ライフサイエンスコーパス: cTnI

1 cTnI can be phosphorylated by protein kinase A (PKA) at

2 cTnI concentrations were significantly higher in rejecti

3 cTnI levels increased over time and were a strong marker

4 cTnI levels were detectable in 968 (96.4%) subjects at b

5 cTnI QAEH is similar in these four residues to ssTnI and

6 cTnI QAEH molecular dynamics simulations demonstrated al

7 cTnI was abnormal in only 1 patient.

8 cTnI was measured in 418 serum samples, including 35 pai

9 cTnI was measured with a high-sensitivity assay (Abbott

10 cTnI was measured with a high-sensitivity assay in 3824

11 cTnI(WT), cTnI(R146G), and cTnI(R21C) were complexed int

12 cTnI[39-60] binds to the hydrophobic face of cCTnC, stab

13 TnI-R145G/S23D/S24D Ca(2+)-bound cTnC(1-161)-cTnI(1-172)-cTnT(236-285), and cTnI-R145G/PS23/PS24 Ca(2

14 tions of cTnI-R145G Ca(2+)-bound cTnC(1-161)-cTnI(1-172)-cTnT(236-285), cTnI-R145G/S23D/S24D Ca(2+)-b

15 TnI-R145G/PS23/PS24 Ca(2+)-bound cTnC(1-161)-cTnI(1-172)-cTnT(236-285), respectively.

16 ex structure (including residues cTnC 1-161, cTnI 1-172, and cTnT 236-285) with the N-terminus of cTn

17 bound cTnC(1-161)-cTnI(1-172)-cTnT(236-285), cTnI-R145G/S23D/S24D Ca(2+)-bound cTnC(1-161)-cTnI(1-172

18 In addition, cTnI provided no incremental prognostic information to t

19 and 60 +/- 17, respectively, with additional cTnI release occurring after 150 min of reperfusion.

20 Antibodies against cTnI are immobilized on the sensor surface for specific

21 ed with the LKB1 complex alone did not alter cTnI phosphorylation or phosphospecies distribution.

22 Although cTnI is unique to myocardium, cTnT can be re-expressed i

23 ast, cTnI[1-37] remains disordered, although cTnI[19-37] is electrostatically tethered to the negativ

24 d cTnC(1-161)-cTnI(1-172)-cTnT(236-285), and cTnI-R145G/PS23/PS24 Ca(2+)-bound cTnC(1-161)-cTnI(1-172

25 lix C of cTnC (residues 56, 59, and 63), and cTnI (residue 145) in the presence of either cTnI RCM mu

26 PKA-mediated phosphorylation of cMyBP-C and cTnI each independently contribute to enhance myofilamen

27 TnT and CK-MB in the absence of clinical and cTnI evidence of myocardial injury.

28 target binding, cTnI[148-158] for cNTnC and cTnI[39-60] for cCTnC.

29 A negative copeptin and cTnI at baseline ruled out AMI for 58% of patients, with

30 Both abnormal copeptin and cTnI were predictors of death at 180 days (p < 0.0001 fo

31 The interaction between N-cTnC and cTnI stabilizes the Ca(2+)-induced opening of N-cTnC and

32 myocytes expressing wild-type (WT) cTnI and cTnI A164H, whereas the A164R variant showed increased m

33 showed the selectivity of detecting cTnT and cTnI in human serum with wide dynamic range.

34 g surface confinement of the target cTnT and cTnI molecules on to the electrode surface.

35 biomarkers (NT-proBNP, H-FABP, hs-cTnT, and cTnI) strongly associated with the primary outcome.

36 erences compared with normal, and myomir and cTnI levels were only captured near the detection limit.

37 comparison to mammalian cTnI, cTnI QAEH and cTnI AH showed increased contractility and slowed relaxa

38 er, our results suggest that cTnI(R146G) and cTnI(R21C) blunt PKA modulation of activation and relaxa

39 cTnI(WT), cTnI(R146G), and cTnI(R21C) were complexed into cardiac troponin and exch

40 n (Tmax) was maintained for cTnI(R146G)- and cTnI(R21C)-exchanged myofibrils, and Ca(2+) sensitivity

41 this effect was blunted for cTnI(R146G)- and cTnI(R21C)-exchanged myofibrils.

