ライフサイエンスコーパス: cardiac troponin I

1 tinin, cardiac myosin-binding protein C, and cardiac troponin I).

2 letal troponin I but not when it is bound to cardiac troponin I.

3 istidine, which is replaced by an alanine in cardiac troponin I.

4 as cAMP-response element binding protein and cardiac troponin I.

5 ed hearts, as evidenced by 54% reduced serum cardiac troponin I.

6 diac troponin C for the regulatory region of cardiac troponin I.

7 igens of two antibodies raised against human cardiac troponin I.

8 experimental work was carried out with human cardiac troponin I.

9 omplex formed between cardiac troponin C and cardiac troponin I.

10 troponin C bound to the isolated N-domain of cardiac troponin I.

11 ding to residues 85-93, when bound to intact cardiac troponin I.

12 r Tm180 littermates, which express wild-type cardiac troponin I.

13 xation rate increased in myocytes expressing cardiac troponin-I.

14 tion sites previously identified in purified cardiac troponin-I.

15 ors showed extraordinary sensitivity towards cardiac troponin I [1.7microA/(ng/mL) in phosphate buffe

16 After bisphosphorylation of cardiac troponin I(1-80) the apparent K(d) increased to

17 c troponin C(F20W/N51C)(AEDANS) complexed to cardiac troponin I(1-80) was used to monitor binding of

18 or intact cardiac troponin C bound to either cardiac troponin I(1-80)/troponin I(129-166) or troponin

19 .59 (95% CI, 1.76-3.83) for high-sensitivity cardiac troponin I, 1.65 (95% CI, 1.12-2.44) for NT-proB

20 regulatory domain of cardiac troponin C for cardiac troponin I(129-166) and provides further evidenc

21 The apparent K(d) for cardiac troponin I(129-166) binding to cardiac troponin

22 ponin I(1-80) was used to monitor binding of cardiac troponin I(129-166) to the regulatory domain of

23 roponin I(129-166) complex demonstrated that cardiac troponin I(129-166), corresponding to the adjace

24 se, 1 splice acceptor site, and 3 missense), cardiac troponin I (2 missense), and alpha-cardiac myosi

25 4 (307-1312) ng/L, hs-cTnI (high sensitivity cardiac troponin I) 6.3 (3.4-13.0) ng/L, hs-CRP (high se

26 The device can detect serum cardiac troponin I, a biomarker of cardiac disease to 10

27 ensitivity by a single histidine substituted cardiac troponin I (A164H) would protect the whole anima

28 ssociated with PAPP-A stratified by baseline cardiac troponin I [Accu-TnI >0.04 mug/l], p interaction

29 croarray analysis of serum biomarkers (e.g., cardiac troponin I) afforded up to 130-fold enhancement

30 ning reduces the incidence of postprocedural cardiac troponin I after elective PCI and confers an MAC

31 Patients with an MACCE had a higher mean cardiac troponin I after PCI (+/-SD): 2.07+/-6.99 versus

32 protein coding exons of cardiac troponin T, cardiac troponin I, alpha-tropomyosin, and cardiac actin

33 Cardiac troponin is an independent predictor of cardiova

34 In addition, plasma concentration of cardiac troponin I, an established diagnostic marker for

35 rary primary prevention population, baseline cardiac troponin I and BNP were associated with the risk

36 We used cardiac troponin I and C-reactive protein as the targets

37 ding the myocardial differentiation markers, cardiac troponin I and cardiac alpha-actin, are absent,

38 e also noted raised plasma concentrations of cardiac troponin I and collagen fibril deposition in the

39 n of CMBK resulted in higher serum levels of cardiac troponin I and elevated amounts of reactive oxyg

40 changes in circulation (ie, detectable serum cardiac troponin I and elevated serum soluble intercellu

41 he measurement of the heart attack indicator cardiac troponin I and is shown to successfully combine

42 phenotype, restoring normal serum levels for cardiac troponin I and normal cardiac muscle morphology.

