ライフサイエンスコーパス: TnT

1 TnT in insects contains a highly-diverged structure cons

2 TnT may serve as a bridge between the Ca(2+) sensor (TnC

3 ts Tm*146-TnI, Tm*146-troponin C, and Tm*146-TnT using fluorescence-labeled TnI, mass spectrometry, a

4 icles was capped by a gelsolin (segment 1-3)-TnT fusion protein (substituting for normal TnT), and th

5 iment with adeno-associated virus serotype 9 TnT-MEK1-CA nearly abolished the detrimental phenotype o

6 diac Trpm7 deletion (before embryonic day 9; TnT/Isl1-Cre) results in congestive heart failure and de

7 A TnT sensitive layer was prepared by electropolymerisatio

8 nC complexes to fully relax the fibers after TnT displacement was also compromised.

9 3.7, actin filaments containing high-alanine TnT had an elevated ATPase rate like that obtained when

10 High-alanine TnT-containing cardiac muscle preparations had increased

11 ics revealed that at pCa 8, the high-alanine TnT-containing filaments did not enter the first inactiv

12 t transition was abolished with high-alanine TnT.

13 hanges in the affinity of some, but not all, TnT mutants for Tm relative to WT TnT.

14 rdiac troponin T mutants (TnT(1-44Delta) and TnT(45-74Delta)) that have a divergent effect on the ove

15 cho Bernardo Study with plasma NT-proBNP and TnT measured at baseline (1997 to 1999) and followed up

16 f TnC (the sensor), TnI (the regulator), and TnT (the link to the muscle thin filament) have been det

17 s that the long framework helices of TnI and TnT, presumed to be a Ca(2+)-independent structural doma

18 Tn is composed of TnC, TnI, and TnT.

19 and detectable TnT vs. low NT-proBNP and any TnT: 3.20, 95% CI: 1.91 to 5.38, p < 0.001).

20 analyzed all four reported mutants: Arg63His TnT, Arg91Gly beta-TM, Arg174Gln TnI, and a TnI truncati

21 tients, with mice expressing the more benign TnT-R278C mutant (R278C) that does not affect myofilamen

22 bitory effect on binary interactions between TnT and other thin filament proteins, TnI, TnC and Tm.

23 Those with both TnT and NT-proBNP elevations are at even higher risk, an

24 unohistochemistry detected ssTnT and cardiac TnT in nuclear bag fibres, whereas fast skeletal muscle

25 to adult and fetal isoforms of human cardiac TnT (HCTnT3-DeltaE96 and HCTnT1-DeltaE106, respectively)

26 We generated a human cardiac TnT variant in which we replaced seven C-terminal Lys an

27 de that C-terminal basic residues in cardiac TnT are critical for the regulation of cardiac muscle co

28 -92W and R-92L missense mutations in cardiac TnT known to alter the flexibility of the TnT tropomyosi

29 KO mice have significantly increased cardiac TnT.

30 ut mice have significantly increased cardiac TnT.

31 earts in which the endogenous intact cardiac TnT was partially replaced by cTnT-ND showed lowered con

32 st, mu-calpain treatment of isolated cardiac TnT resulted in nonspecific degradation, suggesting that

33 with an abnormally spliced myopathic cardiac TnT (cTnT).

34 demonstrated in naturally occurring cardiac TnT isoforms, indicating a physiological significance.

35 utations in the TM-binding domain of cardiac TnT alter thin filament structure and flexibility suffic

36 mice contain a significant level of cardiac TnT and a low molecular weight splice form of ssTnT.

37 ibres contain a significant level of cardiac TnT and the low molecular weight splice form of ssTnT.

38 ssTnT and a compensatory increase of cardiac TnT in intrafusal nuclear bag fibres may increase myofil

39 ssTnT and a compensatory increase of cardiac TnT in nuclear bag fibres would increase myofilament Ca(

40 ion that removes amino acids 1-71 of cardiac TnT.

41 Dynamic features of rat cardiac TnT (cTnT) and rat fast skeletal TnT (fsTnT) reconstitut

42 eins were complexed with recombinant cardiac TnT/TnC and exchanged into skinned rat cardiac trabecula

43 scle TnT NH2-terminus spliced to the cardiac TnT core.