42 assessed the association between smoking and cTnI and the impact of smoking on the associations betwe

43 hrough structural effects on tropomyosin and cTnI.

44 mplete the immunosensor, abbreviated as anti-cTnI(BSA)/NAC-CdAgTe QDs/AuNPs/GCE.

45 The sensing element, anti-cTnI, was then covalently bound to the composite materia

46 ilized antibody for cardiac troponin I (anti-cTnI) on a photoresponsive composite material consisting

47 with antibody anti-cardiac Troponin I (anti-cTnI) to detect cardiac marker antigen Troponin I (cTnI)

48 trode was then modified with monoclonal anti-cTnI antibodies via Schiff reaction based chemistry.

49 Immobilization of anti-cTnI Ab on CNFs and the detection of human-cTnI were exa

50 action of target cTnI with its specific anti-cTnI antibody.

51 The anti-cTnI was covalently conjugated to afGQDs through carbodi

52 Using a novel high-sensitive assay, cTnI levels could be determined in nearly all elderly st

53 hese results suggest that the RCM-associated cTnI R145W mutation induces a permanent structural state

54 The association between cTnI levels and cardiovascular end points is stronger in

55 mpact of smoking on the associations between cTnI levels and the incidence of acute myocardial infarc

56 modifies the prognostic relationship between cTnI and outcomes remain unclear.

57 urface that is stabilized by target binding, cTnI[148-158] for cNTnC and cTnI[39-60] for cCTnC.

58 n a model with clinical indicators plus BNP, cTnI, ST2, PAPP-A, and MPO (each p</=0.01) [corrected].

59 1pg/mL in human serum was achieved for both cTnI and cTnT.

60 The interaction can be abolished by cTnI phosphorylation at Ser22 and Ser23, an important me

61 tractile activation that can be modulated by cTnI phosphorylation.

62 that altering C-I interactions by PKA, or by cTnI phosphomimetic mutations (S23D/S24D-cTnI), directly

63 evation myocardial infarctions undetected by cTnI at 0 h were detected with copeptin >14 pmol/l in 10

64 ne transduction of adult cardiac myocytes by cTnIs with specific helix 4 ssTnI substitutions, Q157R/A

65 MNP-captured cTnI molecules resulted in spectral responses up to 6-fo

66 ically, this resulted in significant cardiac cTnI and PLN phosphorylation and improved heart performa

67 residues to ssTnI and nonmammalian chordate cTnIs, whereas cTnI AH is similar to fish cTnI in these

68 r bundles exchanged with troponin containing cTnI pseudo-phosphorylated at Ser-150 demonstrate increa

69 In contrast, cTnI, measured using 2 sensitive assays, was persistentl

70 In contrast, cTnI[1-37] remains disordered, although cTnI[19-37] is e

71 tly stabilize this Ca(2+)-sensitizing N-cTnC-cTnI interaction through structural effects on tropomyos

72 phorylation and this mutation alter the cTnC-cTnI (C-I) interaction, which plays a crucial role in mo

73 decrease KCa and pCa50, and weaken the cTnC-cTnI (C-I) interaction.

74 hat a histidine button engineered into cTnI (cTnI A164H) specifically enhances inotropic function in

75 of the inhibitory subunit of troponin, cTnI (cTnI(1-39)), is a target for phosphorylation by protein

76 In comparison to mammalian cTnI, cTnI QAEH and cTnI AH showed increased contractility and

77 cardiac injury (NT-proBNP, H-FABP, hs-cTnT, cTnI, and CK-MB).

78 estigations, and measurements of serum cTnT, cTnI, creatine kinase (CK), creatine kinase myocardial b

79 A series of single cysteine cTnI mutants was generated, labeled with the fluorophore

80 f N-cTnC and is presumed to also destabilize cTnI-actin interactions that work together with steric e

81 demonstrate a good selectivity for detecting cTnI.

82 an-cTnI analytes and is capable of detecting cTnI at concentrations as low as approximately 0.2 ng/mL

83 al responses up to 6-fold higher than direct cTnI adsorption on the GNR sensor.

84 To distinguish cTnI from cMyBP-C/titin phosphorylation effects on the f

85 m for recombinant troponin containing either cTnI R145W, PKA/PKC phosphomimetic charge mutations (S23

86 uggest that phosphorylation by PKA of either cTnI or cMyBP-C/titin independently reduces the pCa(50)

87 cTnI (residue 145) in the presence of either cTnI RCM mutation or cTnI PKC phosphomimetic.