43 ncreased expression of the maturation marker cardiac troponin I and significantly increased action po

44 enes, and despite their close proximity, the cardiac troponin I and slow skeletal troponin T genes sh

45 s, such as cardiac alpha-myosin heavy chain, cardiac troponin I and T, atrial natriuretic factor, and

46 Cardiac troponin I and T, regulatory components of the c

47 TnT1, -2, or -3 and reconstituted with human cardiac troponin I and troponin C (HCTnI.TnC) complex sh

48 chia coli, purified, and combined with human cardiac troponins I and C to reconstitute human cardiac

49 High-sensitivity assays can quantify cardiac troponins I and T (hs-cTnI, hs-cTnT) in individu

50 rs of a recent coronary occlusion (including cardiac troponin I) and their respective contribution.

51 protein kinase C phosphorylation of purified cardiac troponin I, and although this cluster was not ac

52 lattice expands after PKA phosphorylation of cardiac troponin I, and when present, cMyBP-C, may stabi

53 gens, like cardiac myosin heavy chain-alpha, cardiac troponin-I, and adenine nucleotide translocator

54 fabricated with an immobilized antibody for cardiac troponin I (anti-cTnI) on a photoresponsive comp

55 dots (afGQDs) conjugated with antibody anti-cardiac Troponin I (anti-cTnI) to detect cardiac marker

56 vels of B-type natriuretic peptide (BNP) and cardiac troponin I are associated with adverse outcomes

57 Three separate clusters within cardiac troponin I are phosphorylated by protein kinase

58 kinase C-dependent phosphorylation sites in cardiac troponin-I are likely responsible for the accele

59 f the method and provide validation, we used cardiac troponin I as analyte and monitored the time cou

60 xhibits five times lower detection limit for cardiac troponin I assay with a high selectivity.

61 he impact of implementing a high-sensitivity cardiac troponin I assay with sex-specific diagnostic th

62 Use of the high-sensitivity cardiac troponin I assay with sex-specific thresholds in

63 ons at presentation using a high-sensitivity cardiac troponin I assay.

64 ntervention for such patients, the dosage of cardiac troponin I at admission could not help in the de

65 roperties and still enabled the detection of cardiac troponin I at pg/mL concentrations in 10% serum

66 ombinant PKD catalytic domain phosphorylates cardiac troponin I at Ser22/Ser23 and reduces myofilamen

67 phospholamban (at Ser16 site; p = 0.04) and cardiac troponin I (at Ser23/24 sites; p = 0.01), veloci

68 e found that TpP correlated only weakly with cardiac troponin I, B-type natriuretic peptide, and high

69 implified Pulmonary Embolism Severity Index, cardiac troponin I, brain natriuretic peptide, and lower

70 us biomolecular recognition of model analyte cardiac troponin I by two antibody fragments brought the

71 of the clinical biomarker of cardiac injury, cardiac troponin-I, by 52+/-17% (P=1.01x10(-2)).

72 rched to evaluate if an early measurement of cardiac troponin I can help to detect a recent coronary

73 rdial injury was defined as high-sensitivity cardiac troponin I concentration >99th centile of 16 ng/

74 acute coronary syndrome, a high-sensitivity cardiac troponin I concentration of less than 5 ng/L ide

75 Plasma cardiac troponin I concentration was measured with a hig

76 e myocardial injury (high-sensitivity plasma cardiac troponin I concentration, 4.3 ng/L [interquartil

77 y, as assessed by serial measurements of the cardiac troponin I concentration.

78 consecutive patients (n=2122) with elevated cardiac troponin I concentrations (>/=0.05 microg/L) at

79 ocardial ischemia, and an increase in plasma cardiac troponin I concentrations (1.4 [0.8-2.5] versus

80 We measured cardiac troponin I concentrations in 725 participants (6

81 ospective studies measuring high-sensitivity cardiac troponin I concentrations in patients with suspe

82 Cardiac troponin I concentrations were less than 5 ng/L

83 rating age, sex, and paired high-sensitivity cardiac troponin I concentrations, was trained on 3,013

84 Myocyte replacement with a cardiac troponin I containing a Thr144 substituted with

85 The N-domain of cardiac troponin I contains two protein kinase C phospho

86 diac troponin C for the regulatory region of cardiac troponin I (corresponding to residues 128-180).

