ライフサイエンスコーパス: protein C

1 heavy chain) and MYBPC3 (beta-myosin-binding protein C).

2 lfate-accelerated antithrombin and activated protein C.

3 ivity of rTMD23 was independent of activated protein C.

4 increased phosphorylation of myosin-binding protein C.

5 be prevented by recombinant human activated protein C.

6 ed as an anticoagulant factor that activates protein C.

7 clinical trial was human recumbent activated protein C.

8 vational and randomized studies of activated protein C.

9 ere or from the truncation of myosin binding protein C.

10 nts treated with recombinant human activated protein C.

11 idosis, have decreased circulating levels of protein C.

12 ymatic activity of factor VIIa and activated protein C.

13 ells expressing low levels of myosin-binding protein C.

14 mmonest being MYBPC3 encoding myosin-binding protein C.

15 d blockade activity for its ligand activated protein C.

16 f its targets, troponin I and myosin-binding protein C.

17 dent pathways defined by the chromosome axis proteins C(2)M and ORD.

18 Cardiac myosin-binding protein C, a cardiac-specific myofilament protein, is pr

19 Protein C, a secretory vitamin K-dependent anticoagulant

20 proliferation by inhibiting a retinoblastoma protein/c-Abl interaction leading to greater c-Abl activ

21 t: phosphorylation of cardiac myosin binding protein-C accelerates cross bridge binding to actin, the

22 This would promote systemic protein C activation and early cessation of thrombin gen

23 the fibrinogen gamma' peptide also inhibited protein C activation by the thrombin/thrombomodulin comp

24 protein C anticoagulant pathway by promoting protein C activation.

25 This molecule was also impaired in protein C activation.

26 diminished fibrinogen cleavage and increased protein C activation.

27 Hence, availability of a protein C activator would afford a therapeutic for patie

28 an innovative step toward the development of protein C activators of clinical and diagnostic relevanc

29 ulation of circulating levels of fibrinogen, protein C activity, and antifibrinolytic proteins and de

30 nvertases, because both R198A and R221A lack protein C activity.

31 Early treatment with an activated protein C analog restored BSCB integrity that developed

32 phase of coagulation via rapid activation of protein C and consequent inactivation of factors Va and

33 of more mature neurons, e.g., human neuronal protein C and D (HuC/D).

34 ting pharmacological quantities of activated protein C and effectively diagnoses protein C deficiency

35 e TEG profile and platelet count, endotoxin, Protein C and fibrinogen were independent predictors of

36 assessing the association between activated protein C and mortality resulted in a 9% shift in the ac

37 g coagulation factors II, VII, IX, and X and proteins C and S) or plasma.

38 oke cases and controls, including quantified proteins C and S, antithrombin, factors VIII/IX/XI, fibr

39 inetochore microtubule binders by centromere proteins C and T (CENP-C and CENP-T).

40 e VDAC, bacterial porin OmpC (outer membrane protein C), and bacterial channel-forming toxin alpha-he

41 Anti-histone IgG, recombinant activated protein C, and heparin were equally effective in abrogat

42 he natural anticoagulants (ie, antithrombin, protein C, and protein S), were assessed, and data on ri

43 heads, the cardiac isoform of myosin-binding protein-C, and titin will aid in understanding of the st

44 can be elicited by a S. Typhi outer-membrane protein C- and F-based subunit vaccine (porins).

45 between serum anti-OmpC IgA (Outer membrane protein C), anti-GP2 (anti-glycoprotein 2) IgG and anti-

46 EPCR plays a crucial role in the protein C anticoagulant pathway by promoting protein C a

47 These results demonstrate that the protein C anticoagulant system can be successfully targe

48 Cytoprotection by activated protein C (aPC) after ischemia-reperfusion injury (IRI)

49 ase-activated receptor 1 (PAR1) by activated protein C (APC) and thrombin elicits paradoxical cytopro

50 Activated protein C (APC) breaks down the complex that produces th

51 by purified CK1 did not affect its activated protein C (APC) cofactor activity in activated partial t