88 PKA cannot phosphorylate either cTnI S23/24 variant, leaving cMyBP-C/titin as PKA target

89 te cTnIs, whereas cTnI AH is similar to fish cTnI in these four residues.

90 Monoclonal antibodies for cTnI were covalently immobilized on the nanowire surface

91 e as current enzyme-linked immuno-assays for cTnI.

92 howed relative increased calcium binding for cTnI QAEH compared to cTnI.

93 Importantly, this effect was blunted for cTnI(R146G)- and cTnI(R21C)-exchanged myofibrils.

94 ontributions of ~67 and ~33% for cMyBP-C for cTnI, respectively.

95 Maximal tension (Tmax) was maintained for cTnI(R146G)- and cTnI(R21C)-exchanged myofibrils, and Ca

96 al histidine ionization may be necessary for cTnI A164H to act as a molecular sensor capable of modul

97 PKA phosphorylation decreased pCa50 for cTnI(WT)-exchanged myofibrils but not for either mutatio

98 elerated the early slow phase relaxation for cTnI(WT) myofibrils, especially at Ca(2+) levels that th

99 ns influence the affinity of cardiac TnC for cTnI (KC-I) or contractile kinetics during beta-adrenerg

100 Therefore, we generated cTnI knock-in mouse models carrying an R21C mutation to

101 e using alternative biomarkers (haematocrit, cTnI-hs, cystatin C, or creatinine clearance) also outpe

102 Furthermore, exchange with cTn having cTnI serines 23/24 mutated to aspartic acids to mimic ph

103 148-158] presented to cNTnC, and this is how cTnI[19-37] indirectly modulates the calcium affinity of

104 Here, we tested how cTnI(R146G) or cTnI(R21C) influences contractile activat

105 Hs-cTnI levels were measured at presentation and after 1 ho

106 hs-cTnI was measured (Abbott assay) using sex-specific 99th

107 Cardiac troponin was detectable in 80.0% (hs-cTnI: 82.6%; hs-cTnT: 69.7%).

108 2DS2VASc (P=0.004 for hs-cTnT and P=0.022 hs-cTnI) and 0.61 for ATRIA scores (P=0.005 hs-cTnT and P=0

109 We directly compared all 4 hs-cTnI-based rule-out strategies: limit of detection (LOD,

110 ed statistically significant after adding hs-cTnI to the model.

111 utoff (hs-cTnI<5 ng/L), 1-hour algorithm (hs-cTnI<5 ng/L and 1-hour change<2 ng/L), and the 0/1-hour

112 C (AUC, 0.924), hs-cTnT (AUC, 0.927), and hs-cTnI (AUC, 0.922) and superior to cTnI measured by a con

113 Reclassification Improvement +0.256) and hs-cTnI (Net Reclassification Improvement +0.308; both P<0.

114 Elevated BNP and hs-cTnI identify candidates for targeted risk reduction.

115 logy 0/1-hour algorithm using hs-cTnT and hs-cTnI in patients with RD, defined as an estimated glomer

116 iminatory power comparable to hs-cTnT and hs-cTnI in the diagnosis of AMI and may perform favorably i

117 Simultaneous elevations of BNP and hs-cTnI over clinical cutoffs were strongly associated with

118 d C indices of 0.65 with both hs-cTnT and hs-cTnI, in comparison with 0.60 for CHA2DS2VASc (P=0.004 f

119 ailable high-sensitivity (hs) cTn assays (hs-cTnI, Abbott; hs-cTnT, Roche) among 2300 consecutive pat

120 curve of 0.94 for hs-cTnT (0.92 for both hs-cTnI assays).

121 he Diagnostics; hs-cTnI, Beckman-Coulter; hs-cTnI Siemens) in a blinded fashion at presentation and s

122 aseline and serial high-sensitivity cTnI (hs-cTnI) measurements for myocardial infarction and 30- and

123 ion (LOD, hs-cTnI<2 ng/L), single cutoff (hs-cTnI<5 ng/L), 1-hour algorithm (hs-cTnI<5 ng/L and 1-hou

124 ith 3 assays (hs-cTnT, Roche Diagnostics; hs-cTnI, Beckman-Coulter; hs-cTnI Siemens) in a blinded fas

125 Combinations of normal and elevated hs-cTnI (>26.2 ng/L) and BNP (>100 pg/mL) were also studied

126 tile ranges) were 5.6 (3.3-10.5) ng/L for hs-cTnI and 39 (15, 94) pg/mL for BNP.

