ライフサイエンスコーパス: TnI

1 TnI levels are strong predictors of risk, and change mod

2 TnI levels increased in 23.0%, were unchanged in 51.3%,

3 TnI levels were measured at baseline and after 1 year in

4 TnI levels were related to CHD death and MI after adjust

5 TnI, CRP, GDF-15, MPO, PlGF, and sFlt-1 levels increased

6 TnI-directed autoimmune myocarditis (TnI-AM), a CD4(+) T

7 TnI-I release facilitates the repositioning of tropomyos

8 TnI-PP mice demonstrated a reduced myofilament Ca(2+) se

9 While Tm*146-TnI was produced only in the absence of Ca(2+), the prod

10 A tryptic peptide from Tm*146-TnI with a molecular mass of 2601.2 Da that was not pres

11 determined to be crosslinked products Tm*146-TnI, Tm*146-troponin C, and Tm*146-TnT using fluorescenc

12 ve suggested that, in the absence of Ca(2+), TnI interacts with Tm and actin in reconstituted muscle

13 serine to alanine substitution at Ser23/24; TnI(PKA-)) were bred with mice expressing non-phosphoryl

14 the rate-limiting step in de-activation; 3), TnI induces opening; 4), there is an incompletely deacti

15 ed based on a BNP higher than 81 pg/mL and a TnI higher than 0.1 ng/mL and compared with Mayo 2004 wi

16 TnT, Arg91Gly beta-TM, Arg174Gln TnI, and a TnI truncation mutant (Arg156ter).

17 the rate of Tn dissociation is by favoring a TnI-TnC interaction over a TnI-actin-Tm interaction.

18 dges shift the regulatory equilibrium from a TnI-actin-Tm interaction to a TnC-TnI interaction that l

19 is by favoring a TnI-TnC interaction over a TnI-actin-Tm interaction.

20 st that the switch activates in two steps: a TnI-independent Ca(2+)-priming step followed by TnI-depe

21 nce of Ca(2+), support the hypothesis that a TnI-Tm interaction maintains Tm at the outer domain of a

22 mine, whereas expression of phosphor-ablated TnI alone had little effect on the acceleration of contr

23 atified by baseline cardiac troponin I [Accu-TnI >0.04 mug/l], p interaction = 0.87).

24 With thermally activated TnI kinks (kink energy B approximately k(B)T), TnI also

25 Net reclassification improvement by adding TnI to the baseline model for CHD death and MI was 4.8%

26 bound troponin C and release of the adjacent TnI-I from actin.

27 eptidase complex subunit 1) subunit, affects TnI-directed autoimmune pathology of the heart.

28 on was elevated in wild-type (wt) mice after TnI immunization.

29 n T (TnT), and troponin C] or with actin and TnI.

30 Age, sex, and BNP and TnI concentrations were similar between the 25 patients

31 ggest that the phosphorylation of MyBP-C and TnI contributes significantly to the rates of force deve

32 CaMK2 inhibition reduced both MyBP-C and TnI phosphorylation and decreased active force without c

33 es before and after inhibition of MyBP-C and TnI phosphorylation using the calcium/calmodulin kinase

34 promotes compensatory changes in MyBP-C and TnI phosphorylation, which when normalized do not restor

35 o beta(1)-adrenergic stimulation, MyBP-C and TnI were phosphorylated to a similar level in TG-RLC(P-)

36 on Ca(2+) binding, structural dynamics, and TnI interaction independently.

37 e (BNP), and creatine kinase-MB (CK-MB), and TnI and BNP by CART.

38 ce for significant interplay between MHC and TnI isoforms that is essential for tuning cardiac contra

39 d to study how the interplay between MHC and TnI modulate muscle length-mediated effect on crossbridg

40 ces the phosphorylation of phospholamban and TnI as well as contraction responses induced by 10 micro

41 ing PKA phosphorylation of phospholamban and TnI for myocyte contraction responses under beta(1)AR st

42 mal PKA phosphorylation of phospholamban and TnI, and myocyte contraction responses.

