ライフサイエンスコーパス: TTD

1 TTD < 9 days identifies patients at high risk of transmi

2 TTD is caused by mutations in DNA repair/transcription g

3 TTD is caused by variations in 10 genes: 3 nucleotide ex

4 TTD is now freely accessible at:

5 TTD mutants lose or retain helicase activity but map to

6 TTD was summarised using a stratified Cox proportional h

7 TTD was the time from withdrawal of life-sustaining trea

8 We followed a cohort of 36 TTD patients from 2001 to 2013.

9 UNC8531 was cocrystallized with the 53BP1 TTD to guide further optimization efforts, leading to UN

10 A mouse with a TTD mutation has now been found to display remarkable si

11 an Sgf29 orthologue in Dictyostelium with a TTD that specifically recognizes the H3K4me3 modificatio

12 All TTD hair samples had reduced sulfur content.

13 Its reduction characterizes all TTD cases so far investigated, both the PS-TTD with muta

14 letion of 716-730 are found in both XP-D and TTD cell strains.

15 es include the familiar COSMIC, Drugbank and TTD.

16 ins intermediate between those of normal and TTD individuals.

17 ifferences between xeroderma pigmentosum and TTD and illustrate the value of suppressor genetics for

18 type I in the ECM of cell/tissue systems and TTD patient skin.

19 ated with higher percentages of CD4+ TEM and TTD cells.

20 orts of combined clinical features of XP and TTD.

21 XPC and TTD/XPD cell lines were complemented using retroviral tr

22 bal repair rate, in the complemented XPC and TTD/XPD cells, almost all of the CPDs at "hotspots" for

23 In both XPC and TTD/XPD complemented lines, CPD repair on the non-transc

24 We found that the apo TTD-PHD module in solution comprises a dynamic ensemble

25 uding key residues across the autoinhibitory TTD-PBR interface.

26 tandem Tudor domain (TTD) in BAHCC1 (BAHCC1(TTD)) selectively reads H4K20me1 for facilitating replic

27 In summary, this study identifies BAHCC1(TTD) as an effector transducing H4K20me1 signals into MC

28 nd cellular analyses demonstrate that BAHCC1(TTD) preferentially recognizes H4K20me1 to promote the r

29 etion of BAHCC1, or disruption of the BAHCC1(TTD):H4K20me1 interaction, reduces H4K20me1 levels and M

30 is and in the phenotypic differences between TTD and XP.

31 d graft survival and no relationship between TTD and graft survival.

32 o further delineate the relationship between TTD and outcome.

33 rm of the tricothiodystrophy disorder called TTD-A(2).

34 hat the specific mutations in XPD that cause TTD result in reduced expression of the beta-globin gene

35 , respectively), whereas some characteristic TTD clinical, laboratory, and imaging findings were abse

36 D domain, resulting in creation of a coupled TTD-PHD module.

37 plicably associated with (XP) or without (CS/TTD) cancer.

38 In the therapeutic target database (TTD), nine categories of established druggability charac

39 base (CTD) and Therapeutic Targets Database (TTD), respectively.

40 d half the LD50 and decreased time to death (TTD) of wild type and complement B. anthracis Sterne in

41 and-down times based on donor time to death (TTD).

42 and down in relation to donor time to death (TTD).

43 Although true time delay (TTD) elements(12) solve this problem and service a broad

44 Switching to camizestrant-CDK4/6i delayed TTD and reduced the risk of deterioration in patient-rep

45 . aeruginosa had similar times to detection (TTD) (P = 0.352); however, antibiotic-containing BacT/Al

46 We assessed the time to detection (TTD) and growth of 2 Pseudomonas aeruginosa isolates in

47 The mean times to detection (TTD) for M. tuberculosis complex were 14.4 days for BACT

48 re the sensitivities and times to detection (TTD) of BacT/Alert Pediatric FAN (PF) and Bactec Peds Pl

49 The 1G test time to detection (TTD) of Mtb and simultaneous DST was 17-days, while the

50 AM concentration and MGIT time to detection (TTD) showed a good inverse relationship (r = -0.803, p <

51 d for concordance, median time to detection (TTD), and diagnostic performance based on 2013 Musculosk

52 n on test sensitivity and time to detection (TTD).

53 We hypothesize that time-to-detection (TTD) in liquid culture of spontaneously produced sputum

54 econdary endpoints of time to deterioration (TTD) in pain, physical functioning, breast symptoms and

55 Time to deterioration (TTD), change in overall status, and patient-reported tol

56 ording to five periods of time to diagnosis (TTD).