127 A scores (P=0.005 hs-cTnT and P=0.034 for hs-cTnI).

128 rtality increased in patients with higher hs-cTnI concentrations and any level of renal dysfunction.

129 sing high-sensitivity cardiac troponin I (hs-cTnI) have been identified.

130 and high-sensitivity cardiac troponin I (hs-cTnI) were determined in plasma samples obtained at stud

131 and high-sensitivity cardiac troponin I (hs-cTnI) were included in adjusted models.

132 y increased significantly with increasing hs-cTnI tertile (1.3%, 6.0%, and 10.4%, respectively).

133 -out strategies: limit of detection (LOD, hs-cTnI<2 ng/L), single cutoff (hs-cTnI<5 ng/L), 1-hour alg

134 TnT or standard-sensitivity cTnI (but not hs-cTnI) led to an increase in AUC to 0.931 (P<0.0001) and

135 ), as well as serum biomarkers (NTproBNP, hs-cTnI, and PICP).

136 mance but not the rule-out performance of hs-cTnI for myocardial infarction, and mortality increased

137 c CDVs and parallel measurements of other hs-cTnI assays.

138 s can quantify cardiac troponins I and T (hs-cTnI, hs-cTnT) in individuals with no clinically manifes

139 ) and those measuring hs-cTnT rather than hs-cTnI (p = 0.027).

140 Similar findings were obtained with the hs-cTnI assays.

141 ng the C statistics, cMyC was superior to hs-cTnI and standard sensitivity cTnI (P<0.05 for both) and

142 Using hs-cTnI, patients with RD had comparable sensitivity of rul

143 ment +0.149 versus hs-cTnT, +0.235 versus hs-cTnI (P<0.001).

144 Patients with hs-cTnI concentration exceeding concentrations in the 99th

145 lectivity and high sensitivity against human-cTnI analytes and is capable of detecting cTnI at concen

146 i-cTnI Ab on CNFs and the detection of human-cTnI were examined using electrochemical impedance spect

147 used in combination with cardiac troponin I (cTnI) <99 th percentile and a nondiagnostic electrocardi

148 s for cardiac injury are cardiac troponin I (cTnI) and cardiac troponin T (cTnT) which have been cons

149 ndent phosphorylation of cardiac troponin I (cTnI) and phospholamban (PLN).

150 idelines regard cTnT and cardiac troponin I (cTnI) as equally sensitive and specific for the diagnosi

151 a novel high-sensitivity cardiac troponin I (cTnI) assay for this purpose.

152 hancement of LSPR assay, cardiac troponin I (cTnI) for myocardial infarction diagnosis was used as a

153 Cardiac troponin I (cTnI) functions as the molecular switch of the thin fila

154 The cardiac isoform of troponin I (cTnI) has a unique 31-residue N-terminal region that bin

155 to detect cardiac marker antigen Troponin I (cTnI) in blood based on fluorescence resonance energy tr

156 e regulatory function of cardiac troponin I (cTnI) involves three important contiguous regions within

157 -adrenergic stimulation, cardiac troponin I (cTnI) is phosphorylated by protein kinase A (PKA) at sit

158 smoking and circulating cardiac troponin I (cTnI) levels are associated with the risk of acute myoca

159 ardiomyopathy-associated cardiac troponin I (cTnI) mutations, R146G and R21C, are located in differen

160 site-specific changes in cardiac Troponin I (cTnI) phosphorylation, as well as a unique distribution

161 th a similar increase in cardiac troponin I (cTnI) protein, the established marker for heart injury.

162 The cardiac troponin I (cTnI) R145W mutation is associated with restrictive card

163 The cardiac troponin I (cTnI) R21C (cTnI-R21C) mutation has been linked to hyper

164 to demonstrate reduced card-iac troponin I (cTnI) release from ischemic rat hearts perfused with thi

165 Cardiac troponin I (cTnI) was measured by using a novel, high-sensitive assa

166 binding assay to detect cardiac Troponin I (cTnI) was used as an example to demonstrate the function

167 label-free detection of cardiac troponin I (cTnI), a biomarker for diagnosis of acute myocardial inf

168 -terminus (Ser-23/24) of cardiac troponin I (cTnI), cardiac myosin-binding protein C (cMyBP-C) and ti

169 In myofilaments PKA targets troponin I (cTnI), myosin binding protein-C (cMyBP-C) and titin.

170 in-binding protein-C and cardiac troponin I (cTnI), we sought to define if phosphorylation of one of

171 nsitive immunosensing of Cardiac Troponin I (cTnI).

