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-I release facilitates the repositioning of tropomyos

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

8 nI) regulatory region peptides: TnI(96-115), TnI(96-131) and TnI(96-139).

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

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

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

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

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

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

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

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

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

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

25 pans the seven-site spacing between adjacent TnI molecules.

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

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

28 2)s(-1), 1.2x10(-2)s(-1) for TnI(96-131) and TnI(96-139) peptides, respectively.

29 egion peptides: TnI(96-115), TnI(96-131) and TnI(96-139).

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

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

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

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

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

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

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

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

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

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

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

41 sin chain in a blocking position; myosin and TnI compete for actin and induce oppositely-directed cha

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

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

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

45 mal PKA phosphorylation of phospholamban and TnI.

46 equilibrium binding curves for myosin-S1 and TnI as a function of their first-order affinities K(S1)

47 Multiple isoforms of TnT, Tm, and TnI are differentially expressed in both cardiac develop

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

49 view of the interactions between the TnC and TnI proteins of the troponin complex.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

67 is detached by the actin binding of TnI, but TnI is more efficiently detached by myosin when the kink

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

69 tension development was markedly enhanced by TnI replacement but not by TnT or Tm isoform replacement

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

92 diac development and disease, but concurrent TnI, Tm, and TnT isoform switching has hindered assignme

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

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

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

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

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

98 k(off)=2.0x10(-2)s(-1), 1.2x10(-2)s(-1) for TnI(96-131) and TnI(96-139) peptides, respectively.

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

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

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

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

103 levels or functional differences between HCM TnI and ssTnI could help explain these divergent organ-l

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

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

106 hs-TnI was also significantly associated with cardiac death

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

131 N-terminal extension of cardiac troponin I (TnI) by PKA modulates Ca(2+) release from the troponin c

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

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

134 osin (Tm), troponin T (TnT), and troponin I (TnI) form an allosteric regulatory complex that is requi

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

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

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

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

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

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

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

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

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

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

145 onin C (TnC) and rabbit skeletal troponin I (TnI) regulatory region peptides: TnI(96-115), TnI(96-131

146 terminal domain of an isoform of troponin I (TnI) specific to the troponin-tropomyosin (Tc-Tm) comple

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

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

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

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

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

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

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

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

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

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

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

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

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

160 A) targets contractile proteins, troponin-I (TnI) and myosin binding protein C (MyBP-C) in the heart

161 ablished that the interaction of troponin-I (TnI), the inhibitory subunit of Tn, with actin is requir

162 gulation of contraction, and this identifies TnI as a potential target to modify contractile performa

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

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

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

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

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

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

169 re are two separate actin-binding regions in TnI that interact with actin, the molecular mechanism of

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

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

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

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

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

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

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

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

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

179 In binary complexes the mutant TnIs cross-link to both the isolated TnC N-domain and wh

180 rate experiments, greater than 90% of native TnI and 40-50% of native Tm or TnT were specifically rep

181 ion in NTG hearts; (2) replacement of native TnI with ssTnI increases Ca2+ sensitivity of tension but

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

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

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

185 Myosin is detached by the actin binding of TnI, but TnI is more efficiently detached by myosin when

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

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

188 anism is used for coupling the detachment of TnI to calcium binding by TnC.

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

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

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

192 ed heterodimers when mixed with HR domain of TnI.

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

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

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

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

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

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

199 hin filaments and the inhibitory function of TnI appear to be insensitive to changes in charge (+/-2)

200 1 antibody reduced inflammation in hearts of TnI-immunized wt mice.

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

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

203 ely replaced by the slow skeletal isoform of TnI (ssTnI-TG) lacking the phosphorylation sites for PKA

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

205 Cardiac myocytes express two isoforms of TnI during development.

206 g modifiers of mutant Drosophila isoforms of TnI.

207 Baseline measurements of TnI, CRP, and BNP were performed in 450 patients in OPUS

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

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

210 the role of PKA-dependent phosphorylation of TnI and MyBP-C on LDA in the heart, we examined LDA in s

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

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

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

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

215 issense mutation in the inhibitory region of TnI replaces an arginine residue at position 145 with a

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

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

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

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

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

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

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

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

224 pse and to release the inhibitory segment of TnI.

225 ch to constrain separate helical segments of TnI.

226 to bind with an affinity similar to that of TnI(96-131) by fluorescence analysis (K(d)=380nM), its b

227 Titration of TnI replacement from >90% to <30% revealed a dominant fu

228 Gene transfer of TnI isoforms or mutants into adult cardiac myocytes is u

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

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

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

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

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

234 gly, although the inhibitory region peptide (TnI(96-115)) was observed to bind with an affinity simil

235 troponin I (TnI) regulatory region peptides: TnI(96-115), TnI(96-131) and TnI(96-139).

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

237 increased in association with diminished PKA TnI phosphorylation.

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

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

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

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

242 Over this range of isoform replacement, TnI, but not Tm or TnT embryonic isoforms, influenced ca

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

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

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

246 , including patients discharged after single TnI measurement.

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

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

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

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

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

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

253 dominant functional effect of slow skeletal TnI to modulate regulation.

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

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

256 with a concurrent decrease in slow skeletal TnI.

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

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

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

260 Troponin itself consists of three subunits, TnI, TnC, and TnT, widely characterized as being respons

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

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

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

264 The TnI peptide conjugates were then captured via dimerizati

265 ture of the interactions between TnC and the TnI-TnT component differs significantly between the card

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

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

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

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

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

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

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

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

274 T is reduced by prior phosphorylation of the TnI.

275 he inhibitory peptide residues preceding the TnI switch helix.

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

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

278 fined essential sequence elements within the TnI regulatory region.

279 ant in hydrophobic interactions between this TnI region and TnC's N-domain cleft.

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

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

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

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

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

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

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

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

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

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

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

291 with which the hydrophobic patch presents to TnI.

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

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

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

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

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

297 Using TnI mutants with photocrosslinking probes attached to ge

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.