57 in a linker region connecting the different TTD and PHD histone modification-binding domains causes

58 ddition, our work suggests that differential TTD binding properties across the KDM4 demethylase famil

59 n secondary end points of time to discharge (TTD), time to discontinuation of IV opioids (TTDIVO), an

60 terms of time-to-treatment discontinuation (TTD) and extended- to standard-interval pembrolizumab pr

61 estimate time to treatment discontinuation (TTD) and overall survival (OS).

62 al (PFS), time to treatment discontinuation (TTD), and time to next treatment (TTNT) are alternative

63 Time to treatment discontinuation (TTD), probability of discontinuation, and treatment pers

64 xcept for time-to-treatment discontinuation (TTD), which began at treatment initiation.

65 (OS), and time to treatment discontinuation (TTD).

66 logy and concerted effort in drug discovery, TTD and other databases were highly expected to facilita

67 ved in trichothiodystrophy group A disorder (TTD-A), was key in the completion of the PInC.

68 protein, termed the tat transduction domain (TTD), has been shown to mediate transfer of biomolecules

69 ters through its hybrid tandem tudor domain (TTD) (1, 2), providing a model for how these modificatio

70 volutionarily conserved tandem Tudor domain (TTD) in BAHCC1 (BAHCC1(TTD)) selectively reads H4K20me1

71 , which binds the 53BP1 tandem Tudor domain (TTD) with an IC(50) of 0.47 +/- 0.09 muM in a TR-FRET as

72 blocks interaction of a tandem tudor domain (TTD) with H3K9me3 by occupying an essential peptide-bind

73 ting the isolated UHRF1 tandem Tudor domain (TTD), which recognizes the heterochromatin-associated hi

74 acts with H3K4me3 via a tandem tudor domain (TTD).

75 Donor TTD was not associated with recipient 12-month eGFR on a

76 cohort study of DCD kidney recipients, donor TTD was not associated with posttransplant outcomes, in

77 ell-known databases, such as HMDB, DrugBank, TTD and PubMed etc.

78 ork reveals a mechanism by which the dynamic TTD-PHD module can be allosterically targeted with small

79 Eleven TTD patients with characterized mutations in the XPD gen

80 lysis and log-rank test were used to examine TTD.

81 DNA complex is thermodynamically favored for TTD-containing DNA over undamaged DNA, most likely becau

82 tify the expression alterations specific for TTD primary dermal fibroblasts.

83 Raman spectra of hairs from TTD patients and normal donors revealed a larger contrib

84 f the tandem tudor domain-plant homeodomain (TTD-PHD) histone reader module, including its 20-residue

85 d tandem Tudor domain and plant homeodomain (TTD-PHD) of UHRF1, thus mediating ortholog-specific UHRF

86 We assessed what impact TTD had on outcomes following DCD liver transplantation.

87 We examined what impact TTD had on pancreas graft outcomes following donors afte

88 Utilizing IMC for PJI detection improves TTD by nearly 2 days while improving diagnostic accuracy

89 r and tissue homeostasis, ECM alterations in TTD were shown to impact on the migration and wound-heal

90 highlights the relevance of ECM anomalies in TTD pathogenesis and in the phenotypic differences betwe

91 tically less favored disulfide conformers in TTD hairs.

92 grade correlated with a 3.2-day decrease in TTD (P < .001), and this correlation persisted after adj

93 ention-to-treat principle, no differences in TTD were observed between standard- and extended-interva

94 lagens of the extracellular matrix (ECM), in TTD patients mutated in XPD compared with their healthy

95 ecruitment on the PTGIS promoter is found in TTD but not in XP cells.

96 taglandin I(2) synthase (PTGIS) are found in TTD cells.

97 for reduced expression of a specific gene in TTD.

98 lts expand the spectrum of genes involved in TTD to include genes implicated in amino acid charging o

99 by the observation that double mutations in TTD that abolished its interaction with Rpa12 also great

100 The defect is observed in TTD and not in XP and is specific for fibroblasts, which

101 has been identified previously, but only in TTD patients with no features of XP.

102 reatment RESET placebo showed a reduction in TTD of 23.1 hours (P = .062) and in TTDIVO of 30.1 hours

103 MMP-1 transcriptional up-regulation in TTD is caused by an erroneous signaling mediated by reti

104 dentify a distinct phenotype relationship in TTD caused by TTDN1 mutations and suggest a different me

105 osphorylation of TFIIEalpha was also seen in TTD cells with mutations in ERCC2, which encodes the XPD

106 Candidate surrogate end points included TTD; TTNT; PFS based on imaging reports only; PFS based

107 Increasing TTD was not associated with graft survival (adjusted haz

108 Log-rank test indicated TTD was significantly longer for patients on OTX-101 vs.

109 ured structural features of breaks in intact TTD hairs.