87 Binding of the anchoring region of cardiac troponin I (corresponding to residues 34-71) to

88 ompe disease, the relationship between cTnT, cardiac troponin I, creatine kinase (CK), CK-myocardial

89 Cardiac troponin I (cTI) release occurs frequently after

90 Cardiac troponin I (cTI) was measured to quantify the de

91 farction (AMI) when used in combination with cardiac troponin I (cTnI) <99 th percentile and a nondia

92 The Ca(2+)-induced interaction between cardiac troponin I (cTnI) and actin plays a key role in

93 myocardial fibrosis, blocked increased serum cardiac troponin I (cTnI) and brain type natriuretic pep

94 most specific markers for cardiac injury are cardiac troponin I (cTnI) and cardiac troponin T (cTnT)

95 The LC-MS analysis of recombinant cardiac troponin I (cTnI) and cTnI extracted from human

96 ic peptide (BNP), alone and in comparison to cardiac troponin I (cTnI) and high-sensitivity C-reactiv

97 in association with phosphorylation of both cardiac troponin I (cTnI) and phospholamban (PLB).

98 Elucidating the relative roles of cardiac troponin I (cTnI) and phospholamban (PLN) in bet

99 ing in PKA-site dependent phosphorylation of cardiac troponin I (cTnI) and phospholamban (PLN).

100 study determined the prevalence of increased cardiac troponin I (cTnI) and T (cTnT) in end-stage rena

101 al 273 residues of gamma2 as bait identified cardiac troponin I (cTnI) as a putative interactor.

102 Practice guidelines regard cTnT and cardiac troponin I (cTnI) as equally sensitive and speci

103 formance metrics of a novel high-sensitivity cardiac troponin I (cTnI) assay for this purpose.

104 delta phosphorylates the myofilament protein cardiac troponin I (cTnI) at Ser(23)/Ser(24) when it is

105 it was demonstrated that AMPK phosphorylates cardiac troponin I (cTnI) at Ser-150 in vitro.

106 r PKC-dependent multisite phosphorylation of cardiac troponin I (cTnI) at Ser-23 and Ser-24 (also PKA

107 induces protein kinase A phosphorylation of cardiac troponin I (cTnI) at Ser23/24 to alter the inter

108 ecrease in linker flexibility in response to cardiac troponin I (cTnI) binding.

109 ith 99mTc sestamibi and measurement of serum cardiac troponin I (cTnI) both can identify patients wit

110 evidence that multi-site phosphorylation of cardiac troponin I (cTnI) by protein kinase C is importa

111 G demonstrated a complete replacement of the cardiac troponin I (cTnI) by ssTnI.

112 The N-terminal domain of cardiac troponin I (cTnI) comprising residues 33-80 and

113 PKA-dependent phosphorylation of cardiac troponin I (cTnI) contributes significantly to b

114 in kinase C (PKC)-induced phosphorylation of cardiac troponin I (cTnI) depresses the acto-myosin inte

115 y syndromes (ACS) according to the degree of cardiac troponin I (cTnI) elevation.

116 )O(4) MNPs in the enhancement of LSPR assay, cardiac troponin I (cTnI) for myocardial infarction diag

117 We sought to evaluate cardiac troponin I (cTnI) for predicting early clinical

118 Cardiac troponin I (cTnI) functions as the molecular swi

119 Cardiac troponin I (cTnI) geometric mean decreased by 34

120 e performed on 242 patients in whom cTnT and cardiac troponin I (cTnI) had been previously run.

