ライフサイエンスコーパス: cTnI

1 cTnI concentrations were significantly higher in rejecti

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

3 cTnI QAEH molecular dynamics simulations demonstrated al

4 cTnI was abnormal in only 1 patient.

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

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

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

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

9 cTnI, but not cTnT, was associated with myocardial infar

10 cTnI-G203S or age-matched wt mice were treated with acti

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

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

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

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

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

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

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

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

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

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

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

22 After the characterization analysis, cTnI imprinted electrode was developed in the presence o

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

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

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

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

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

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

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

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

31 High-sensitivity cTnT and cTnI were measured in serum from 19 501 individuals in G

32 and contrast (1) the association of cTnT and cTnI with CVD and non-CVD outcomes, and (2) their determ

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

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

35 ith a significant reduction in NT-proBNP and cTnI, suggesting improvement in myocardial wall stress.

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

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

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

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

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

41 hrough structural effects on tropomyosin and cTnI.

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

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

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

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

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

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

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

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

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

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

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

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

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

55 Both cTnI and cTnT had strong associations with CVD death and

56 Both cTnI and cTnT were strongly associated with CVD risk in

57 1pg/mL in human serum was achieved for both cTnI and cTnT.

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

59 tractile activation that can be modulated by cTnI phosphorylation.

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

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

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

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

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

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

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

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

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

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

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

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

72 demonstrate a good selectivity for detecting cTnI.

73 m-resolved molecular fingerprints of diverse cTnI proteoforms to establish proteoform-pathophysiology

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

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

76 ology, highly organized sarcomeres, elevated cTnI expression and mitochondrial distribution and funct

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

78 (95% CI, 1.17-1.32) and 1.11 (1.04-1.19) for cTnI and cTnT, respectively; ratio of hazard ratios 1.12

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

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

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

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

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

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

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

86 tride quantum dots (BNQDs) was presented for cTnI detection in plasma samples.

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

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

89 using cardiac troponin I mutation Gly203Ser (cTnI-G203S) is associated with increased mitochondrial m

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

91 148-158] presented to cNTnC, and this is how cTnI[19-37] indirectly modulates the calcium affinity of

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

93 hs-cTnI (Siemens) rose faster and reached a higher peak.

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

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

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

97 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

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

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

100 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

101 with an hs-cTnT assay and an alternative hs-cTnI assay with even higher analytic sensitivity (limit

102 An hs-cTnI cutoff of 2.5 ng/L, derived previously in mostly as

103 Using the cTnT, hs-cTnI (Siemens), and hs-cTnI (Abbott) concentrations at 0 and 180 minutes, 1 (11

104 : hs-cTnT (Roche), hs-cTnI (Siemens), and hs-cTnI (Abbott).

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

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

107 elded an NPV of 66% (CI, 59% to 72%), and hs-cTnI concentrations less than 2 ng/L yielded an NPV of 6

108 BNP, NT-proBNP, hs-cTnT, and hs-cTnI concentrations provide useful diagnostic and progno

109 BNP, NT-proBNP, hs-cTnT and hs-cTnI concentrations were measured in a blinded fashion.

110 accuracy of BNP, NT-proBNP, hs-cTnT, and hs-cTnI concentrations, alone and against the ones of clini

111 BNP, NT-proBNP, hs-cTnT, and hs-cTnI cut-offs, achieving pre-defined thresholds for sens

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

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

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

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

116 BNP, NT-proBNP, hs-cTnT, and hs-cTnI were significantly higher in cardiac syncope vs. ot

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

118 .94; 95% CI: 0.93 to 0.96; p = 0.213) and hs-cTnI-Architect (AUC: 0.92; 95% CI: 0.90 to 0.93; p < 0.0

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

120 continuous relationship between baseline hs-cTnI and risk for adverse events, using 2 Food and Drug

121 at 30 days were examined across baseline hs-cTnI concentrations.

122 ng 2 Food and Drug Administration-cleared hs-cTnI assays, an optimized threshold of <5 ng/l safely id

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

124 Using the cTnT, hs-cTnI (Siemens), and hs-cTnI (Abbott) concentrations at 0

125 Combining BNP/NT-proBNP with hs-cTnT/hs-cTnI further improved diagnostic accuracy to an AUC of 0

126 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

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

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

129 milarly, using the alternative assays for hs-cTnI or hs-cTnT, no cutoff achieved the target performan

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

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

132 ared high-sensitivity cardiac troponin I (hs-cTnI) assays.

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

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

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

136 eks: high-sensitivity cardiac troponin I (hs-cTnI), N-terminal pro-B-type natriuretic peptide (NT-pro

137 o between-group differences in changes in hs-cTnI, CRP, uric acid, or urine protein-creatinine ratio

138 very low hs-cTn concentrations, including hs-cTnI concentrations less than 2.5 ng/L, do not generally

139 indings in a secondary analysis including hs-cTnI-Architect for central adjudication.

140 Increased hs-cTnI (Siemens) concentrations were first detectable 15 m

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

142 natriuretic peptide) 624 (307-1312) ng/L, hs-cTnI (high sensitivity cardiac troponin I) 6.3 (3.4-13.0

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

144 tudy sought to examine single measurement hs-cTnI to identify patients at low and high risk for acute

145 No hs-cTnI cutoff reached both performance characteristics pre

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

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

148 eriods before and after implementation of hs-cTnI assay (Abbott) using sex-specific 99th percentiles.