43 mal PKA phosphorylation of phospholamban and TnI.

44 ecutive patients who had BNP, NT-proBNP, and TnI drawn simultaneously to create the staging system an

45 terleukin-17 production in heart tissue, and TnI-directed humoral autoimmune responses, was also pres

46 not occur in mice expressing both Tm180 and TnI-PP.

47 tion of a coiled-coil heterodimer of TnT and TnI has been recently confirmed by the crystal structure

48 Several regions of TnT and TnI were unfolded even at low temperature, suggesting in

49 oBNP) and cardiac troponins T and I (TnT and TnI) for prognostication, but many centers do not offer

50 R regions alone of the fast skeletal TnT and TnI, as defined earlier, were insufficient to form a coi

51 the embryonic/fetal isoforms of Tm, TnT, and TnI by using gene transfer.

52 astolic relaxation compared to wild-type and TnI(PKA-) mice.

53 ntractile response compared to wild-type and TnI(PKA-) mice.

54 The TnIf and TnIs enhancers were activated by matching fast and slow

55 increase in Ca2+ sensitivity, and Arg156ter TnI generated significantly higher maximum force.

56 s: Arg63His TnT, Arg91Gly beta-TM, Arg174Gln TnI, and a TnI truncation mutant (Arg156ter).

57 We measured cTnI using a sensitive assay (TnI-Ultra, Siemens Healthcare Diagnostics, Deerfield, Il

58 the NH(2)-lobe and the NH(2)-lobe-associated TnI switch helix, implying that Ca(2+) greatly stabilize

59 The response curves obtained at TnI concentrations ranging from 0 to 10 mug/mL, using bo

60 Baseline TnI levels and change at 1 year are independent predicto

61 Baseline TnI tertiles were <0.006 ng/ml, 0.006 to <0.018 ng/ml, a

62 altered intermolecular interactions between TnI helix 4 and cTnC helix A, specifically revealing a n

63 How this signal is transmitted between TnI and troponin C (TnC), resulting in accelerated Ca(2+

64 expression of the embryonic isoforms of both TnI and MHC had functional effects that were not previou

65 main of TnC removes the inhibitory effect by TnI on the contraction.

66 -independent Ca(2+)-priming step followed by TnI-dependent opening.

67 LMP2 and LMP7 by immunization with a cardiac TnI peptide.

68 d irreversibly replaced by the adult cardiac TnI (cTnI) isoform.

69 soform is substituted into the adult cardiac TnI isoform at codon 164.

70 f-antigen responses directed against cardiac TnI (troponin I).

71 210), when reconstituted with either cardiac TnI.TnC or ssTnI.TnC, significantly decreased Ca(2+) sen

72 of a mouse line in which the entire cardiac TnI gene was deleted, we investigated the effect of enha

73 g transgenic expression of exogenous cardiac TnI to rescue the postnatal lethality of a mouse line in

74 stidine residue present in the fetal cardiac TnI isoform is substituted into the adult cardiac TnI is

75 ese results support a novel role for cardiac TnI PKA phosphorylation in the rate-dependent enhancemen

76 These results suggest that Thr144 in cardiac TnI modulates cardiac myofilament length-dependent activ

77 Native cardiac TnI was near completely replaced in one transgenic line

78 ighly conserved TnT-binding helix of cardiac TnI (cTnI) in wild turkey hearts in concurrence with an

79 conclude that bisphosphorylation of cardiac TnI elicits its effects by weakening the interaction bet

80 The inhibitory region of cardiac TnI spans from residue 138 to 149.

81 vidence that specific replacement of cardiac TnI with ssTnI has a protective effect on the LV systoli

82 mice were generated that overexpress cardiac TnI in which the serine residues normally targeted by PK

83 nstrated that ROCK-II phosphorylated cardiac TnI (cTnI) at S23, S24, and T144 and cardiac TnT (cTnT)

84 skeletal troponin I (ssTnI) replaced cardiac TnI (cTnI) indicates the significance of a His in ssTnI

85 ansients, and 3) an inability of the cardiac TnI to completely inhibit activation in the absence of C

86 s with the structure of the upstream cardiac TnI gene.