44 at the molecular pathogenesis of the cardiac TnT mutation-related cardiomyopathies is different for e

45 uction of the NH2-terminal truncated cardiac TnT (cTnT-ND), indicating a myofibril-associated proteol

46 -expressing the N-terminal truncated cardiac TnT (cTnT-ND).

47 olecules: (1) NH2-terminal truncated cardiac TnT and (2) chimera proteins consisting of an acidic or

48 Here we report a truncated cardiac TnT produced during myocardial ischemia reperfusion.

49 hares a high degree of homology with cardiac TnT (CTnT).

50 no acid substitution in the highly conserved TnT-binding helix of cardiac TnI (cTnI) in wild turkey h

51 ent as well as impaired contractility in DCM TnT-R173W iPSC-CMs.

52 nt of sarcomeric proteins in presence of DCM TnT-R173W.

53 -associated protease and is known to degrade TnT.

54 regulated actin filaments containing Delta14 TnT and acrylodan-labeled tropomyosin did not show the f

55 Regulated actin containing Delta14 TnT had ATPase activities in the absence of Ca2+ that we

56 lier that regulated actin containing Delta14 TnT was more readily activated than wild-type regulated

57 with both elevated NT-proBNP and detectable TnT had poorer survival (HR for high NT-proBNP and detec

58 rvival (HR for high NT-proBNP and detectable TnT vs. low NT-proBNP and any TnT: 3.20, 95% CI: 1.91 to

59 Participants with detectable TnT (>/=0.01 ng/ml, n = 39) had an increased risk of all

60 Apparently healthy adults with detectable TnT or elevated NT-proBNP levels are at increased risk o

61 of myofilament Ca(2+) sensitivity in Tm(DM)+TnT(1-44Delta) fibers.

62 276N)+TnT(WT) fibers but increased in Tm(DM)+TnT(45-74Delta) fibers; however, TnT(45-74Delta) did not

63 ss-bridge detachment (g) decreased in Tm(DM)+TnT(WT) and Tm(H276N)+TnT(WT) fibers but increased in Tm

64 sin or actin-tropomyosin yet avoided docking TnT domains that lack known or predicted structure.

65 here that C-terminally truncated Drosophila TnT (TpnT-CD70) retains binding of tropomyosin, troponin

66 truncations of the endogenous and exogenous TnT, despite different amino acid sequences at the cleav

67 C2C12 myotubes, but unlike intact exogenous TnT, truncated slow TnT protein was not detected.

68 oponin T (TnT) mutants (TnT-I79N, TnT-F110I, TnT-R278C), we found that increasing myofilament Ca sens

69 th-old transgenic (Tg) mice expressing F110I-TnT and R278C-TnT did not develop significant hypertroph

70 fibers from transgenic mice expressing F110I-TnT demonstrated increased Ca(2+) sensitivity of force a

71 ) sensitivity of force was observed in F110I-TnT-reconstituted human cardiac muscle preparations.

72 hetic TnT MIP receptor had high affinity for TnT with a KD of 2.3x10(-13) M.

73 sin-associated protein, is required for full TnT inactivation at low Ca(2+) and for limiting its acti

74 Changing TnG to GnT, TnT, or GnG drastically reduced ureDp activation (to 0.5

75 g) decreased in Tm(DM)+TnT(WT) and Tm(H276N)+TnT(WT) fibers but increased in Tm(DM)+TnT(45-74Delta) f

76 Yet it is not known how TnT mutation causes dysfunction of sarcomere microdomain

77 d in Tm(DM)+TnT(45-74Delta) fibers; however, TnT(45-74Delta) did not alter g, demonstrating that S229

78 Hs-TnT, but not NT-proBNP, was associated with OSA after ad

79 Hs-TnT, NT-proBNP, and GDF-15 are predictors of cardiovascu

80 Hs-TnT, NT-proBNP, and GDF-15 were determined and assessed

81 Adding hs-TnT levels to the CHA2DS2VASc score improved the C stati

82 and stroke in patients with NSTE-ACS and hs-TnT >/=14.0 ng/L in both invasively and noninvasively ma

83 and stroke in patients with NSTE-ACS and hs-TnT >/=14.0 ng/L in both invasively and noninvasively ma

84 minal pro-B-type natriuretic peptide) and hs-TnT (high-sensitivity troponin T), circulating SN levels

85 n did not affect changes in NT-proBNP and hs-TnT values, and these biomarkers were not associated wit

86 minal pro-B-type natriuretic peptide, and hs-TnT, hs-TnI levels in the fourth compared with the 3 low

87 endently of conventional risk markers and hs-TnT.