121 ucture conserved in all troponin I isoforms, cardiac troponin I (cTnI) has an N-terminal extension th

122 Multiple mutations in cardiac troponin I (cTnI) have been associated with fami

123 e sought to evaluate the prognostic value of cardiac troponin I (cTnI) in asymptomatic, ambulatory pa

124 We compared levels of phosphorylation of cardiac troponin I (cTnI) in control myocytes with phosp

125 ifically monophosphorylates Ser(23) of human cardiac troponin I (cTnI) in isolation and in the trimer

126 The regulatory function of cardiac troponin I (cTnI) involves three important conti

127 Cardiac troponin I (cTnI) is a highly sensitive and spec

128 Cardiac troponin I (cTnI) is a phosphoprotein subunit of

129 Cardiac troponin I (cTnI) is a sensitive and specific ma

130 Phosphorylation of cardiac troponin I (cTnI) is critical in modulating cont

131 Residue Ser151 of cardiac troponin I (cTnI) is known to be phosphorylated

132 During beta-adrenergic stimulation, cardiac troponin I (cTnI) is phosphorylated by protein k

133 Human cardiac Troponin I (cTnI) is the first sarcomeric protei

134 Cardiac troponin I (cTnI) is the inhibitory subunit of c

135 The R21C substitution in cardiac troponin I (cTnI) is the only identified mutatio

136 The cardiac troponin I (cTnI) isoform contains a unique N-te

137 Both tobacco smoking and circulating cardiac troponin I (cTnI) levels are associated with the

138 ar mechanisms whereby cardiomyopathy-related cardiac troponin I (cTnI) mutations affect myofilament a

139 Cardiac troponin I (cTnI) mutations can cause familial h

140 Two hypertrophic cardiomyopathy-associated cardiac troponin I (cTnI) mutations, R146G and R21C, are

141 in preparations containing either wild-type cardiac troponin I (cTnI) or a mutant cTnI with an R146G

142 aE106, respectively) and studied with either cardiac troponin I (CTnI) or slow skeletal troponin I (S

143 Endotoxemic rat hearts show increased cardiac troponin I (cTnI) phosphorylation at serines 23

144 Cardiac troponin I (cTnI) phosphorylation modulates myoc

145 t proteins revealed site-specific changes in cardiac Troponin I (cTnI) phosphorylation, as well as a

146 , which coincided with a similar increase in cardiac troponin I (cTnI) protein, the established marke

147 The precise mechanism of cardiac troponin I (cTnI) proteolysis in myocardial stun

148 The cardiac troponin I (cTnI) R145W mutation is associated w

149 The cardiac troponin I (cTnI) R21C (cTnI-R21C) mutation has

150 ischemic preconditioning (IPC) to attenuate cardiac troponin I (cTnI) release after elective PCI.

151 A novel finding is a fragment of cardiac troponin I (cTnI) that had increased amounts in

152 ostic implications of low-level increases in cardiac troponin I (cTnI) using a current-generation sen

153 Cardiac troponin I (cTnI) was determined on admission in

154 Cardiac troponin I (cTnI) was measured by using a novel,

155 ition, a competitive binding assay to detect cardiac Troponin I (cTnI) was used as an example to demo

156 r isoforms of myosin light chain 1 and 2 and cardiac troponin I (cTnI) were expressed, with no differ

157 Mutations in cardiac troponin I (cTnI) were identified as causal for

158 highly sensitive and label-free detection of cardiac troponin I (cTnI), a biomarker for diagnosis of

159 the enrichment and comprehensive analysis of cardiac troponin I (cTnI), a gold-standard cardiac bioma

160 difies PKCdelta-dependent phosphorylation of cardiac troponin I (cTnI), a myofilament regulatory prot

161 Cardiac troponin I (cTnI), a sensitive and specific mark

162 We therefore investigated the release of cardiac troponin I (cTnI), a sensitive and specific mark

163 pro b-type natriuretic peptide (NT-proBNP), cardiac troponin I (cTnI), and fibrinogen- were rapidly

164 ondary structure of the inhibitory region of cardiac troponin I (cTnI), and the change in the separat

165 with an established role of PKD in targeting cardiac troponin I (cTnI), caPKD expression led to a mar

166 PKA targets the N-terminus (Ser-23/24) of cardiac troponin I (cTnI), cardiac myosin-binding protei

167 g over a range of cut points, alone and with cardiac troponin I (cTnI), in patients with non-ST-eleva

168 the PKD catalytic domain as bait, identified cardiac troponin I (cTnI), myosin-binding protein C (cMy

169 also no difference in PKA phosphorylation of cardiac troponin I (cTnI), phospholamban, or ryanodine r

170 ssed by tracking phosphorylation of CREB and cardiac troponin I (cTnI), two physiologically relevant

171 ncluding titin, myosin-binding protein-C and cardiac troponin I (cTnI), we sought to define if phosph

172 al infarction biomarkers, myoglobin (MG) and cardiac troponin I (cTnI), were quantified at biological

173 osed for the ultrasensitive immunosensing of Cardiac Troponin I (cTnI).