52 of the structure of Gla domain of activated Protein C (APC) complexed with soluble endothelial Prote

53 The coagulation protease activated protein C (aPC) confers cytoprotective effects in variou

54 Activated protein C (APC) is a blood protease with anticoagulant a

55 Activated protein C (APC) is a multifunctional serine protease wit

56 Activated protein C (APC) is a protease with anticoagulant and cel

57 Activated protein C (APC) is an anticoagulant protease that initia

58 lial barrier protective effects of activated protein C (APC) require the endothelial protein C recept

59 920-->Arg, FVNara) associated with activated protein C (APC) resistance and a severe thrombotic pheno

60 Activated protein C (APC) resistance, often associated with the fa

61 gnaling, whereas its activation by activated protein C (APC) stimulates cytoprotective and antiinflam

62 e a microenvironment enriched with activated protein C (aPC) that retains EPCR(+) LT-HSCs by limiting

63 compared the protective effect of activated protein C (APC) to that of the Food and Drug Administrat

64 K3A-APC is a recombinant analog of activated protein C (APC) which is an endogenous protease with mul

65 The homeostatic blood protease, activated protein C (APC), can function as (1) an antithrombotic o

66 of the natural protein C pathway, activated protein C (aPC), exerts pleiotropic effects on coagulati

67 ed to play a key role in mediating activated protein C (APC)-induced cytoprotective effects, includin

68 echanisms, including production of activated protein C (APC).

69 PR(221) downward arrow results in activated protein C (APC; residues 222-461).

70 otein C receptor (EPCR) by the Gla-domain of protein C/APC is responsible for the beta-arrestin-2 bia

71 Finally, administration of PF4/44mer-DNA protein C aptamer complexes in mice induced anti-PF4/apt

72 anti-nucleolar and pro-apoptotic effects of protein C are flavivirus-species specific.

73 commonly known as an important cofactor for protein C as well as a direct inhibitor of multiple coag

74 s was sufficient to interfere with activated protein C-barrier protective activities in human brain e

75 We conclude that factor VII and protein C bind preferentially to monoester phosphates, w

76 We hypothesize that factor VII and protein C bind preferentially to the monoester phosphate

77 bitors that block recognition of VEEV capsid protein (C) by the host importin (IMP) alpha/beta1 nucle

78 her proteins such as synemin, myosin binding protein C (C-protein), glycogen debranching enzyme and r

79 two vital Plasmodium berghei G-actin-binding proteins, C-CAP and profilin, in combination with three

80 known interactor Casitas B-lineage lymphoma protein (c-CBL), conducted a peptide array screen based

81 Okp1 directly associates with the centromere protein C (CENP-C) homologue Mif2 to form a cooperative

82 fl), directly interacts with the centromeric protein C (CENP-C).

83 tants for the centromere proteins centromere protein-C (CENP-C) and chromosome alignment 1 (CAL1) to

84 ac troponin I (cTnI), cardiac myosin-binding protein C (cMyBP-C) and titin.

85 rdiac sarcomere, both cardiac myosin binding protein C (cMyBP-C) and troponin-I (cTnI) are prominent

86 Cardiac myosin binding protein C (cMyBP-C) has a key regulatory role in cardiac

87 Cardiac myosin-binding protein C (cMyBP-C) is a component of the thick filament

88 Cardiac myosin-binding protein C (cMyBP-C) is a thick-filament-associated prote

89 Cardiac myosin-binding protein C (cMyBP-C) regulates actin-myosin interaction a

90 ts accessory protein, cardiac myosin binding protein C (cMyBP-C), are the two most common causes of h

91 cture and dynamics of cardiac myosin-binding protein C (cMyBP-C), focusing on the N-terminal region.