110 These changes make TTD hairs excessively prone to breakage and weathering.

111 The mean TTD were shorter in the Peds Plus system controls (14.2

112 Median TTD in the entire cohort was 13 min (interquartile range

113 Median TTD was 15 minutes (range, 0-407 minutes), with 885 kidn

114 Median TTD was 354 days for patients receiving OTX-101 vs. 241

115 ative percentages by day detected and median TTD of initial and follow-up specimens were analyzed.

116 d median TTRFD by 56.3 hours, reduced median TTD by 41.5 hours, and reduced median TTDIVO by 50.5 hou

117 The median TTD of PJI by cultures was 51 (21-410) hours compared to

118 was 2.0 (95% CI, 1.5-2.5) years; the median TTD was 1.5 (95% CI, 1.0-2.1) years.

119 5.8 (95% CI, 5.6-6.1) years, and the median TTD was 4.2 (95% CI, 4.1-4.4) years.

120 The median TTD-MTBC for BacT/Alert (n = 3 sites) was 18 days, with

121 The median TTD-MTBC for MGIT (n = 6 sites) was 14 days.

122 to 85% for cultures (P < 0.001) with median TTD of 12 (0.5-127) hours compared to 52 (21-174) hours

123 ponding to an increase of 221 hours for MGIT TTD during the first 14 days of treatment, a treatment d

124 entrations correlated with increases of MGIT TTD in individual patients.

125 si-true time delay (Q-TTD) that miniaturizes TTD elements and breaks fundamental channel-capacity lim

126 ycobacteria (TTD-all, n = 1547) and of MTBC (TTD-MTBC, n = 466) over 6-month periods from primarily (

127 ts of time to detection of all mycobacteria (TTD-all, n = 1547) and of MTBC (TTD-MTBC, n = 466) over

128 defects, mirroring phenotypes observed in NP-TTD patient cells.

129 ain neurodevelopmental phenotypes seen in NP-TTD.

130 n non-photosensitive trichothiodystrophy (NP-TTD), functionally links intron lariat processing to spl

131 genes as well as the nonphotosensitive (NPS)-TTD.

132 Here we present the identification of an NPS-TTD-associated gene, threonyl-tRNA synthetase (TARS), fo

133 ts a biomarker that combines all PS- and NPS-TTD cases and distinguishes them from XP.

134 variants as new gene defects that cause NPS-TTD.

135 fferent non-photosensitive forms of TTD (NPS-TTD), which do not appear to show features of premature

136 associated with non-photosensitive TTD (NPS-TTD); these include MPLKIP (also called TTDN1), GTF2E2 (

137 ly large group of these individuals with NPS-TTD have remained genetically uncharacterized.

138 roup of uncharacterized individuals with NPS-TTD.

139 Patients suffering from XP and 50% of TTD afflicted individuals are photosensitive and have a

140 nsitivity is present in approximately 50% of TTD patients but is not associated with an elevated freq

141 CD4+ cells (residues 632-651 and 950-969 of TTD and 271-290, 321-350, 351-370, 411-430, and 431-450

142 The extension of reduced abundance of TTD factors to translation as well as transcription rede

143 Analysis of TTD of positive MTBC cultures in broth can predict the p

144 n primary fibroblasts from a large cohort of TTD or XP cases with mutations in ERCC2/XPD gene, we ide

145 We studied the correlation of TTD with the risk of transmission of infection from inde

146 We now extend the definition of TTD from a transcription syndrome to a "gene-expression"

147 ed linear regression (change per doubling of TTD, -0.25; 95% CI, -0.68 to 0.19; P = .27), nor with de

148 Duration of TTD, defined as time from WLST to donor mechanical asyst

149 urvival rather than focus on the duration of TTD.

150 asize this phenomenon as a common feature of TTD.

151 thesis that many of the clinical features of TTD result from inadequate expression of a diverse set o

152 abinas brittle hair syndrome, a mild form of TTD.