87 phy in transgenic (TG) mice in which cardiac TnI was replaced with ssTnI and in nontransgenic (NTG) l

88 When complexed with cardiac TnI.TnC or ssTnI.TnC, both TnT1 DCM mutations strongly d

89 T)-treated fibers reconstituted with cardiac TnI.troponin C (TnC) or ssTnI.TnC significantly increase

90 In this conformation, TnI(1-32) interacts with the N-lobe of cardiac troponin

91 ntly less with the thin filaments containing TnI(T144A) than that with the wild-type TnI.

92 Cyanogen bromide digestion of the covalent TnI-TnC complex formed from intact troponin demonstrates

93 Pravastatin decreased TnI levels by 0.003 ng/ml versus placebo (p = 0.002).

94 of embryonic vs. cardiac isoforms of either TnI or MHC on cardiac muscle function and contractile dy

95 Lower threshold of hs-TnI and EXL-TnI was more discriminatory for overall mortality (Log-r

96 The autoimmune signature during experimental TnI-AM, with high immunoproteasome expression, immunoglo

97 toimmunity were investigated in experimental TnI-AM and in 2 cases of ICI-related myocarditis.

98 the affinity of the immobilized peptides for TnI was somewhat reduced, overall, these results demonst

99 ng affinity of gold-immobilized peptides for TnI was studied and compared with that of phage-immobili

100 niques show that the binding is specific for TnI as compared to a streptavidin (SA) control.

101 , has been immobilized on a gold surface for TnI detection.

102 Protection from TnI-directed autoimmune heart pathology with improved ca

103 lectron microscopy reconstruction showed how TnI binding to both actin and tropomyosin at low Ca2+ co

104 hs-TnI and high-sensitivity troponin T provide complementar

105 hs-TnI and high-sensitivity troponin T were only modestly c

106 hs-TnI correlated moderately with hs-TnT (r = 0.44) and N-t

107 hs-TnI was also significantly associated with cardiac death

108 hs-TnI was observed to have a stronger association with inc

109 Adding hs-TnI levels to the CHA2DS2VASc score improved c-statistic

110 An early-discharge strategy using an hs-TnI assay and TIMI score </= 1 had similar safety as pre

111 In multivariable analysis, hs-TnI was significantly associated with stroke or systemic

112 ding of no ischemic electrocardiogram and hs-TnI </= 26.2 ng/l with the TIMI = 0 and TIMI </= 1 pathw

113 n I measured by a high-sensitivity assay (hs-TnI) is associated with incident cardiovascular disease

114 tructed to determine associations between hs-TnI and incident coronary heart disease (CHD; myocardial

115 The associations between hs-TnI concentrations and clinical outcomes were evaluated

116 In patients with stable CAD, hs-TnI concentrations are associated with cardiovascular ri

117 Combining hs-TnI and BNP improved to predict long-term outcome (p = 0

118 Combining hs-TnI with BNP helped better risk stratification.

119 In conclusion, hs-TnI levels correlated with the degree of LV dysfunction

120 Detectable hs-TnI levels were observed in 85% of the study population.

121 st quintile, hs-TnI <=1.3 ng/L), elevated hs-TnI (highest quintile, hs-TnI >=3.8 ng/L) was associated

122 Elevated hs-TnI is strongly associated with increased global CVD inc

123 rthermore, applying a lower threshold for hs-TnI performed better for outcome prediction than a recom

124 diagnostic pathway integrating 0- and 2-h hs-TnI results, Thrombolysis In Myocardial Infarction (TIMI

125 In total, 98.5% of patients had hs-TnI concentrations higher than the detection level (1.2

126 lidate a new high-sensitivity troponin I (hs-TnI) assay in a clinical protocol for assessing patients

127 High-sensitivity cardiac troponin I (hs-TnI) levels at baseline were assessed in 3,623 patients

128 High-sensitivity troponin-I (hs-TnI) measurement improves risk assessment for cardiovasc

129 In adjusted models, in comparison to low hs-TnI (lowest quintile, hs-TnI <=1.3 ng/L), elevated hs-Tn

130 embolism ranged from 0.76% in the lowest hs-TnI quartile to 2.26% in the highest quartile (>10.1 ng/

131 0.03 for both), while higher threshold of hs-TnI (p = 0.75) and RXL-TnI were not (p = 0.30).

