2 variants and the development of an electroche

286 ing peptide transactivator of transcription (TAT).

287 The transacting activator of transduction (TAT) protein plays a key role in the progression of AIDS

288 Using TAT-tagged peptides and chimeric constructs that are una

289 evels were associated with increases in VAT, TAT, and BMI (16%, 9%, and 2.5%, respectively; P < .04)

290 n domain of the human immunodeficiency virus TAT protein (Tat), an Angiopep peptide (Ang-2), and the

291 The W317A TAT-RasGAP(317-326) point mutant, known to have impaired

292 NF-kappaB inhibitor-treated groups, whereas TAT levels were elevated in all three groups with a peak

293 dies provide a structural explanation of why TAT-SF1 must be displaced before the stable addition of

294 r performance in the pole test compared with TAT.beta-Gal-treated controls.

295 Blocking neutrophil degranulation with TAT-SNAP23 fusion protein significantly reduced the chem

296 Here, we use NPs functionalized with TAT (transactivator of transcription) peptide (T-NPs) as

297 cological blockade of Cx43 hemichannels with TAT-Gap19 also significantly decreased infarct volume in

298 These changes were linked with TAT-Gap19-induced suppression of ATP signaling and activ

299 In vitro treatment of synaptosomes with TAT-NET-Thr(30) (wild-type peptide) completely blocked c

300 In addition, TAT-CBD3, but not CBD3 without TAT or TAT-scramble peptide, inhibited increases in cyto

301 IV-1 protein, TAT-CBD3, but not CBD3 without TAT, attenuated N-methyl-d-aspartate receptor (NMDAR) ac