153 or the different non-photosensitive forms of TTD (NPS-TTD), which do not appear to show features of p

154 The mechanism of TTD-mediated membrane translocation is currently unknown

155 To study the mechanism of TTD-mediated membrane translocation, the TTD was fused t

156 donors and markedly irregular in sections of TTD hairs possibly reflecting abnormalities in melanin d

157 A model for the first step of TTD-mediated entry into cells is presented.

158 hildren showing clinical features typical of TTD who harbor different homozygous missense mutations i

159 nding pockets that are in close proximity on TTD and so has the potential to be evolved into more pot

160 gnized both toxoids, those of 1 subject only TTD, and those of 1 only DTD.

161 petes with linker binding, and promotes open TTD-PHD conformations that are less efficient at H3K9me3

162 Laboratories should analyze their own TTD data to inform protocol decisions.

163 PG-TTD has been shown to bind to heparin by isothermal titr

164 n of streptococcal protein G (PG) to form PG-TTD.

165 heteronuclear relaxation measurements of PG-TTD in complex with heparin show that the TTD becomes le

166 NMR studies of PG-TTD in the free state indicated that the structure of th

167 Heteronuclear relaxation measurements of PG-TTD in the free state show that the TTD moiety of PG-TTD

168 he free state show that the TTD moiety of PG-TTD is relatively mobile (e.g., the average S(2) value o

169 ed that the structure of the PG moiety of PG-TTD was not perturbed by the presence of the TTD and tha

170 d that heparin binds to the TTD moiety of PG-TTD.

171 und to be associated with non-photosensitive TTD (NPS-TTD); these include MPLKIP (also called TTDN1),

172 The photosensitive TTD (PS-TTD) forms exhibits in addition to progressive n

173 l TTD cases so far investigated, both the PS-TTD with mutations in TFIIH coding genes as well as the

174 -free photosensitive trichothiodystrophy (PS-TTD) and the cancer-prone xeroderma pigmentosum (XP) are

175 The photosensitive TTD (PS-TTD) forms exhibits in addition to progressive neuropath

176 em by introducing a quasi-true time delay (Q-TTD) that miniaturizes TTD elements and breaks fundament

177 The XPD(R658H) TTD protein, like XPD(T46I/R658H), is codominant when ov

178 anslation as well as transcription redefines TTD as a syndrome in which proteins involved in gene exp

179 2 to Trp correlates with highly UV-sensitive TTD cell strains, and mutation of Arg683 to Trp correlat

180 erall, we demonstrated superior sensitivity, TTD, and antibiotic neutralization in the Bactec Peds Pl

181 Short TTD (<9 days) was associated with an increased risk of t

182 A very short TTD was associated with increased risk of graft loss, po

183 de at diagnosis predicts patients with short TTD.

184 -containing BacT/Alert bottles had a shorter TTD compared with antibiotic-containing Bactec bottles f

185 nd revealed increasing accuracy with shorter TTD (<4.5 years before diagnosis: area under the curve =

186 h its first 15 amino acids, depleted in some TTD-A patients.

187 d DNA binding and transcription termination (TTD) domains.

188 demethylation by KDM4C and demonstrated that TTD-mediated recognition of H3K4me3 stimulates demethyla

189 We found no evidence that TTD impacts pancreas graft survival after DCD simultaneo

190 by DBR1 variations, further indicating that TTD is a disorder of RNA metabolism (RNAopathy).

191 ndings extend our previous observations that TTD mutations affect the stability of the corresponding

192 Our findings support the theory that TTD is caused by transcriptional impairments that are di

193 The TTD for MAC in each system were 10.0 days for BACTEC MGI

194 The TTD peptides and DTD peptides 271-290 and 331-350 were r

195 l rearrangement of the domains, allowing the TTD to bind H3K9me3.

196 le hydrogen-bonding interactions between the TTD and dATP than between the TTD and dGTP.

197 ns between the TTD and dATP than between the TTD and dGTP.

198 ve hydrogen-bonding interactions between the TTD and the enzyme that hold the TTD more rigidly in pla

199 er, protein-protein interactions between the TTD with the Rpa12 subunit of RNA pol I seem to be an in

200 replication termination is distinct from the TTD.

201 between the TTD and the enzyme that hold the TTD more rigidly in place.

202 conformations, with the linker lying in the TTD peptide-binding groove.

203 When P. aeruginosa was isolated, the TTD was typically <26 h, and no differences between Bact

204 mobile (e.g., the average S(2) value of the TTD and PG core are approximately 0.54 and approximately

205 TTD was not perturbed by the presence of the TTD and that the TTD moiety is in an extended conformati

206 inker is anchored in a surface groove of the TTD domain, resulting in creation of a coupled TTD-PHD m

207 ur data indicate that the brittleness of the TTD hair is dependent upon abnormalities at several leve

208 T base pair formed at the 3' position of the TTD in the previous step of Pol eta function.

209 bound to heparin (average S(2) value of the TTD is 0.69 in the presence of heparin).