149 The implementation of hs-cTnI assay together with sex-specific 99th percentiles w

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

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

152 For high-risk patients, hs-cTnI >=120 ng/l resulted in positive predictive values f

153 ical performance of a point-of-care (POC)-hs-cTnI assay in patients with suspected myocardial infarct

154 The POC-hs-cTnI-TriageTrue assay provides high diagnostic accuracy

155 The area under the curve (AUC) for POC-hs-cTnI-TriageTrue at presentation was 0.95 (95% confidence

156 rectly compare diagnostic accuracy of POC-hs-cTnI-TriageTrue versus best-validated central laboratory

157 ed the derivation and validation of a POC-hs-cTnI-TriageTrue-specific 0/1-h algorithm.

158 he prognostic accuracy of BNP, NT-proBNP, hs-cTnI, and hs-cTnT for MACE was moderate-to-good (AUC 0.7

159 iet, the fruit-and-vegetable diet reduced hs-cTnI levels by 0.5 ng/L (95% CI, -0.9 to -0.2 ng/L) and

160 h the control diet, the DASH diet reduced hs-cTnI levels by 0.5 ng/L (CI, -0.9 to -0.1 ng/L) and NT-p

161 itivity (hs) cTn assays: hs-cTnT (Roche), hs-cTnI (Siemens), and hs-cTnI (Abbott).

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

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

164 Upon implementation of the hs-cTnI assay, proportion of patients with troponin levels

165 The hs-cTnI cutoff of 2.5 ng/L provided an NPV of 70% (95% CI,

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

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

168 Similar findings emerged when using hs-cTnI.

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

170 atients as low risk at presentation, with hs-cTnI >=120 ng/l identifying high-risk patients.

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

172 ute MI enrolled across 29 U.S. sites with hs-cTnI measured using the Atellica IM TnIH and ADVIA Centa

173 blunted by human TnI, suggesting that human cTnI phosphorylation by cMLCK modifies the functional co

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

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

176 er cardiac troponin T (cTnT) and troponin I (cTnI) are equivalent measures of risk in this setting.

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

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

179 Cardiac troponin I (cTnI) geometric mean decreased by 34% in the pooled mava

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

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

182 rylates Ser(23) of human cardiac troponin I (cTnI) in isolation and in the trimeric troponin complex

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

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

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

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

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

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

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

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

191 omprehensive analysis of cardiac troponin I (cTnI), a gold-standard cardiac biomarker, directly from

192 tic peptide (NT-proBNP), cardiac troponin I (cTnI), and fibrinogen- were rapidly (5 min) analyzed fro

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

194 nsitive immunosensing of Cardiac Troponin I (cTnI).

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

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

197 lonal antibodies against cardiac troponin I (cTnI).

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

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

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

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

202 The cardiac Troponin-I (cTnI) is one of the subunits of cardiac troponin complex

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

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

205 am genetic causes of low-grade elevations in cTnI and cTnT appear distinct, and their associations wi

206 Elevations in cTnI are more strongly associated with some CVD outcomes

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

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

209 erations in six biochemical intermediates in cTnI-G203S hearts consistent with increased anaplerosis.

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

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

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

213 Interestingly, cTnI-R145G blunted the intrasubunit interactions between

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

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

216 cium sensitivity and alters calpain-mediated cTnI proteolysis.

217 (0.1-50 mg/L), NT-proBNP (50-10,000 pg/mL), cTnI (1-10,000 pg/mL), and fibrinogen (0.1-5 mg/mL).

218 sence of 100.0 mM pyrrole containing 25.0 mM cTnI.

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

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

221 By contrast, cTnT, but not cTnI, was associated with non-CVD death; ratio of hazard

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

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

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

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

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

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

228 These NPs enable the sensitive enrichment of cTnI (<1 ng/mL) with high specificity and reproducibilit

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

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

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

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

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

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

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

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

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

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

239 ed isoproterenol-mediated phosphorylation of cTnI and PLN.

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

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

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

243 ry, potentially by decreasing proteolysis of cTnI.

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

245 Moreover, the selectivity of cTnI imprinted glassy carbon electrode (GCE) was investi

246 rain source configuration for the sensing of cTnI.

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

248 After that, the analytical studies of cTnI in plasma samples were performed by using cTnI impr

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

250 involved interactions with the N-terminus of cTnI.

251 72, and cTnT 236-285) with the N-terminus of cTnI.

252 examine the efficacy of in vivo treatment of cTnI-G203S mice with a peptide derived against the alpha

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

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

255 that AID-TAT treatment of precardiomyopathic cTnI-G203S mice, but not mice with established cardiomyo

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

257 12-17) were exchanged (~93%) for recombinant cTnI in which the two PKA sites were mutated to either p

258 erved that human cMLCK phosphorylates rodent cTnI to a much smaller extent in vitro and in situ, sugg

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

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

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

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

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

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

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

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

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

268 Due to its myocardial specificity, cTnI is widely used for the diagnosis of AMI diseases.

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

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

271 ardiac biomarkers including troponin I or T (cTnI or cTnT), creatine kinase-MB (CK-MB), and myoglobin

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

273 an serum albumin (>10(10) more abundant than cTnI).

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

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

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

277 dentify biomarkers of HCM resulting from the cTnI mutation Gly203Ser, and present a safe, preventativ

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

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

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

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

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

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

292 nI in plasma samples were performed by using cTnI imprinted biosensor.

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 ad genome-wide significant associations with cTnI, and a different set of 4 loci (4 single-nucleotide

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

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

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