132 Lower threshold of hs-TnI and EXL-TnI was more discriminatory for overall mort

133 The comparative association of hs-TnI and high-sensitivity troponin T with incident CVD ev

134 ith warfarin are consistent regardless of hs-TnI levels.

135 The addition of hs-TnI to the Pooled Cohort Equation model improved risk pr

136 sma levels of B-type natriuretic peptide, hs-TnI (high-sensitivity troponin I), CRP (C-reactive prote

137 ad positive hs-TnI while 27% had positive hs-TnI using recommended thresholds (16 ng/L for female and

138 g a threshold of 6 ng/L, 77% had positive hs-TnI while 27% had positive hs-TnI using recommended thre

139 ng/L), elevated hs-TnI (highest quintile, hs-TnI >=3.8 ng/L) was associated with greater incident CHD

140 omparison to low hs-TnI (lowest quintile, hs-TnI <=1.3 ng/L), elevated hs-TnI (highest quintile, hs-T

141 At randomization, hs-TnI was analyzed in 14 821 atrial fibrillation patients

142 l as blood sampling for high-sensitivity (hs-TnI) and conventional troponin I (EXL-LOCI and RXL) asse

143 The hs-TnI assay detected troponin (>/=1.3 ng/L) in 98.5% patie

144 The hs-TnI level is independently associated with a raised risk

145 o-B-type natriuretic peptide, and hs-TnT, hs-TnI levels in the fourth compared with the 3 lower quart

146 ted to assess prediction improvement when hs-TnI was added to traditional risk factors used in the Po

147 o calcium was significantly blunted by human TnI, suggesting that human cTnI phosphorylation by cMLCK

148 n binding protein-C (MyBP-C) and troponin I (TnI) acts coordinately to change the rates of force gene

149 rotein kinase A-phosphorylatable troponin I (TnI) and MyBP-C, we examined in vivo haemodynamic functi

150 Two key myofilaments proteins, troponin I (TnI) and myosin binding protein-C (MyBP-C), are phosphor

151 Troponin I (TnI) and myosin heavy chain (MHC) are two contractile re

152 es encoding slow TnT and cardiac troponin I (TnI) are closely linked.

153 Troponin T (TnT) and troponin I (TnI) are two evolutionarily and functionally linked subu

154 and myofilament proteins such as troponin I (TnI) by protein kinase A (PKA).

155 e natriuretic peptide (BNP), and troponin I (TnI) concentrations and electrocardiographic, echocardio

156 The myofilament protein troponin I (TnI) has a key isoform-dependent role in the development

157 Autoimmune response to cardiac troponin I (TnI) induces inflammation and fibrosis in the myocardium

158 ted muscle is the release of the troponin I (TnI) inhibitory region (TnI-I) from actin.

159 N-terminal extension of cardiac troponin I (TnI) is bisphosphorylated by protein kinase A in respons

160 Troponin I (TnI) is the molecular switch of the sarcomere.

161 fferent TnT isoform, a different troponin I (TnI) isoform, slow skeletal TnI (ssTnI), is the dominant

162 tnatal increase in expression of troponin I (TnI) isoforms, suggesting that high-level transcription

163 change in contemporary sensitive troponin I (TnI) levels predicts coronary heart disease (CHD) death

164 Using the Troponin I (TnI) locus as a case study, we show that more refined lo

165 giography after single or serial troponin I (TnI) measurement, depending on time of presentation to t

166 a previously unknown variant in troponin I (TnI) were identified.