174 quantities of monoclonal antibodies against cardiac troponin I (cTnI).

175 ied by increases in the level of a truncated cardiac troponin I (cTnI-ND) from restricted removal of

176 re disorganization and reduced expression of cardiac troponin-I (cTnI) and cardiac troponin-T (cTnT).

177 oped for rapid and simultaneous screening of cardiac Troponin-I (cTnI) and cardiac-Troponin-T (cTnT)

178 um myoglobin, creatine-kinase-MB (CK-MB) and cardiac troponin-I (cTnI) for predicting the infarct-rel

179 The cardiac Troponin-I (cTnI) is one of the subunits of card

180 Cardiac troponins I (cTnI) and T (cTnT) are useful for a

181 C(81-161), in a complex with the N domain of cardiac troponin I, cTnI(33-80), and compared it with a

182 ophic cardiomyopathy (HCM)-associated mutant cardiac troponin I (cTnIR145G; R146G in rodents) has bee

183 Low concentrations of high-sensitivity cardiac troponin I determined on presentation to the eme

184 es corresponding to the inhibitory region of cardiac troponin I (e.g. hcTnI128-153) to F-actin to for

185 vely enrolled and serial echocardiograms and cardiac troponin I evaluations were performed.

186 We discuss a current concept of cardiac troponin I function in the A-band region of the

187 Myocardial injury was assessed by cardiac troponin I (>0.40 ng/mL), myocardial infarction

188 Cardiac troponin I has a limited role in predicting mort

189 into porcine skinned fibers along with human cardiac troponin I (HCTnI) and troponin C (HCTnC), and t

190 sed the functional consequences of the human cardiac troponin I (hcTnI) hypertrophic cardiomyopathy R

191 The human cardiac troponin I (hcTnI) mutation R145W has been assoc

192 ies of the unique N-terminal region of human cardiac troponin I (hcTnI), predicted a possible intramo

193 several mutations in the gene encoding human cardiac troponin I (HCTnI).

194 fter adjusting for clinical characteristics, cardiac troponin I, high-sensitivity C-reactive protein,

195 Drug Administration-cleared high-sensitivity cardiac troponin I (hs-cTnI) assays.

196 myocardial infarction using high-sensitivity cardiac troponin I (hs-cTnI) have been identified.

197 c troponin T (hs-cTnT), and high-sensitivity cardiac troponin I (hs-cTnI) were determined in plasma s

198 Quartiles of BNP and high-sensitivity cardiac troponin I (hs-cTnI) were included in adjusted m

199 ed at baseline and 8 weeks: high-sensitivity cardiac troponin I (hs-cTnI), N-terminal pro-B-type natr

200 High-sensitivity cardiac troponin I (hs-TnI) levels at baseline were asse

201 tionship between changes in high-sensitivity cardiac troponin I (hsTnI) and cardiovascular outcomes.

202 We measured high-sensitivity cardiac troponin I (hsTnI) in 12 956 and BNP in 11 076 p

203 of the sarcomere and potential signaling to cardiac troponin I in a network involving the ends of th

204 on of caspase-3, and increased expression of cardiac troponin I in cardiomyocytes.

205 terferences when electrochemically detecting cardiac troponin I in complex biological samples.

206 terations occurred on individual residues of cardiac troponin I in heart failure, likely reflecting a

207 valuated the performance of high-sensitivity cardiac troponin I in those with and without renal impai

208 in kinase catalysed phosphorylation of human cardiac troponin I in vitro.

209 injury, and markedly reduced elaboration of cardiac troponin-I in coronary effluent during ESHP.