88 Immediately prior to cell application, hs-TnT levels to measure myocardial injury and NT-proBNP le

89 hs was inversely correlated with baseline hs-TnT (r=-0.27, P=0.001).

90 fter elective PCI depends on the baseline hs-TnT level.

91 After adjustment, baseline hs-TnT levels (hazard ratio [HR]: 1.22; 95% confidence inte

92 .014 mug/l; n = 2,721); elevated baseline hs-TnT levels (hs-TnT >0.014 mug/l) with no further rise po

93 The associations between baseline hs-TnT levels and outcomes were evaluated using adjusted Co

94 patients with or without raised baseline hs-TnT levels is unclear.

95 rocedure (n = 516); and elevated baseline hs-TnT levels with a further rise post-procedure (n = 1,647

96 18.2%) in patients with elevated baseline hs-TnT levels with a further rise post-procedure (p < 0.001

97 16.0%) in patients with elevated baseline hs-TnT levels with no further rise post-procedure; and 155

98 95% CI: 0.91 to 1.69; p = 0.165) baseline hs-TnT levels.

99 tly, only patients with elevated baseline hs-TnT>/=15.19 pg/mL (upper tertile) demonstrated a signifi

100 We assessed the association between hs-TnT and cardiac structure and function, and the effect o

101 rel in the noninvasive group CONCLUSIONS: Hs-TnT, NT-proBNP, and GDF-15 are predictors of cardiovascu

102 Elevated hs-TnT in the myocardial injury range (>0.014 mug/L) was fo

103 Elevated hs-TnT predicts substantial benefit of ticagrelor over clop

104 Patients with elevated hs-TnT were older and had more severe heart failure.

105 no longer significant after adjusting for hs-TnT (P=0.09).

106 t hs-TnT quartile to 2.13% in the highest hs-TnT quartile (adjusted hazard ratio [HR]: 1.94; 95% conf

107 Decreases in hs-TnT with LCZ696 in parallel with improvement in N-termin

108 2,721); elevated baseline hs-TnT levels (hs-TnT >0.014 mug/l) with no further rise post-procedure (n

109 seline and post-procedural hs-TnT levels (hs-TnT </=0.014 mug/l; n = 742); nonelevated baseline but e

110 tes calculated per SD increase of the log hs-TnT scale).

111 ined unchanged in patients in the 2 lower hs-TnT tertiles.

112 embolism ranged from 0.87% in the lowest hs-TnT quartile to 2.13% in the highest hs-TnT quartile (ad

113 h higher levels of concomitantly measured hs-TnT among women but not men, in whom other comorbidities

114 In the same models, hs-TnT concentrations were associated with the incidence of

115 ut no apparent benefit was seen at normal hs-TnT.

116 Levels of hs-TnT are often elevated in patients with AF.

117 test the hypothesis that serum levels of hs-TnT correlate with cell retention and determine the resp

118 ial injury as measured by serum levels of hs-TnT predicts the reduction of NT-proBNP serum levels at

119 We evaluated the impact of hs-TnT reporting on care and outcome among chest pain patie

120 Increasing levels of hs-TnT were associated with increasing risk of cardiovascul

121 Levels of hs-TnT were measurable in 93.5% of patients; 75% had levels

122 endently associated with higher levels of hs-TnT, suggesting that subclinical myocardial injury may p

123 erwent polysomnography and measurement of hs-TnT.

124 ct of LCZ696, compared with valsartan, on hs-TnT over 36 weeks.

