ライフサイエンスコーパス: TnT

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

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

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

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

5 A TnT sensitive layer was prepared by electropolymerisatio

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

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

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

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

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

11 arly twofold symmetrical assembly of TnI and TnT subunits penetrated asymmetrically by the dumbbell-s

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

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

14 Both intact TnT and TnT N-terminal fragment (TnT N47) bound terbium with hig

15 tested and found to bind both intact TnT and TnT N47.

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

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

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

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

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

21 TnI (cTnI) at S23, S24, and T144 and cardiac TnT (cTnT) at S278 and T287.

22 rid troponin (skeletal TnI, TnC, and cardiac TnT) than with all cardiac troponin.

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

24 -92W and R-92L missense mutations in cardiac TnT known to alter the flexibility of the TnT tropomyosi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

40 e results suggest that patients with certain TnT mutations may respond to certain pathological situat

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

42 -associated protease and is known to degrade TnT.

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

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

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

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

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

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

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

50 In addition to a different TnT isoform, a different troponin I (TnI) isoform, slow

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

52 276N)+TnT(WT) fibers but increased in Tm(DM)+TnT(45-74Delta) fibers; however, TnT(45-74Delta) did not

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

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

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

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

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

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

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

60 ent (R278C-TnT) or only slightly less (F110I-TnT) than that of non-Tg and WT-Tg littermates.

61 irst time, we discovered that a chicken fast TnT isoform with a unique Tx motif (HEEAH)(n) binds calc

62 ated cardiomyopathy (DCM) mutations in fetal TnT and fetal troponin affect the functional properties

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

64 Both intact TnT and TnT N-terminal fragment (TnT N47) bound terbium with high affinity indicating tha

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

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

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

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

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

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

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

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

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

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

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

76 endently of conventional risk markers and hs-TnT.

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

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

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

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

81 .014 mug/l; n = 2,721); elevated baseline hs-TnT levels (hs-TnT >0.014 mug/l) with no further rise po

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

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

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

85 18.2%) in patients with elevated baseline hs-TnT levels with a further rise post-procedure (p < 0.001

86 16.0%) in patients with elevated baseline hs-TnT levels with no further rise post-procedure; and 155

87 95% CI: 0.91 to 1.69; p = 0.165) baseline hs-TnT levels.

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

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

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

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

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

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

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

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

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

97 2,721); elevated baseline hs-TnT levels (hs-TnT >0.014 mug/l) with no further rise post-procedure (n

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

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

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

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

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

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

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

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

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

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

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

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

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

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

112 erwent polysomnography and measurement of hs-TnT.

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

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

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

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

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

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

119 ; 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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

151 Both intact TnT and TnT N-terminal fragment (TnT N47) bound terbium

152 ium was tested and found to bind both intact TnT and TnT N47.

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

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

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

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

157 ntial dominant negative effect of the mutant TnT fragment.

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

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

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

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

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

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

164 hat calcium bound to the tertiary complex of TnT and the tropomyosin dimer with a fast on-rate (10(6)

165 ](3-)/[Fe(CN)6](4-) and the concentration of TnT in buffer over the range 0.009-0.8 ng/mL, with a det

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

167 al importance of the functional diversity of TnT isoforms.

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

169 he formation of a coiled-coil heterodimer of TnT and TnI has been recently confirmed by the crystal s

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

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

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

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

174 of TnT may contribute to the pathogenesis of TnT-linked FHC through different mechanisms.

175 ts confirmed that the individual peptides of TnT were monomeric but formed heterodimers when mixed wi

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

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

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

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

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

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

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

183 se results suggest that different regions of TnT may contribute to the pathogenesis of TnT-linked FHC

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

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

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

187 addition to the conserved core structure of TnT.

188 d preserving the conserved core structure of TnT.

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

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

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

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

193 Peak TnT measurement added incremental prognostic value to di

194 Peak TnT measurement added incremental prognostic value to di

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

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

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

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

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

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

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

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

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

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

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

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

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

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

209 at the termini, hence they lack the primary TnT(1)-tropomyosin interaction, allowing study of exon 6

210 as unchanged between the wild type and R205A TnT.

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

212 the maximal ATPase was not different (R278C-TnT) or only slightly less (F110I-TnT) than that of non-

213 in human fibers reconstituted with the R278C-TnT mutant.

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

215 idues N-terminal to the conserved HR region (TnT residues 165-178) are essential for the stable coile

216 57033 mimicked the effects of Ca-sensitizing TnT mutants and produced pause-dependent ventricular ect

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

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

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

220 binant deletion mutants of the fast skeletal TnT to determine the minimal sequence required for stabl

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

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

223 Intact slow TnT mRNA was readily detected in patient muscle, indicat

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

225 sponsible for the instability of mutant slow TnT in ANM muscle.

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

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

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

229 n two alternatively spliced isoforms of slow TnT mRNA.

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

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

232 nce of intact or prematurely terminated slow TnT polypeptide in Amish nemaline myopathy (ANM) patient

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

234 The slow TnT-(1-179) fragment has substantially lower affinity fo

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 cells, producing the expected truncated slow TnT protein.

239 evelopmentally regulated and tissue specific TnT isoforms.

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

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

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

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

244 this study was to elucidate how troponin T (TnT) dilated cardiomyopathy (DCM) mutations in fetal TnT

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

246 exon 11 of slow skeletal muscle troponin T (TnT) gene (TNNT1) causes an autosomal-recessive inherite

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

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

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

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

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

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

253 Numerous troponin T (TnT) isoforms are generated by alternative RNA splicing

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

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

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

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

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

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

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

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

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

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

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

265 sociated with phosphorylation of troponin T (TnT), troponin I (TnI), and myosin-binding protein C (C-

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

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

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

269 These results suggest that TnT may play a role in modulating the calcium-mediated r

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

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

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

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

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

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

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

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

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

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

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

284 ated different secondary structures of these TnT mutants.

285 The metal binding behavior of this TnT isoform was first investigated using terbium as a ca

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

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

288 Tm*174 mainly crosslinked to TnT.

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

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

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

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

293 adily detectable fluorescence variation upon TnT binding.

294 ent of the coiled-coil formed by the various TnT peptides with TnI HR domain.

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

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

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

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

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

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

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