167 Ca(2+)-dependent interaction of troponin I (TnI) with actin.tropomyosin (Tm) in muscle thin filament

168 llosteric sensor for Ca(2+), and troponin I (TnI), an allosteric reporter.

169 atory proteins troponin T (TnT), troponin I (TnI), and beta-tropomyosin (beta-TM) have been shown to

170 phorylation of phospholamban and troponin I (TnI), and contraction responses.

171 phorylation of troponin T (TnT), troponin I (TnI), and myosin-binding protein C (C-protein).

172 hree subunits, troponin C (TnC), troponin I (TnI), and troponin T (TnT).

173 scriminators in serum by LR were troponin I (TnI), B-type natriuretic peptide (BNP), and creatine kin

174 hich a helix of another subunit, troponin I (TnI), binds.

175 stuzumab therapy: ultrasensitive troponin I (TnI), high-sensitivity C-reactive protein (CRP), N-termi

176 h nanomolar affinity for cardiac troponin I (TnI), previously identified from a polyvalent phage disp

177 members of troponin T (TnT) and troponin I (TnI), two subunits of the Ca(2+)-regulatory troponin com

178 ncrease in expression of cardiac troponin I (TnI), with a concurrent decrease in slow skeletal TnI.

179 n-binding protein-C (MyBP-C) and troponin I (TnI).

180 Change in TnI was defined as moving up or down 1 tertile or >/=50%

181 city was associated with interval changes in TnI (HR: 1.38 per SD; 95% confidence interval: 1.05 to 1

182 H-sensitive 'histidine button' engineered in TnI produces a titratable molecular switch that 'senses'

183 Early increases in TnI and MPO levels offer additive information about the

184 In landmark analyses, increases in TnI levels were associated with increased numbers of CHD

185 d trans-species-specific residues located in TnI's helix 4 using structure/function and molecular dyn

186 ressing non-phosphorylatable PKA residues in TnI and MyBP-C (DBL(PKA-)).

187 ate the functional significance of increased TnI phosphorylation in endotoxemia, we studied the contr

188 hly protected properties for the interacting TnI helix 1 and TnC COOH-domain.

189 properties were observed for the interacting TnI switch helix and TnC NH(2)-domain, contrasting with

190 C, and Tm*146-TnT using fluorescence-labeled TnI, mass spectrometry, and Western blot analysis.

191 same monocysteine mutations into full-length TnI, we were able to probe the environment of the N-term

192 Thus, MHC-TnI interplay may provide a developmentally dependent me

193 In the isolated heart, histidine-modified TnI improves systolic and diastolic function and mitigat

194 ion level was reduced from 1.02 to 0.3 molPi/TnI (EC50 P/unP = 1.8 +/- 0.2, p < 0.001).

195 TnI-directed autoimmune myocarditis (TnI-AM), a CD4(+) T-cell-mediated disease, was induced i

196 gulatory regions: to the start of the nearby TnI helix 1 and to the COOH terminus of the TnT-TnI coil

197 the mechanism, we focused on several notable TnI isoform and trans-species-specific residues located

198 res a nearly twofold symmetrical assembly of TnI and TnT subunits penetrated asymmetrically by the du

199 between actin and Ca-TnC for the binding of TnI.

200 tituted with actin and troponin [composed of TnI, troponin T (TnT), and troponin C] or with actin and

201 ral interactions of the regulatory domain of TnI (the "inhibitory" subunit of troponin) with tropomyo

202 ow that a region in the C-terminal domain of TnI interacts with Tm in the absence of Ca(2+), support

203 s the C terminus of the regulatory domain of TnI to move away from the actin surface by 6.3A, lateral

204 ed heterodimers when mixed with HR domain of TnI.

205 Moreover, expression of TnI-PP in Tm180 hearts inhibited modifications in the ac

206 ng evidence that the N-terminal extension of TnI interacts with the N-terminal domain of TnC.