210 Although most of the TTD patients are photosensitive, patients with TTDN1 mut

211 atively investigated the contribution of the TTD to the catalysis of H3K9me3 demethylation by KDM4C a

212 GTP binding at both thymine positions of the TTD, most likely due to more persistent and stable hydro

213 We previously proposed that some of the TTD-specific features derive from subtle transcription d

214 The findings support the TTD equivalence of standard- and extended-interval pembr

215 PG-TTD in complex with heparin show that the TTD becomes less dynamic when bound to heparin (average

216 rbed by the presence of the TTD and that the TTD moiety is in an extended conformation.

217 ts of PG-TTD in the free state show that the TTD moiety of PG-TTD is relatively mobile (e.g., the ave

218 eridine-1-carboximidamide, that binds to the TTD groove, competes with linker binding, and promotes o

219 scopy demonstrated that heparin binds to the TTD moiety of PG-TTD.

220 of TTD-mediated membrane translocation, the TTD was fused to the C-terminus of a model cargo protein

221 led from new-generation thiophenthiadiazole (TTD)-based NIR-II fluorophores HLAnP (n = 1-4) for simul

222 quence analysis of the ERCC2 cDNA from three TTD cell strains (TTD1V1, TTD3VI, and TTD1RO) revealed m

223 n of CD4+ cell-enriched blood lymphocytes to TTD and DTD and individual synthetic universal epitopes

224 se also impairing transcription give rise to TTD.

225 the epitope peptides correlated with that to TTD or DTD, consistent with recognition of the peptides

226 ggested that tetanus and diphtheria toxoids (TTD and DTD, respectively) contain "universal" epitopes

227 Trichothiodystrophy (TTD) is a complex disorder caused by mutations in the XP

228 Trichothiodystrophy (TTD) is a rare autosomal recessive disorder characterize

229 Trichothiodystrophy (TTD) is a rare hereditary neurodevelopmental disorder de

230 Trichothiodystrophy (TTD) is a rare multisystem disorder, characterized by su

231 Trichothiodystrophy (TTD), a rare, autosomal recessive, multisystem developme

232 ma pigmentosum (XP) and trichothiodystrophy (TTD) are rare heritable diseases.

233 kayne syndrome (CS) and trichothiodystrophy (TTD)), which are inexplicably associated with (XP) or wi

234 ma pigmentosum (XP) and trichothiodystrophy (TTD).

235 ayne syndrome (CS), and trichothiodystrophy (TTD).

236 e multi-system disorder trichothiodystrophy (TTD), in which there is no skin cancer predisposition, o

237 he multisystem disorder trichothiodystrophy (TTD), which share only cutaneous photosensitivity.

238 developmental disorder trichothiodystrophy (TTD).

239 e clinical phenotype of trichothiodystrophy (TTD) in several patients who display intermediate UV sen

240 diagnostic hallmark of trichothiodystrophy (TTD), a rare recessive disease associated with a wide sp

241 r from 15 patients with trichothiodystrophy (TTD), a rare inherited disorder with brittle, cystine-de

242 Better performance was observed when using TTD instead of CTD when drug-indication associations app

243 pe phase-shifting structure with 3D variable TTD reflectors within a sub-wavelength footprint.

244 of graft loss was significantly greater when TTD <=14 min.

245 e multi-system abnormalities associated with TTD are the result of a subtle deficiency in basal trans

246 HBV-SNPs showed significant association with TTD after adjustment for HBV genotype, 24 of which could

247 Similar patterns of associations with TTD were observed.

248 d a standard incubator at 37 degrees C, with TTD and CFU being monitored for up to 72 h.

249 f Arg658 to either His or Cys correlate with TTD cell strains with intermediate UV-sensitivity, mutat

250 th 885 kidneys transplanted from donors with TTD over 1 hour and 303 kidneys transplanted from donors

251 nd 303 kidneys transplanted from donors with TTD over 2 hours.

252 t is found in about half of individuals with TTD; all of these individuals harbor bi-allelic mutation

253 y, and renal function in both fast aging Xpd(TTD/TTD) and naturally aged mice.

254 pair genes ERCC1 and XPD (Ercc1(d/-) and Xpd(TTD) mice), we explored age-dependent vascular function

255 ium-dependent vasodilator dysfunction in Xpd(TTD) animals was increased.