125 Preprocedural hs-TnT elevation remained an independent predictor of 1-yea

126 dural hs-TnT levels (peak post-procedural hs-TnT >0.014 mug/l; n = 2,721); elevated baseline hs-TnT l

127 Peak post-procedural hs-TnT findings were not associated with mortality in patie

128 r the prognostic value of post-procedural hs-TnT level after elective PCI depends on the baseline hs-

129 ctive PCI, an increase in post-procedural hs-TnT level did not offer prognostic information beyond th

130 ; p < 0.001) but not peak post-procedural hs-TnT levels (HR: 1.04; 95% CI: 0.85 to 1.28; p = 0.679) w

131 nonelevated baseline and post-procedural hs-TnT levels (hs-TnT </=0.014 mug/l; n = 742); nonelevated

132 ted baseline but elevated post-procedural hs-TnT levels (peak post-procedural hs-TnT >0.014 mug/l; n

133 ted baseline but elevated post-procedural hs-TnT levels; 50 (16.0%) in patients with elevated baselin

134 nonelevated baseline and post-procedural hs-TnT levels; 54 (3.8%) in patients with nonelevated basel

135 who had baseline and peak post-procedural hs-TnT measurements available.

136 LCZ696 treatment reduced hs-TnT to a greater extent at 12 weeks (12% reduction; P=0.

137 Because stable hs-TnT levels are common in patients with a clinical diagno

138 asurement of high-sensitivity troponin T (hs-TnT) and N-terminal pro B-type natriuretic peptide (NT-p

139 High-sensitivity troponin T (hs-TnT) and N-terminal prohormone of brain naturetic peptid

140 High-sensitivity troponin T (hs-TnT) assays promise greater discrimination of evolving m

141 -proBNP) and high-sensitivity troponin T (hs-TnT) can be used as surrogate markers and whether geneti

142 tic value of high-sensitivity troponin T (hs-TnT) elevation after elective percutaneous coronary inte

143 of elevated high-sensitivity troponin T (hs-TnT) in 298 patients with heart failure with preserved e

144 tic value of high-sensitivity troponin T (hs-TnT) in addition to clinical risk factors and the CHA2DS

145 sts to measure high-sensitive troponin T (hs-TnT) serum levels revealed the presence of ongoing minut

146 ween OSA and high-sensitivity troponin T (hs-TnT), cardiac structure, and CV outcomes differs by sex.

147 mportance of high-sensitivity troponin T (hs-TnT), N-terminal pro-brain natriuretic peptide (NT-proBN

148 t of high-sensitivity cardiac troponin T (hs-TnT).

149 The hs-TnT level is independently associated with an increased

150 mortality, and bleeding regardless of the hs-TnT level.

151 warfarin are consistent regardless of the hs-TnT level.

152 Patients were allocated to hs-TnT reporting (hs-report) or standard reporting (std-rep

153 artile range, 11.6-13.1) years follow-up, hs-TnT was related to risk of death or incident heart failu

154 sively managed patients; in patients with hs-TnT <14.0 ng/L, there was no difference between ticagrel

155 sively managed patients; in patients with hs-TnT <14.0 ng/L, there was no difference between ticagrel

156 hs-TnI correlated moderately with hs-TnT (r = 0.44) and N-terminal pro-B-type natriuretic pep

157 OSA was independently associated with hs-TnT among women (P=0.03) but not in men (P=0.94).

158 hin the heart was closely associated with hs-TnT levels in patients with chronic ischemic heart failu

159 characterisation of a novel sensor for human TnT based on a molecularly-imprinted electrosynthesised

160 e (NT-proBNP) and cardiac troponins T and I (TnT and TnI) for prognostication, but many centers do no

161 pressing troponin T (TnT) mutants (TnT-I79N, TnT-F110I, TnT-R278C), we found that increasing myofilam

162 in TNT1's tropomyosin-binding domain impairs TnT's contribution to inhibitory tropomyosin positioning

163 Our model simulation of the data implicates TnT as a participant in the process by which SL- and XB-

164 Glu-rich long C-terminal extension of insect TnT functions as a myofilament Ca(2+) buffer/reservoir a

165 Vertebrate and invertebrate TnTs have conserved core structures, reflecting conserve

166 ATPase rate like that obtained when the last TnT 14 residues were deleted.

167 cardiac-specific constitutively active MEK1 (TnT-MEK1-CA) was administrated to rescue cardiac dysfunc

168 region, we investigated two classes of model TnT molecules: (1) NH2-terminal truncated cardiac TnT an

169 ) expresses exclusively slow skeletal muscle TnT (ssTnT) together with cardiac forms of troponin I an

170 isting of an acidic or basic skeletal muscle TnT NH2-terminus spliced to the cardiac TnT core.