207 ural evidence that a C-terminal extension of TnI is anchored on actin at low Ca(2+) and competes with

208 We attribute this to an extension of TnI linking the troponin core domain to actin at low (bu

209 ave studied the interaction of a fragment of TnI consisting of residues 1-64 (I1-64) with troponin C

210 ions between several N-terminal fragments of TnI, residues 1-18 (I1-18), residues 1-29 (I1-29), and r

211 1 antibody reduced inflammation in hearts of TnI-immunized wt mice.

212 ion shows that the long framework helices of TnI and TnT, presumed to be a Ca(2+)-independent structu

213 xation effects, indicating the importance of TnI-Tm interactions in maintaining the blocked state.

214 Alternatively, before induction of TnI-AM or after establishment of autoimmune myocarditis,

215 ) mice that express the embryonic isoform of TnI, slow skeletal TnI (ssTnI), were treated with propyl

216 Cardiac myocytes express two isoforms of TnI during development.

217 Using the well-established model of TnI-induced experimental autoimmune myocarditis (EAM), w

218 7C(+/-)) is in the fetal/neonatal paralog of TnI, a gene thought to be expressed in the heart up to t

219 to be crucial factors in the pathogenesis of TnI-induced EAM, because inhibition of HMGB1 and ablatio

220 ness due to prevention of phosphorylation of TnI at PKA-sensitive sites.

221 sphorylation, and reduced phosphorylation of TnI compared with Tm180 mice.

222 opose that cMLCK-mediated phosphorylation of TnI is functionally significant and represents a critica

223 preventing the induction and progression of TnI-AM when self-reactive CD4(+) T cells were primed.

224 nclude that a localized N-terminal region of TnI comprised of amino acids 33-80, which interacts with

225 kening the interaction between the region of TnI immediately C-terminal to the phosphorylation sites

226 ral part of Tm with the C-terminal region of TnI.

227 ous information on the N-terminal regions of TnI that interact with TnC: I1-18 does not bind to TnC w

228 Our results indicate that the response of TnI promoter sequences to electrical stimulation is cons

229 To resolve the mechanistic role of TnI in activation we performed stopped-flow FRET measure

230 To more directly delineate the role of TnI PKA phosphorylation, transgenic mice were generated

231 To examine the roles of TnI and MyBP-C phosphorylation in beta-adrenergic-mediat

232 The inhibitory segment of TnI changes conformation from an extended loop in the pr

233 f the sensor binds the inhibitory segment of TnI in the Ca(2+)-activated state.

234 pse and to release the inhibitory segment of TnI.

235 roponin core domain, the C-terminal third of TnI, and tropomyosin under the influence of a 64-residue

236 rter constructs harbouring 2.7 and 2.1 kb of TnIs and TnIf regulatory sequences, respectively.

237 d to determine the effects of pravastatin on TnI levels.

238 present in the tryptic peptides of Tm*146 or TnI was identified using HPLC and matrix-assisted laser

239 d addition of a lacking component (Ca(2+) or TnI) and deactivation after rapid chelation of Ca(2+).

240 and approximately 34% ssTnI of total MHC or TnI, respectively, allowing us to test the functional ef

241 ic (TG) mice expressing non-phosphorylatable TnI protein kinase A (PKA) residues (i.e. serine to alan

242 increased in association with diminished PKA TnI phosphorylation.

243 oil's NH(2)-terminal base plus the preceding TnI loop with which the base interacts.

244 etween TnT and other thin filament proteins, TnI, TnC and Tm.

245 RTFs reconstituted with the mutant R37C TnI exhibited reduced Ca(2+)-binding sensitivity due to

246 e of the troponin I (TnI) inhibitory region (TnI-I) from actin.

247 ineered TnC mutants with weakened regulatory TnI interactions, the apparent exchange rate at pCa 4 in

248 igher threshold of hs-TnI (p = 0.75) and RXL-TnI were not (p = 0.30).

249 horylated cardiac troponin I (S23D and S24D; TnI-PP).

250 Replacing wild-type TnI with S45E TnI, that favors the inactive state, did not restore the

251 uscle troponin composed of TnC (the sensor), TnI (the regulator), and TnT (the link to the muscle thi

252 , including patients discharged after single TnI measurement.