92 The cardiac isoform [cardiac myosin binding protein C (cMyBP-C)] is essential for normal cardiac fun

93 Phosphorylation of cardiac myosin-binding protein-C (cMyBP-C) by protein kinase A accelerates the

94 Although mutations in cardiac myosin binding protein-C (cMyBP-C) cause heart disease, its role in mus

95 Cardiac myosin binding protein-C (cMyBP-C) is a member of the immunoglobulin (I

96 Cardiac myosin-binding protein-C (cMyBP-C) is a thick filament protein that mod

97 Cardiac myosin-binding protein-C (cMyBP-C) is a thick filament-associated prote

98 ighly correlated with cardiac myosin-binding protein-C (cMyBP-C) protein level.

99 regulatory subunit of cardiac myosin-binding protein-C (cMyBP-C) that modulates actin and myosin inte

100 MYBPC3, which encodes cardiac myosin binding protein-C (cMyBP-C).

101 Cardiac myosin-binding protein C (cMyC) is a cardiac-restricted protein that is

102 Plasma activated protein C concentrations in activated protein C overexpr

103 n-12, acetylated tubulin, and human neuronal protein C/D, as well as choline acetyltransferase, tyros

104 s against acetylated tubulin, human neuronal protein C/D, choline acetyltransferase, tyrosine hydroxy

105 ethods for collecting and analysing membrane protein CD data, highlighting where protocols for solubl

106 ctivated protein C and effectively diagnoses protein C deficiency in human plasma.

107 -1) deficiency in 2, and 1 patient each with protein C deficiency, anticardiolipin antibodies, factor

108 for antithrombin deficiency; 1.1% (0.7%) for protein C deficiency; and 1.0% (0.7%) for protein S defi

109 Homozygous cardiac myosin binding protein C-deficient (Mybpc(t/t)) mice develop dramatic c

110 rogen receptor and by CCAAT/enhancer-binding protein (C/EBP) beta (CEBPB).

111 und to associate with CCAAT-enhancer-binding protein (C/EBP) beta and cooperate with VDR and C/EBPbet

112 CCAAT/Enhancer Binding Protein (C/EBP) beta function is frequently deregulated

113 transcription factor, CCAAT/enhancer-binding protein (C/EBP) delta as a critical downstream target of

114 ilon, a member of the CCAAT/enhancer binding protein (C/EBP) family of transcription factors, is excl

115 (BZip) domain of the CCAAT/enhancer-binding protein (C/EBP) fused to fluorescent proteins.

116 hat the UPR-regulated CCAAT/enhancer-binding protein (C/EBP) homologous protein (CHOP) participates i

117 g to the induction of CCAAT/enhancer binding protein (C/EBP) transcription factors.

118 ionally controlled by CCAAT/enhancer-binding protein (C/EBP)-beta and -delta.

119 p40 promoter requires CCAAT enhancer-binding protein (C/EBP)-beta and nuclear factor kappaB (NFkappaB

120 transcription factor CCAAT/enhancer binding protein (C/EBP)beta, known to be involved in macrophage

121 CCAAT/enhancer-binding protein (C/EBPalpha) can appoint mouse bone marrow (MBM)

122 at TRIB2 relieves the liver tumor suppressor protein C/EBPalpha-mediated inhibition of YAP/TEAD trans

123 actor, PU.1, and with CCAAT enhancer binding proteins, C/EBPalpha and C/EBPepsilon.

124 rotein 1 (AP1), SMAD, CCAAT/enhancer-binding protein (C/EBPbeta), and cAMP-response element-binding p

125 CCAAT/enhancer binding proteins (C/EBPs) are expressed in various tissues, incl

126 action between GR and CCAAT-enhancer-binding proteins (C/EBPs), since the GR can regulate gene expres

127 lity resulted in a 9% shift in the activated protein C effect estimate toward the null (odds ratio fr

128 Inhibition of SCD reduced surfactant protein C expression and suppressed rhinovirus-induced I

129 variant in a candidate gene (myosin binding protein C, fast type [MYBPC2] and vacuolar protein sorti

130 r cellular caspase 8 (FLICE)-like inhibitory protein (c-FLIP) is required for TNFalpha-induced protec

131 t cellular caspase 8 (FLICE)-like inhibitory protein (c-FLIP) promotes cell survival in death recepto

132 sociated with cellular FLICE-like inhibitory protein (c-FLIP) turnover and that gamma-secretase inhib

133 with a decrease in cellular FLICE-inhibitory protein (c-FLIP).