171 ofibrils overexpressing fast skeletal muscle TnT produced similar NH2-terminal truncations of the end

172 ear bag fibres, whereas fast skeletal muscle TnT was detected in nuclear chain fibres, and cardiac al

173 ntial dominant negative effect of the mutant TnT fragment.

174 ition, two mouse cardiac troponin T mutants (TnT(1-44Delta) and TnT(45-74Delta)) that have a divergen

175 om mice expressing troponin T (TnT) mutants (TnT-I79N, TnT-F110I, TnT-R278C), we found that increasin

176 -TnT fusion protein (substituting for normal TnT), and the other end was capped by tropomodulin.

177 beta peptides in the biological activity of TnT was primarily modulatory.

178 ardiomyopathy is by changing the affinity of TnT for Tm within the TNT1 region.

179 concile with the high, 20 nM K(d) binding of TnT onto tropomyosin.

180 a/beta exons, we constructed combinations of TnT cDNAs from a single human fetal fast skeletal TnTbet

181 ](3-)/[Fe(CN)6](4-) and the concentration of TnT in buffer over the range 0.009-0.8 ng/mL, with a det

182 ions alter the COOH-terminal conformation of TnT and thin filament Ca2+-activation, yet the functiona

183 al importance of the functional diversity of TnT isoforms.

184 conclusion, the Ca2+-sensitizing effects of TnT mutations may reduce the responsiveness of mouse hea

185 under the influence of a 64-residue helix of TnT located at the overlap of adjacent tropomyosins are

186 eased ratios of slow versus fast isoforms of TnT, TnI, and myosin.

187 Minimally elevated levels of TnT, a marker of cardiomyocyte injury, have been found i

188 calpain-mediated proteolytic modification of TnT may act as an acute mechanism to adjust muscle contr

189 of troponin, probably representing parts of TnT or the troponin core domain, to promote tropomyosin

190 nylenediamine (o-PD) film in the presence of TnT as a template was performed in acetate buffer (0.5 M

191 o-PD) on a gold electrode in the presence of TnT as a template.

192 cating a muscle cell-specific proteolysis of TnT when it is not integrated into myofilaments.

193 the f peptide in the N-terminal T1 region of TnT, has a strong inhibitory effect on binary interactio

194 removing the NH2-terminal variable region of TnT, the mu-calpain-mediated proteolytic modification of

195 ed in the tropomyosin (Tm) binding region of TnT, TNT1 (residues 80-180).

196 Several regions of TnT and TnI were unfolded even at low temperature, sugge

197 The structure-function relationship of TnT may be explored for the development of new treatment

198 es, expanding the classic structural role of TnT to a dynamic role regulating sarcomere function.

199 vation, yet the functional core structure of TnT and the mechanism of NH2-terminal modulation are not

200 addition to the conserved core structure of TnT.

201 d preserving the conserved core structure of TnT.

202 C, indicating a preserved core structure of TnT.

203 th the affinity changes observed in vitro of TnT mutants for Tm.

204 involved a strong cross-bridge influence on TnT's interaction with actin-Tm.

205 Patients' TnT levels were measured 6 to 12 hours after surgery and

206 Peak TnT measurement added incremental prognostic value to di

207 Patients with a peak TnT value of 0.01 ng/mL or less, 0.02, 0.03-0.29, and 0.

208 lity compared with the reference group (peak TnT </= 0.01 ng/mL): peak TnT of 0.02 ng/mL (adjusted ha

209 lity compared with the reference group (peak TnT</=0.01 ng/mL): peak TnT of 0.02 ng/mL (adjusted haza

210 eference group (peak TnT</=0.01 ng/mL): peak TnT of 0.02 ng/mL (adjusted hazard ratio [aHR], 2.41; 95

