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 mutants lose or retain helicase activity but map to

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

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

6 All TTD hair samples had reduced sulfur content.

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

8 ins intermediate between those of normal and TTD individuals.

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

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

11 orts of combined clinical features of XP and TTD.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

32 Eleven TTD patients with characterized mutations in the XPD gen

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

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

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

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

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

38 tically less favored disulfide conformers in TTD hairs.

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

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

41 for reduced expression of a specific gene in TTD.

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

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

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

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

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

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

48 ured structural features of breaks in intact TTD hairs.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

79 2 to Trp correlates with highly UV-sensitive TTD cell strains, and mutation of Arg683 to Trp correlat

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

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

82 de at diagnosis predicts patients with short TTD.

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

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

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

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

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

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

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

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

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

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

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

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

95 replication termination is distinct from the TTD.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

126 developmental disorder trichothiodystrophy (TTD).

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

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

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

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

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

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

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

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

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