134 The cytosolic protein c-FLIP (cellular Fas-associated death domain-lik

135 creased expression of the activity-dependent protein c-Fos in the NAcc, specifically the shell subreg

136 ter binding by the AP-1 transcription factor proteins c-Fos and c-Jun have been demonstrated in all t

137 of chaperones Bip and Hsp70 as well as AP-1 proteins c-Fos and JunB, in addition to molecular signat

138 MYBPC3 (Myosin-binding protein C) founder mutations account for 35% of hypertro

139 Once in the circulation, activated protein C functions as an anticoagulant, anti-inflammato

140 o 5 to 10 nM), and the addition of exogenous protein C further decreased thrombin generation.

141 en the myosin heavy chain and myosin-binding protein C genotype-positive patients.

142 etween myosin heavy chain and myosin-binding protein C genotype-positive patients.

143 n MLY2, myosin heavy chain 6, myosin-binding protein C), glucose metabolism proteins (pyruvate dehydr

144 Activated protein C has anticoagulant and anti-inflammatory proper

145 perform quantification of trypsin-resistant proteins (C-hordeins) through analysis of their semi- or

146 as mediated by upregulation of antiapoptotic protein (c-IAP-2) through calmodulin-dependent kinase-II

147 homeostasis of critical RNA- and DNA-binding proteins, (c) impaired cytoskeleton function, and (d) no

148 stitutively enhanced expression of activated protein C impairs host defense during severe Gram-negati

149 rotease thrombin activates the anticoagulant protein C in a reaction that requires the cofactor throm

150 e conclude that prior convertase cleavage of protein C in hepatocytes is critical for its thrombin ac

151 ation and function of cardiac myosin-binding protein C in human heart failure.

152 diagnostic tool for monitoring the level of protein C in plasma.

153 ors of APC are members of the serpin family: protein C inhibitor (PCI) and alpha1-antitrypsin (alpha1

154 Protein C inhibitor (PCI) is a serpin with broad proteas

155 Myosin binding protein C is a thick filament protein of vertebrate stri

156 at phosphorylation of cardiac myosin binding protein-C is a key regulator of the kinetics and amplitu

157 Circumsporozoite protein (CS) is the antigenic target for RTS,S, the most

158 C3, encoding cMyBP-C (cardiac myosin-binding protein C), is the most frequently mutated HCM gene.

159 ve mutant of the basic region leucine zipper protein c-Jun, a major constituent of the AP-1 transcrip

160 species, muscle insulin signalling, IBalpha protein, c-Jun phosphorylation, inflammatory gene (toll-

161 (ATF3), which, in association with accessory proteins (c-Jun dimerization protein 2 [JDP2], ATF2, and

162 The three JUN proteins (c-JUN, JUNB, and JUND) can have both redundant

163 We have investigated the role of Jun family proteins (c-Jun, JunB, and JunD) in TGF-beta effects on

164 entified a biallelic splice-site mutation in protein C kinase delta (PRKCD), causing the absence of t

165 Measles virus (MV) lacking expression of C protein (C(KO)) is a potent activator of the double-stra

166 rch solutions to recombinant human activated protein C, large multicenter randomized controlled trial

167 e THBD, results in high plasma TM levels and protein C-mediated suppression of thrombin generation.

168 The refined NRG-GBM-RPA consisting of MGMT protein, c-Met protein, and age revealed greater separat

169 is G+LVH- population, cardiac myosin-binding protein C mutation carriers had twice the prevalence of

170 stimulation increases cardiac myosin binding protein C (MyBP-C) and troponin I phosphorylation to acc

171 order of the myosin heads and myosin binding protein C (MyBP-C) decreased in the sarcomere length ran

172 Myosin-binding protein C (MyBP-C) is an accessory protein of striated m

173 Myosin binding protein C (MyBP-C) is expressed in striated muscles, whe

174 e the level of troponin I and myosin binding protein C (MyBP-C) phosphorylation in their hearts befor

175 Myosin binding protein-C (MyBP-C) is a key regulatory protein in heart

176 roteins, troponin I (TnI) and myosin binding protein-C (MyBP-C), are phosphorylated following beta-ad

177 tified as the 140-kDa cardiac myosin binding protein C (MyBPC).