211 erence group (peak TnT </= 0.01 ng/mL): peak TnT of 0.02 ng/mL (adjusted hazard ratio [aHR], 2.41; 95

212 ultivariable analysis demonstrated that peak TnT values of at least 0.02 ng/mL, occurring in 11.6% of

213 ultivariable analysis demonstrated that peak TnT values of at least 0.02 ng/mL, occurring in 11.6% of

214 We repeated this analysis, adding the peak TnT measurement during the first 3 postoperative days as

215 o die within 30 days for the model with peak TnT measurement vs without (C index = 0.85 vs 0.81; diff

216 g noncardiac surgery, the peak postoperative TnT measurement during the first 3 days after surgery wa

217 as unchanged between the wild type and R205A TnT.

218 nic (Tg) mice expressing F110I-TnT and R278C-TnT did not develop significant hypertrophy or ventricul

219 Our results, using the recombinant TnT isoforms in different functional in vitro assays, sh

220 olecule-based activation of AMPK can restore TnT microdomain interactions, and partially recovers sar

221 57033 mimicked the effects of Ca-sensitizing TnT mutants and produced pause-dependent ventricular ect

222 nsgenic mice expressing the Ca2+-sensitizing TnT-I79N mutant (I79N), which causes a high rate of sudd

223 rat cardiac TnT (cTnT) and rat fast skeletal TnT (fsTnT) reconstituted cardiac muscle preparations we

224 on the biological function of fast skeletal TnT and this can be correlated with changes in the Ca2+

225 ponding 1-41 residues of mouse fast skeletal TnT.

226 The genes encoding slow TnT and cardiac troponin I (TnI) are closely linked.

227 etectable amount of truncated or intact slow TnT proteins, indicating a muscle cell-specific proteoly

228 gates the expression and fate of mutant slow TnT in muscle cells.

229 he data demonstrated a critical role of slow TnT in diaphragm function and in the pathogenesis and pa

230 The levels of slow TnT mRNA and protein were significantly reduced in the d

231 n two alternatively spliced isoforms of slow TnT mRNA.

232 ated the effect of enhancer deletion on slow TnT gene expression in vivo and functional consequences.

233 in undifferentiated myoblasts produced slow TnT mRNA but not a detectable amount of truncated or int

234 sted that the 5'-enhancer region of the slow TnT gene overlaps with the structure of the upstream car

235 The slow TnT-deficient (ssTnT-KD) diaphragm muscle exhibited atro

236 unlike intact exogenous TnT, truncated slow TnT protein was not detected.

237 Rapid degradation of the truncated slow TnT protein, rather than instability of the nonsense mRN

238 evelopmentally regulated and tissue specific TnT isoforms.

239 The synthetic TnT MIP receptor had high affinity for TnT with a KD of

240 stic value of detectable cardiac troponin T (TnT) and elevated N-terminal pro-B-type natriuretic pept

241 Troponin T (TnT) and troponin I (TnI) are two evolutionarily and fun

242 The three isoforms of vertebrate troponin T (TnT) are normally expressed in a muscle type-specific ma

243 the physiological effects of the troponin T (TnT) F110I and R278C mutations associated with familial

244 ternative splicing from a single troponin T (TnT) gene produce multiple developmentally regulated and

245 ral and COOH-terminal regions of troponin T (TnT) interact with troponin C, troponin I, and tropomyos

246 Cardiac troponin T (TnT) is a highly sensitive cardiac biomarker for myocard

247 The thin filament protein troponin T (TnT) is a regulator of sarcomere function.

248 minal variable region of cardiac troponin T (TnT) is a regulatory structure that can be selectively r

249 re of the NH2-terminal region of troponin T (TnT) is hypervariable among the muscle type-specific iso

250 Troponin T (TnT) is the thin-filament-anchoring subunit of troponin.

251 The heterogenic nature of troponin T (TnT) isoforms in fast skeletal and cardiac muscle sugges

252 es isolated from mice expressing troponin T (TnT) mutants (TnT-I79N, TnT-F110I, TnT-R278C), we found

253 Three troponin T (TnT) mutants that cause hypertrophic, restrictive, and d

254 Troponin T (TnT) mutations that cause familial hypertrophic cardiomy

255 The loss of slow skeletal muscle troponin T (TnT) results in a recessive nemaline myopathy in the Ami

256 nown that the flexibility of the troponin T (TnT) tail determines thin filament conformation and henc

257 is study, polymer imprinted with troponin T (TnT) was assessed using electrochemical methods and the

258 The C-terminal region of cardiac troponin T (TnT), a tropomyosin-associated protein, is required for

259 n and troponin [composed of TnI, troponin T (TnT), and troponin C] or with actin and TnI.