253 tion with the HR domain of the fast skeletal TnI.

254 The fetal heart expresses the slow skeletal TnI (ssTnI) isoform and shortly after birth ssTnI is com

255 rent troponin I (TnI) isoform, slow skeletal TnI (ssTnI), is the dominant isoform in the embryonic he

256 the embryonic isoform of TnI, slow skeletal TnI (ssTnI), were treated with propylthiouracil (PTU) to

257 cardiac-specific expression of slow skeletal TnI (ssTnI, which lacks the N-terminal protein extension

258 pecific replacement of cTnI by slow skeletal TnI (ssTnI, which lacks the PKA phosphorylation sites) a

259 S23/24A), or gene transfer of slow skeletal TnI, both of which lack PKA phosphorylation sites, signi

260 l in which cTnI is replaced by slow skeletal TnI, which lacks S23 and S24 and in which T144 is replac

261 with a concurrent decrease in slow skeletal TnI.

262 e prominent with a hybrid troponin (skeletal TnI, TnC, and cardiac TnT) than with all cardiac troponi

263 transcriptional control of troponin I slow (TnIs) and fast (TnIf) regulatory sequences by directly s

264 destabilized rather than stabilized specific TnI segments within the coiled-coil and destabilized a r

265 I kinks (kink energy B approximately k(B)T), TnI also binds cooperatively to actin, producing coopera

266 engineered construct representing C-terminal TnI, and then, 3D electron microscopy was used to resolv

267 utually rescuing mutations demonstrated that TnI-TnT interaction is a critical link in the Ca(2+) sig

268 ure the affinity of the TnT peptides for the TnI HR domain.

269 However, the TnI isoforms had greater effects on the Ca(2+) dissociat

270 n) locally, near the binding site and in the TnI switch helix that attaches to the Ca(2+)-saturated T

271 HDX of the TnI COOH terminus indicated that its known role in regul

272 Most of the TnI COOH terminus was protected from H/D exchange, imply

273 tructure, suggests specific movements of the TnI inhibitory regions, and prominently involves troponi

274 ng the presentation to and withdrawal of the TnI inhibitory segment from the thin filament.

275 two switching steps in cTnI: binding of the TnI regulatory region to hydrophobic sites in the N-doma

276 he inhibitory peptide residues preceding the TnI switch helix.

277 In the Ca(2+)-saturated state, the TnI C-terminus dissociates from actin and binds in part

278 c properties of other parts of troponin: the TnI inhibitory peptide region that binds to actin, the T

279 rs and binds specifically, together with the TnI switch helix, in a hydrophobic pocket of TnC upon ac

280 fined essential sequence elements within the TnI regulatory region.

281 y to Ca(2)(+) affinity or indirectly through TnI association.

282 To obtain direct evidence for this Tm-TnI interaction, we performed photochemical crosslinking

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

284 ium from a TnI-actin-Tm interaction to a TnC-TnI interaction that likely enhances calcium binding by

285 s of a new quantitative dynamic model of TnC-TnI allostery.

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

287 In contrast, portions of the TnT-TnI coiled-coil exhibited high protection from exchange,

288 peptide region that binds to actin, the TnT-TnI coiled-coil, and the TnC COOH domain that contains t

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

290 enone-labeled peptide from Tm crosslinked to TnI peptide 157-163.

291 g that muscle shortening may be important to TnI PKA effects.

292 with which the hydrophobic patch presents to TnI.

293 ibrils substituted with C-terminal truncated TnI showed similar compromised relaxation effects, indic

294 Replacing wild-type TnI with S45E TnI, that favors the inactive state, did n

295 ning TnI(T144A) than that with the wild-type TnI.

296 ion of K206I was greater than with wild-type TnI.

297 served changes in cross-bridge kinetics upon TnI phosphorylation.

298 RAGE knockout (RAGE-ko) mice immunized with TnI showed no structural or physiological signs of cardi

299 coil formed by the various TnT peptides with TnI HR domain.

300 verlap region increased proportionately with TnI-TnC regulatory affinity.