178 thogenic 18 bp duplication in myosin binding protein C (MYBPC3) because of low coverage.

179 y genes, lamin A/C (LMNA) and myosin binding protein C (MYBPC3).

180 The protein c-MYC, a transcription factor that has been show

181 e and a disordered peptide from the oncogene protein c-Myc, we describe a "specific-diffuse" binding

182 sing a functional enhanced green fluorescent protein-c-Myc fusion protein under control of the endoge

183 onents myosin heavy chain and myosin binding protein C (MYH7 and MYBPC3) together explain 75% of inhe

184 e spectrum of ineffective therapy (activated protein C), novel therapeutic ideas (statins and extraco

185 f the response regulator nitrogen regulatory protein C (NtrC(R)), the interconversion of this tyrosin

186 ve and inactive state of nitrogen regulatory protein C (NtrC).

187 everal dynein genes and nuclear distribution protein C (nudC), which is an essential component of a s

188 fied and isolated as a cellular receptor for protein C on endothelial cells.

189 in and the cardiac isoform of myosin-binding protein-C on the surface of the myosin filament backbone

190 ment proteins such as cardiac myosin binding protein-C or titin, cause familial hypertrophic cardiomy

191 ng agents such as antihistone IgG, activated protein C, or heparin prevented this effect.

192 Outer surface protein C (OspC) is one of the major lipoproteins expres

193 Wild type and activated protein C overexpressing C57BL/6 mice.

194 ivated protein C concentrations in activated protein C overexpressing mice (median 18.1 ng/mL) were i

195 Activated protein C overexpressing mice demonstrated enhanced susc

196 ulation, were measured in lungs of activated protein C overexpressing mice.

197 orms at a higher molar ratio of carbohydrate/protein ([C]/[P] >5).

198 ending on the molar ratio of carbohydrate to protein ([C]/[P]).

199 vel biological function and mechanism of the protein C pathway in which protein S and the aPC-cleaved

200 n cascade activation, and dysfunction of the protein C pathway may be of specific importance in this

201 s of endothelial integrity (CD31) and of the protein C pathway receptors (endothelial protein C recep

202 The key effector molecule of the natural protein C pathway, activated protein C (aPC), exerts ple

203 cating uncontrolled thrombin generation) and protein C (PC) depletion; this profile resembles the gre

204 Activated protein C (PC) is an anticoagulant involved in the inter

205 production, was increased, and conversion of protein C (PC) to activated PC by CD141-bound thrombin w

206 , there is preferential binding of activated protein C (PC) to Gr1(high)CD11b(high)VLA-3(high) cells

207 The interaction of protein C (PC) with the endothelial PC receptor (EPCR) e

208 brane proteins that partner in activation of protein C (PC).

209 did not affect troponin-I or myosin-binding protein-C phosphorylation in vivo.

210 Cardiac myosin binding protein-C phosphorylation plays an important role in mod

211 e-tracing experiments showed that surfactant protein C-positive (SFTPC-positive) AEC2s self renew and

212 etion of TLR4 or HA synthase 2 in surfactant-protein-C-positive AEC2s leads to impaired renewal capac

213 he natural anticoagulant protease, activated protein C, potently inhibits polyP-mediated proinflammat

214 he anticoagulants antithrombin (Serpinc1) or protein C (Proc) display premature death due to thrombos

215 (hDPP4) under the control of the surfactant protein C promoter or cytokeratin 18 promoter that are s

216 integrin from E10.5 onwards using surfactant protein C promoter-driven Cre.

