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

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

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

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

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

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

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

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

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

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

12 letal troponin I but not when it is bound to 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 Binding of cardiac troponin I-(1-80) decreases conformational excha

20 n C when bound to the NH2-terminal domain of cardiac troponin I-(1-80), and cardiac troponin I-(1-80)

21 with similar correlation times when bound to cardiac troponin I-(1-80).

22 diac troponin C and cardiac troponin C bound cardiac troponin I-(1-80)DD tumble independently.

23 nal domain of cardiac troponin I-(1-80), and cardiac troponin I-(1-80)DD, having serine residues 23 a

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

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

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

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

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

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

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

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

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

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

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

35 Cardiac troponin is an independent predictor of cardiova

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

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

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

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

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

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

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

43 -terminal sequence RRRSS for the function of cardiac troponin I and imply that in human cardiac muscl

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

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

46 and complete sequence of the locus encoding cardiac troponin I and slow skeletal troponin T and ther

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

48 difference does not appear to exist between cardiac troponin I and T in patients with acute coronary

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

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

51 ained with the binary complex formed between cardiac troponin I and the IAANS-labeled cTnC mutant wer

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

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

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

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

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

57 ly significant ranges for creatin kinase MB, cardiac troponin I, and myoglobin agreed well with respo

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

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

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

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

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

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

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

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

66 ss assay alone; CK-MB mass assay followed by cardiac troponin I assay if the CK-MB value is normal; C

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

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

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

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

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

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

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

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

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

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

77 monoclonal antibodies (mAbs) raised against cardiac troponin-I (CdTnI) isolated from canine and huma

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

79 Plasma cardiac troponin I concentration was measured with a hig

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

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

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

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

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

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

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

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

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

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

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

91 Cardiac troponin I (cTI) release occurs frequently after

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

126 luate the diagnostic and prognostic value of cardiac troponin I (cTnI) in emergency department (ED) p

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

145 Cardiac troponin I (cTnI) phosphorylation modulates myoc

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

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

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

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

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

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

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

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

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

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

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

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

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

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

160 d beds for the online determination of human cardiac troponin I (cTnI), a diagnostic marker for myoca

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

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

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

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 ssess the impact of direct current shocks on cardiac troponin I (cTnI), which has greater sensitivity

174 e sought to determine whether measurement of cardiac troponin I (cTnI), which is a serum marker with

175 Phosphorylation of the cardiac troponin I (cTnI)-specific NH2-terminus decrease

176 abeled cTnC when free or when complexed with cardiac troponin I (cTnI).

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

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

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

180 ic performance of serum myoglobin, CK-MB and cardiac troponin-I (cTnI) 60-min ratios was similar.

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

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

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

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

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

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

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

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

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

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

191 Cardiac troponin I has a limited role in predicting mort

192 ides based on the N-terminal region of human cardiac troponin I has been analysed by PAGE and 1H NMR

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

217 sphorylated cardiac specific NH2 terminus of cardiac troponin I interacts with the NH2-terminal domai

218 Cardiac troponin I is a phosphorylation target for endot

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

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

221 Cardiac troponin I is phosphorylated at different sites

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

223 199 (equivalent to Ser200 in mouse) of cTnI (cardiac troponin I) is significantly hyperphosphorylated

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

273 Cardiac troponin is the preferred biomarker for diagnosi

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

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

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

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

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

279 The complexes of importance are: (1) cardiac troponin I (TnI) and monoclonal mouse anti-TnI I

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

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

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

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

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

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

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

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

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

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

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

300 gene transfer was used to replace endogenous cardiac troponin I within the myofilaments of adult card