172 tection of the cardiac biomarker troponin I (cTnI).

173 etection of a cardiac biomarker: Troponin I (cTnI).

174 lonal antibodies against cardiac troponin I (cTnI).

175 s with the actomyosin inhibitory troponin I (cTnI).

176 imultaneous screening of cardiac Troponin-I (cTnI) and cardiac-Troponin-T (cTnT) in a point-of-care s

177 binding protein C (cMyBP-C) and troponin-I (cTnI) are prominent myofilament targets of PKA.

178 performance of cardiac-specific troponin-I (cTnI) concentration levels in serum samples.

179 or the phosphorylation of Ser(23)/Ser(24) in cTnI is to prevent cardiac hypertrophy.

180 The change in cTnI levels was significantly related to male sex (p = 0

181 et as transmitted through related changes in cTnI and tropomyosin) become diminished by decreases in

182 Evolutionary directed changes in cTnI sequence suggest cTnI evolved to favor relaxation p

183 face of cCTnC, stabilizing an alpha helix in cTnI[41-67] and a type VIII turn in cTnI[38-41].

184 justed hazard ratio per log unit increase in cTnI, 1.41; 95% confidence interval, 1.29-1.54).

185 Hyperphosphorylation of this serine in cTnI C terminus impacts heart function by depressing dia

186 helix in cTnI[41-67] and a type VIII turn in cTnI[38-41].

187 yofibrils with the AMPK holoenzyme increased cTnI Ser-150 phosphorylation within the constraints of t

188 osphorylation of cardiac troponin inhibitor (cTnI) and the myosin-binding protein C was reduced by 26

189 AMIs not detected by the initial cTnI alone were picked up with copeptin >14 pmol/l in 23

190 Interestingly, cTnI-R145G blunted the intrasubunit interactions between

191 hown that a histidine button engineered into cTnI (cTnI A164H) specifically enhances inotropic functi

192 This was associated with less cTnI proteolysis in cTnIS200D hearts.

193 In comparison to mammalian cTnI, cTnI QAEH and cTnI AH showed increased contractili

194 the Mean+/-S.E. (n=5) percentage of maximal cTnI release was 30 +/- 7 and 60 +/- 17, respectively, w

195 ic sandwich immunoassay biosensor, measuring cTnI in undiluted blood plasma.

196 Median cTnI levels increased by 45% between both measurements.

197 cium sensitivity and alters calpain-mediated cTnI proteolysis.

198 r-level explanation for how the HCM mutation cTnI-R145G reduces the modulation of cTn by phosphorylat

199 ide is also the target of the point mutation cTnI-R145G, which is associated with hypertrophic cardio

200 patients with elevated cTnT, but with normal cTnI, had any cardiovascular events in either group duri

201 ional analyses determined the association of cTnI concentrations with rejection and International Soc

202 oning impacts the effective concentration of cTnI[148-158] presented to cNTnC, and this is how cTnI[1

203 ciation between increasing concentrations of cTnI and clinical end points in the total study cohort (

204 g is associated with lower concentrations of cTnI, suggesting that substances in tobacco smoke may af

205 oped an improved method for the detection of cTnI release from perfused rat hearts.

206 the sensor surface for specific detection of cTnI with a wide range of concentrations.

207 ylation, as well as a unique distribution of cTnI phosphospecies that were dependent on the LKB1 comp

208 , cTnT linker, I-T arm, regulatory domain of cTnI, the D-E linker of cTnC, and site II cTnC.

209 Furthermore, the blunting effect of cTnI Ser-150 phosphorylation cross-talk can uncouple the

210 The integrated discrimination improvement of cTnI regarding all-cause mortality was 0.014 (p = 0.04),

211 phosphorylated, weakening the interaction of cTnI with cardiac TnC.