217 constructed by insertion of a 12-amino-acid protein C (protC) epitope tag within the UL37 amino acid

218 l vein platelet aggregates and reductions in protein C, protein S, antithrombin and A Disintegrin and

219 nce factor B (PavB) and pneumococcal surface protein C (PspC) are key players for the interaction of

220 titers against group 3 pneumococcal surface protein C (PspC) variants were more likely to be coloniz

221 in A (PspA) and pneumococcal choline-binding protein C (PspC).

222 Because the acute-phase protein C-reactive protein (CRP) is highly upregulated d

223 Here we show that the acute phase protein C-reactive protein (CRP), a ligand for Fc recept

224 prevented binding of C1q and the acute-phase protein C-reactive protein to S. pneumoniae, thereby red

225 ith plasma concentrations of the acute-phase protein, C-reactive protein (CRP), and the adipocytokine

226 showed that most ES-62 was bound to a single protein, C-reactive protein (CRP), in normal human serum

227 eceptors thrombomodulin (TM) and endothelial protein C receptor (EPCR) and that low constitutive expr

228 The endothelial protein C receptor (EPCR) appears to play an important r

229 ypothesize that the occupancy of endothelial protein C receptor (EPCR) by the Gla-domain of protein C

230 s showed that expression of endothelial cell protein C receptor (EPCR) in MPM cells suppresses tumori

231 CIDRalpha1 domains of PfEMP1 and endothelial protein C receptor (EPCR) is associated with severe chil

232 scovery that parasite binding to endothelial protein C receptor (EPCR) is associated with severe dise

233 Loss of endothelial protein C receptor (EPCR) occurs at the sites of Plasmod

234 ral malaria, linking loss of the endothelial protein C receptor (EPCR) on brain vessels, caused by cy

235 mutant mice deficient for either endothelial protein C receptor (EPCR) or PAR1 revealed that the EPCR

236 rhFVIIa also interacts with the endothelial protein C receptor (EPCR) through its gamma-carboxygluta

237 Endothelial cell protein C receptor (EPCR) was first identified and isola

238 r severe malaria isolates impair endothelial protein C receptor (EPCR), a protein involved in coagula

239 nding PfEMP1s also interact with endothelial protein C receptor (EPCR), allowing infected erythrocyte

240 t murine thrombomodulin (TM) and endothelial protein C receptor (EPCR), endothelial membrane proteins

241 recent findings that suggest the endothelial protein C receptor (EPCR), known for its pivotal role in

242 ated protein C (APC) require the endothelial protein C receptor (EPCR), protease-activated receptor (

243 against the neutrophil receptors endothelial protein C receptor (EPCR), protease-activated receptor 3

244 arasite var transcripts encoding endothelial protein C receptor (EPCR)-binding domains, in combinatio

245 s that mediate IE binding to the endothelial protein C receptor (EPCR).

246 dhesion molecule-1 (ICAM-1), and endothelial protein C receptor (EPCR); however, cytoadhesion pattern

247 cord blood CD34(+) cells express endothelial protein C receptor (EPCR/CD201/PROCR) when exposed to th

248 tors in mouse endotoxemia, we found that the protein C receptor (ProcR; EPCR) was required for the no

249 n C (APC) complexed with soluble endothelial Protein C receptor (sEPCR) has position 4 occupied by Ca

250 the protein C pathway receptors (endothelial protein C receptor, thrombomodulin).

251 elated also control retention of endothelial protein C receptor-positive (EPCR(+)) LT-HSCs in the bon

252 hology through interactions with endothelial protein C receptor.

253 cofactor thrombomodulin and the endothelial protein C receptor.

254 The nuclear factor-kappaB protein c-Rel plays a critical role in controlling autoi

255 for appropriate tethering of fV, fVIII, and protein C required for their timely activation by IIa.

256 uggest that functional testing for activated protein C resistance is cheaper and more clinically rele

257 g beta-myosin heavy chain and myosin-binding protein C, respectively, are the 2 most common genes inv

258 A recombinant form of human activated protein C (rhAPC) has shown cytoprotective and anti-infl

259 ) with or without pretreatment of cells with protein C-S195A.