210 RNA signatures correlated with elevations in cardiac Troponin-I in severely injured hearts during EVH

211 oal was to define the role of phosphorylated cardiac troponin-I in the adult myocyte contractile perf

212 F) nanoelectrode arrays for the detection of cardiac troponin-I in the early diagnosis of myocardial

213 ication of cardiac biomarkers (myoglobin and cardiac troponin I) in the clinically significant sensin

214 ectrometry data, 14 phosphorylation sites on cardiac troponin I, including 6 novel residues (S4, S5,

215 A series of cardiac troponin I-interacting kinase (TNNI3K) inhibitor

216 Cardiac troponin I is a phosphorylation target for endot

217 We review how phosphorylation signaling to cardiac troponin I is integrated, with parallel signals

218 Human cardiac troponin I is known to be phosphorylated at mult

219 Cardiac troponin I is phosphorylated at different sites

220 Cardiac troponin I is, however, the best test currently

221 199 (equivalent to Ser200 in mouse) of cTnI (cardiac troponin I) is significantly hyperphosphorylated

222 e molecular mechanism(s) of the mutant human cardiac troponin I (K206I), we tested the Ca(2+) depende

223 Myocardial injury (cardiac troponin I level > or =0.7 ng/mL or creatine kin

224 A positive troponin test was defined as a cardiac troponin I level of 1.0 microg per liter or high

225 Mean cardiac troponin I levels (+/-sd) were significantly low

226 ildren resulted in a significant decrease in cardiac troponin I levels at 24 hrs postoperatively.

227 First, blood cardiac troponin I levels at admission were analyzed to

228 Cardiac troponin I levels were normal in all patients, w

229 , postoperative complications, postoperative cardiac troponin I levels, and duration of stay were col

230 study were to assess the prognostic value of cardiac troponin I levels, measured with a new high-sens

231 In this study, elevated cardiac troponin I levels, which are considered to be a

232 dial IRI, as measured by histology and serum cardiac troponin I levels.

233 a modified HEART score </=3 (which includes cardiac troponin I <0.04 ng/mL at 0 and 3 hours) were ra

234 lic groups used to immobilise antibodies for cardiac troponin I marker.

235 syndrome (n=1218) underwent high-sensitivity cardiac troponin I measurement at presentation and 3 and

236 ital cardiac arrest patients, isolated early cardiac troponin I measurement is modestly predictive of

237 hosphorylation sites in the amino portion of cardiac troponin I-mediated the protein kinase C acceler

238 at, in solution, the regulatory subdomain of cardiac troponin is mobile relative to the remainder of

239 rds measured in transgenic mice expressing a cardiac troponin I mutation (R145G).

240 el we previously identified that HCM causing cardiac troponin I mutation Gly203Ser (cTnI-G203S) is as

241 s: Risk score and clinical outcomes based on cardiac troponin I, N-terminal pro-B-type natriuretic pe

242 Cardiac troponin I, N-terminal pro-B-type natriuretic pe

243 oprotein cholesterol ratio, high-sensitivity cardiac troponin I, NT-proBNP (N-terminal pro-B-type nat

244 ion of smoking and epinephrine initial dose, cardiac troponin I (odds ratio 3.58 [2.03-6.32], p < .00

245 Cardiac troponin (I or T) is the biomarker of choice for

246 l injury as indicated by a positive test for cardiac troponin I or troponin T.

247 ided evidence that protein kinase C-mediated cardiac troponin I phosphorylation accelerates relaxatio

248 unction was associated with normalization of cardiac troponin I phosphorylation and reduced apoptosis

249 the modulation of thin filament activity by cardiac troponin I phosphorylation as an integral and ad

250 at increased myocardial PKD activity induces cardiac troponin I phosphorylation at Ser22/Ser23 and re

251 ar PKD activity was accompanied by increased cardiac troponin I phosphorylation at Ser22/Ser23; this

252 shown to decrease pCa(50), presumably due to cardiac troponin I phosphorylation.

253 drenergic receptor signaling, apoptosis, and cardiac troponin I phosphorylation.

254 The role of cardiac troponin-I phosphorylation in the contractile fu

255 dult rat myocyte contractile performance and cardiac troponin-I phosphorylation.