212 kers exhibited significantly lower levels of cTnI (median, 2.9 ng/L; interquartile range, 2.0-4.1 ng/

213 Detection limit of cTnI with a concentration as low as 0.1ngmL(-1) has been

214 is directly proportional to the logarithm of cTnI concentration between 5.0pgmL(-1) and 20.0ngmL(-1)

215 ntation grade and the performance metrics of cTnI for the detection of AR.

216 e, Ser199 (equivalent to Ser200 in mouse) of cTnI (cardiac troponin I) is significantly hyperphosphor

217 the N terminus and the inhibitory peptide of cTnI that is normally seen with WT-cTn upon PKA phosphor

218 the N-terminus and the inhibitory peptide of cTnI.

219 PKA phosphorylation of cTnI also weakened C-I interaction in the presence of Ca

220 As phosphorylation of cTnI and PLN is critical to myocyte function, titration

221 ed isoproterenol-mediated phosphorylation of cTnI and PLN.

222 Phosphorylation of cTnI at Ser22/23 disrupts domain positioning, explaining

223 g the hypothesis that PKC phosphorylation of cTnI may be maladaptive and potentially associated with

224 upling from the impact of phosphorylation of cTnI mediated by PKA at the Ser-23/Ser-24 target sites.

225 ested the hypothesis that phosphorylation of cTnI modulates length dependence of force generation.

226 ese results indicate that phosphorylation of cTnI serines 23/24 is a key regulator of length dependen

227 t induced by PKC-mediated phosphorylation of cTnI Thr-143.

228 C-I interaction, via PKA phosphorylation of cTnI, may slow thin filament activation and result in in

229 irect evidence of in vivo phosphorylation of cTnI-Ser(42/44) (PKC-specific) sites in an animal model

230 ry, potentially by decreasing proteolysis of cTnI.

231 nd R21C, are located in different regions of cTnI, the inhibitory peptide and the cardiac-specific N

232 n phosphorylation of the S23/S24 residues of cTnI that results in these changes in function.

233 rain source configuration for the sensing of cTnI.

234 ate 150 ns molecular dynamics simulations of cTnI-R145G Ca(2+)-bound cTnC(1-161)-cTnI(1-172)-cTnT(236

235 However, as the N-terminus of cTnI (residues 1-40) has not been resolved in the whole

236 sites S23/S24, located at the N-terminus of cTnI.

237 involved interactions with the N-terminus of cTnI.

238 72, and cTnT 236-285) with the N-terminus of cTnI.

239 We focused on cTnI as troponin can be exchanged in permeabilized stria

240 the presence of either cTnI RCM mutation or cTnI PKC phosphomimetic.

241 Here, we tested how cTnI(R146G) or cTnI(R21C) influences contractile activation and relaxat

242 lation is well understood, the role of other cTnI phosphorylation sites in the regulation of cardiac

243 ylatable cTnI (S23/24A) Tn or phosphomimetic cTnI (S23/24D) Tn.

244 ther wild-type (WT) Tn, non-phosphorylatable cTnI (S23/24A) Tn or phosphomimetic cTnI (S23/24D) Tn.

245 abolic regulatory kinase AMPK phosphorylates cTnI at Ser-150 in vivo to alter cardiac contractile fun

246 at heart preparations optimally precipitated cTnI, allowing its detection in Western blots.

247 ge, electrostatic interaction between R171of cTnI and E15 of cTnC, which structurally phenocopied the

248 The cardiac troponin I (cTnI) R21C (cTnI-R21C) mutation has been linked to hypertrophic card

249 12-17) were exchanged (~93%) for recombinant cTnI in which the two PKA sites were mutated to either p

250 hemia and 60-150 min of reperfusion, reduced cTnI release by 80%.

251 d to hypertrophic cardiomyopathy and renders cTnI incapable of phosphorylation by PKA in vivo.

252 The diagnostic accuracy of BNP, cTnT, and s-cTnI for the diagnosis of ischemic AHF, as quantified by

253 T (cTnT) and sensitive cardiac troponin I (s-cTnI) were also significantly higher in ischemic compare

254 ged with either wild-type cTnI, or S23D/S24D-cTnI recombinant cTn.