260 The interference effect of troponin T (TnT), bovine serum albumin (BSA) and myoglobin (Myo) in

261 wed negligible interference from troponin T (TnT), bovine serum albumin (BSA) and urea under SWV assa

262 The N-terminal half of troponin T (TnT), TNT1, independently promotes tropomyosin-based, st

263 letal muscle regulatory proteins troponin T (TnT), troponin I (TnI), and beta-tropomyosin (beta-TM) h

264 d cardiomyopathy (DCM) mutation, troponin T (TnT)-R173W, display sarcomere protein misalignment and i

265 n C (TnC), troponin I (TnI), and troponin T (TnT).

266 TNNT2 gene that encodes cardiac troponin T (TnT).

267 FRET analyses indicated that the C-terminal TnT region approached Cys-190 of tropomyosin as actin fi

268 We conclude that TnT has a previously unrecognized role in forming the in

269 ineered isogenic controls, we uncovered that TnT-R173W destabilizes molecular interactions of troponi

270 The TnT MIP sensor was shown to have a high affinity to TnT

271 The TnT+ status was associated with adverse clinical and ang

272 tory peptide region that binds to actin, the TnT-TnI coiled-coil, and the TnC COOH domain that contai

273 and hydrophobic complementarity between the TnT tail (TnT1) and tropomyosin, which is difficult to r

274 se at baseline did not materially change the TnT mortality or NT-proBNP mortality associations.

275 ricyanide probe was used to characterise the TnT MIP receptor film.

276 To define the TnT core structure and investigate the regulatory role o

277 two-site model of template affinity for the TnT MIP receptor.

278 By contrast, ablation of Fgf8 in the TnT-Cre domain does not result in OT or RV defects, prov

279 dulates the conformation and function of the TnT core structure to fine-tune muscle contractility.

280 Deletion of the TnT hypervariable NH2-terminus preserved binding to trop

281 The incubation of the TnT MIP receptor-modi fi ed electrode with respect to Tn

282 ac TnT known to alter the flexibility of the TnT tropomyosin-binding domain, we found mutation-specif

283 In contrast, portions of the TnT-TnI coiled-coil exhibited high protection from excha

284 TnI helix 1 and to the COOH terminus of the TnT-TnI coiled-coil.

285 re involved in these activities, whether the TnT C terminus undergoes Ca(2+)-dependent conformational

286 Therefore, TnT potentially contributes to striated muscle relaxatio

287 investigated whether basic residues in this TnT region are involved in these activities, whether the

288 lly rescuing mutations demonstrated that TnI-TnT interaction is a critical link in the Ca(2+) signali

289 sensor was shown to have a high affinity to TnT in comparison with non-imprinted polymer (NIP) elect

290 Tm*174 mainly crosslinked to TnT.

291 eceptor-modi fi ed electrode with respect to TnT concentration resulted in a suppression of the ferro

292 f the MIP-modified electrode with respect to TnT concentration resulted in a suppression of the ferro

293 70 in vivo and normal stoichiometry of total TnT in myofilaments of heterozygous female flies.

294 e to incorporation of unorthodox tropomyosin-TnT crystal structures and complex FRET measurements dur

295 sequence heterogeneity present in wild-type TnT isoforms, irrespective of the stage of development.

296 rol hearts expressing either human wild-type TnT or no transgene (CON).

297 P value approach to determine if there were TnT thresholds that independently altered patients' risk

298 ry heart tube and pharyngeal endoderm, while TnT-Cre is expressed only within the specified heart tub

299 healthy older adults and in conjunction with TnT is unknown.

300 The net reclassification improvement with TnT was 25.0% (P < .001).

301 t not all, TnT mutants for Tm relative to WT TnT.