260 efficiency, and down-regulation by activated protein C showed similar results for the two variants co

261 Myosin Binding Protein-C slow (sMyBP-C) is expressed in skeletal muscle

262 Myosin Binding Protein-C slow (sMyBP-C), encoded by MYBPC1, comprises a

263 Surfactant protein C (SP-C) has been suggested to be an essential e

264 Surfactant protein C (SP-C) is a novel amyloid protein found in the

265 st the ATII cell-specific antigen surfactant protein-C (SP-C) then administered to C57BL/6 mice via t

266 ly target K-RasG12D expression in Surfactant Protein C (SPC)(+) alveolar type 2 cells and in Clara ce

267 mpirical-based approach to the generation of protein CD spectra from atomic coordinates.

268 eed for an application capable of generating protein CD spectra from atomic coordinates.

269 n of EPCR, with subsequent impairment of the protein C system promotes a proinflammatory, procoagulan

270 tor-A (VEGF-A)/VEGF receptor-2 and activated protein C systems, among others.

271 Cox16p, tagged with a dual polyhistidine and protein C tag, co-immunopurified with Cox1p assembly int

272 ll/IL-1 receptor-containing (TIR-containing) protein C (TcpC), which impairs TLR signaling, thereby s

273 vitro, we detected expression of an in-frame protein (C-terminal PB1-F2) from downstream ATGs in PB1-

274 d the vaccine in the entire circumsporozoite protein C-terminal (139 infections), as compared with 33

275 The retinoblastoma protein C-terminal domain (RbC) is necessary for the tum

276 We identified a hydrophobic pocket of the P-protein C-terminal domain as critical to STAT-binding/an

277 either the PIV5 or Nipah virus nucleocapsid protein C-terminal ends are sufficient to direct packagi

278 is that involves the reaction of recombinant protein C-terminal thioesters with N-terminal cysteine (

279 orkflow uses trypsin to enzymatically cleave proteins C-terminal to lysine and arginine residues prio

280 ion whereas in 3'-terminal exons that encode protein C-termini, protein-level selection is significan

281 f the MERS-CoV S protein fused to the RABV G protein C terminus (BNSP333-S1).

282 l tail with the PDZ protein GAIP-interacting protein C terminus, inhibiting its traffic to EEs.

283 ing epitope of HPV thought to include the L1 protein C terminus.

284 t in a +1-bp frameshift and generate a novel protein C terminus.

285 b) class I peptide ligand SIINFEKL at the M2 protein C terminus.

286 MYO6+ and its adaptor GAIP interacting protein, C terminus (GIPC) accumulate at the tips of the

287 a member of the homologous to E6-associated protein C-terminus (HECT)-type family of E3 ligases, wit

288 ieties of different charge and length at the protein C-terminus.

289 proteins (Galpha-binding protein interacting protein, C-terminus and CFTR-associated ligand), PDZ dom

290 status on the association between activated protein C therapy and mortality, an association with con

291 actor X, activated factor VII, and activated protein C to seven different binary lipid compositions.

292 athy is the recurrent MYBPC3 (myosin-binding protein-C) variant c.1504C>T, p.Arg502Trp, which was fou

293 onin inhibitor (cTnI) and the myosin-binding protein C was reduced by 26 and 35%, respectively, in TG

294 and the chaperone domain from prosurfactant protein C, we found that dimethyl sulfoxide (DMSO) can i

295 Decreased levels of Protein C were associated with increased odds for acute

296 corona for the local generation of activated protein C, which inhibits the formation of thrombin.

297 interaction of native cardiac myosin-binding protein C with the thin filament.

298 ouse model expressing cardiac myosin binding protein-C with a non-phosphorylatable Ser282 (i.e. serin

299 t the interactions of cardiac myosin-binding protein-C with its binding partners vary with its phosph

300 ontrolled trial (human recombinant activated Protein C Worldwide Evaluation of Severe Sepsis and sept