255 cTn or exchange of cTn containing S23D/S24D-cTnI resulted in an increase in the rate of early, slow

256 by cTnI phosphomimetic mutations (S23D/S24D-cTnI), directly affects thin filament activation and myo

257 Copeptin levels and a contemporary sensitive cTnI (99 th percentile 40 ng/l; 10% coefficient of varia

258 racy of baseline and serial high-sensitivity cTnI (hs-cTnI) measurements for myocardial infarction an

259 of serial monitoring with a high-sensitivity cTnI assay may offer a low-cost noninvasive strategy for

260 A high-sensitivity cTnI assay seems useful to rule out AR in cardiac transp

261 superior to hs-cTnI and standard sensitivity cTnI (P<0.05 for both) and similar to hs-cTnT at predict

262 of cMyC with hs-cTnT or standard-sensitivity cTnI (but not hs-cTnI) led to an increase in AUC to 0.93

263 In the example assay, several cTnI concentrations ranging from 0 to 250 ng/mL were det

264 availability of thin filament binding sites (cTnI) or altered crossbridge recruitment (cMyBP-C/titin)

265 mensional solution NMR spectroscopy to study cTnI[1-73] in complex with cTnC.

266 ry directed changes in cTnI sequence suggest cTnI evolved to favor relaxation performance in the mamm

267 cence of GQDs based on interaction of target cTnI with its specific anti-cTnI antibody.

268 We conclude that cTnI phosphorylation by AMPK may represent a novel mecha

269 Our data indicate that cTnI is hyperphosphorylated in the failing SHR myocardiu

270 In vitro studies showed that cTnI is a good AMPK substrate and that Ser150 is the pri

271 Our data suggest that cTnI might offer utility for clinical assessment of subj

272 Together, our results suggest that cTnI(R146G) and cTnI(R21C) blunt PKA modulation of activ

273 etween the cTnI N-terminal extension and the cTnI inhibitory peptide, which have been suggested to pl

274 ed the intrasubunit interactions between the cTnI N-terminal extension and the cTnI inhibitory peptid

275 g of homozygous knock-in mice expressing the cTnI-R21C mutation shows that they develop hypertrophy a

276 idge was recapitulated in simulations of the cTnI A164R variant.

277 putationally investigated the effects of the cTnI-R145G mutation on the dynamics of cTn, cTnC Ca(2+)

278 romatography to determine quantitatively the cTnI phosphorylation changes in spontaneously hypertensi

279 erimentally and computationally to study the cTnI N-terminal specific effects of PKA phosphorylation.

280 We found that the cTnI-R145G mutation did not impact the overall dynamics

281 iac-specific N-terminal interaction with the cTnI inhibitory peptide.

282 e cardiomyopathy that is associated with the cTnI R145W mutation.

283 Comparisons were made with the cTnI-R145G/S23D/S24D phosphomimic mutation, which has be

284 ty to enhance myofilament relaxation through cTnI phosphorylation predisposes the heart to abnormal d

285 eversibly replaced by the adult cardiac TnI (cTnI) isoform.

286 ed calcium binding for cTnI QAEH compared to cTnI.

287 Adding copeptin to cTnI allowed safe rule out of AMI with a negative predic

288 lySi NW biosensor, the biosensor response to cTnI biomarker can be improved by at least 16 fold in 50

289 The sensor displayed a linear response to cTnI from 0.001 to 1000 ng mL(-1) with a limit of detect

290 7), and hs-cTnI (AUC, 0.922) and superior to cTnI measured by a contemporary sensitivity assay (AUC,

291 ptide of the inhibitory subunit of troponin, cTnI (cTnI(1-39)), is a target for phosphorylation by pr

292 nous cTn was exchanged with either wild-type cTnI, or S23D/S24D-cTnI recombinant cTn.

293 cTn (pCa50) was significantly decreased when cTnI was phosphorylated by PKA (DeltapCa50 = 0.31).

294 lly under acidic/hypoxic conditions, whereas cTnI facilitates faster relaxation performance.

295 TnI and nonmammalian chordate cTnIs, whereas cTnI AH is similar to fish cTnI in these four residues.

296 However, whether cTnI levels differ according to smoking status and wheth

297 Troponin C (cTnC) interaction with cTnI (C-I interaction) is a critical step in contractile

298 ll complexes, but KC-I was reduced only with cTnI(WT).

299 y between myocytes expressing wild-type (WT) cTnI and cTnI A164H, whereas the A164R variant showed in

300 cTnI(WT), cTnI(R146G), and cTnI(R21C) were complexed into cardiac