256 tein kinase C activation largely depended on cardiac troponin-I phosphorylation.

257 gulatory mechanism, an 11-residue segment of cardiac troponin I previously termed the inhibitory pept

258 We additionally measured human cardiac troponin I protein in 9 human plasma samples, an

259 ural symptoms, ECG ST-segment deviation, and cardiac troponin I release after elective PCI and reduce

260 ocardial injury as measured by a decrease in cardiac troponin I release.

261 ther confirmed by a significant reduction of cardiac troponin-I release and less myocardial apoptosis

262 C and cTnC bound to a C-terminal fragment of cardiac troponin I (residues 147-163).

263 Cardiac troponin T (cTnT) and sensitive cardiac troponin I (s-cTnI) were also significantly high

264 rminal domain novel phosphorylation sites of cardiac troponin I (S165, T180, S198).

265 with mice expressing a pseudophosphorylated cardiac troponin I (S23D and S24D; TnI-PP).

266 sites located in the N-terminal extension of cardiac troponin I (S4, S5, Y25), an increase in phospho

267 Plasma cardiac troponin I samples were obtained at three time p

268 Periprocedural cardiac troponin I significantly increased (F=3.64; P=0.

269 After adjustment for cardiac troponin I, ST-segment deviation, age, sex, diab

270 r the interaction between the Ca(2+) ion and cardiac troponin I subunit.

271 t amplitude but decreased phosphorylation of cardiac troponin I, suggesting direct effects on the con

272 High-sensitivity cardiac troponin I testing is widely used to evaluate pa

273 f peptides afforded higher sensitivities for cardiac troponin I than those prepared by the chemisorpt

274 Cardiac troponin is the preferred biomarker for diagnosi

275 In the adult Tn environment (cTnT3 + cardiac troponin I), the single cTnT3-DeltaN100 and cTnT

276 system has been applied to the detection of cardiac Troponin I, the gold standard biomarker for the

277 The cardiac troponin-I Thr-144 phosphorylation site identifi

278 To evaluate the performance of a cardiac troponin I threshold of 5 ng/L at presentation a

279 The optimum cardiac troponin I threshold was determined at 4.66 ng.m

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

281 Phosphorylation of cardiac troponin I (TnI) by cAMP-dependent protein kinas

282 lation of the unique N-terminal extension of cardiac troponin I (TnI) by PKA modulates Ca(2+) release

283 Autoimmune response to cardiac troponin I (TnI) induces inflammation and fibros

284 The N-terminal extension of cardiac troponin I (TnI) is bisphosphorylated by protein

285 ynthetic peptide with nanomolar affinity for cardiac troponin I (TnI), previously identified from a p

286 e is a progressive increase in expression of cardiac troponin I (TnI), with a concurrent decrease in

287 KEY POINTS: Mutations in genes encoding cardiac troponin I (TNNI3) and cardiac troponin T (TNNT2

288 comeric contractile protein genes identified cardiac troponin I (TNNI3) as the likely disease gene.

289 Cardiac troponin I (TNNI3) gene mutations account for 3%

290 tions to investigate the sarcomeric gene for cardiac troponin I (TNNI3) in 235 patients with dilated

291 : the sarcomeric mutations in genes encoding cardiac troponin I (TNNI3p.98truncation ) and cardiac tr

292 The addition of 2 m urea to the intact cardiac troponin I-troponin C complex significantly incr

293 high sensitivity assay for the detection of cardiac troponin I using electrical double layer gated h

294 he cardiac troponins, cardiac troponin T and cardiac troponin I, using sensitive methods, defines a t

295 Cardiac troponin I was measured in 61,379 patients, and

296 count and myocardial blush grade), and serum cardiac troponin I were assessed before and after PCI.

297 ein and protein kinase C (PKC)-treated mouse cardiac troponin I were enhanced more than 10-fold using

298 evels of serum mediators of inflammation and cardiac troponin I were similar in the two groups.

299 f cardiac muscle can be reduced by replacing cardiac troponin I with its skeletal or neonatal counter

300 tent with physiological data, replacement of cardiac troponin I with slow skeletal troponin I led to