ライフサイエンスコーパス: serpin

1 albumin serine protease inhibitor family (ov-serpin).

2 ibitor (C1INH), a serine protease inhibitor (serpin).

3 conformation would lead to inactive, latent serpin.

4 n to modulate the inhibitory function of the serpin.

5 se proteins endochitinase A, PR-4, PRms, and SerPIN.

6 determines the inhibitory selectivity of the serpin.

7 determining the protease specificity of the serpin.

8 those of well studied human and prokaryotic serpins.

9 -approved small molecule inactivators of any serpins.

10 oteases can be regulated after activation by serpins.

11 PO), regulated by protease inhibitors called serpins.

12 he susceptibility of fibrinolytic enzymes to serpins.

13 s for all tested natural thrombin-inhibiting serpins.

14 rine proteases and their specific inhibitors serpins.

15 ne protease homologs (SPHs) and inhibited by serpins.

16 and is different from other heparin-binding serpins.

17 tial to extend immunomodulatory functions of serpins.

18 At least one isoform of serpin-1 can inhibit hemocyte proteinase 1, another M. s

19 Our results suggest that M. sexta serpin-1 isoforms A, E, and J can inhibit hemolymph prot

20 We identified nine of the 12 serpin-1 isoforms and, through analysis of putative serp

21 We investigated mRNA levels of individual serpin-1 isoforms by quantitative PCR.

22 lasma we used immunoaffinity purification of serpin-1 isoforms from M. sexta plasma, followed by two-

23 rnative splicing produces transcripts for 12 serpin-1 isoforms in Manduca sexta that differ only in t

24 To investigate the presence of individual serpin-1 isoforms in plasma we used immunoaffinity purif

25 dgut chymotrypsin was identified, suggesting serpin-1 isoforms may also function to protect insect ti

26 melanization proteases (IMP-1 and IMP-2) and Serpin-1 mediate hemolymph prophenoloxidase cleavage and

27 1 isoforms and, through analysis of putative serpin-1-proteinase complexes, identified three endogeno

28 ee endogenous M. sexta proteinase targets of serpin-1.

29 HP5 is inhibited by Manduca sexta serpin-4, serpin-1A, and serpin-1J to regulate its activity.

30 ed by Manduca sexta serpin-4, serpin-1A, and serpin-1J to regulate its activity.

31 In addition, a complex of serpin-1K in a complex with M. sexta midgut chymotrypsin

32 Serpin-2 is implicated in the latter activation of Toll

33 e melanization protease (CLIPB8), IMP-1, and Serpin-2.

34 the hinge region in the RCL of Manduca sexta serpin-3 and found they were able to block serpin-3 inhi

35 Serpin-3 associated with Ac-SVAFS-COO(-) had an altered

36 a serpin-3 and found they were able to block serpin-3 inhibitory activity, resulting in suppression o

37 ) displayed robust blocking activity against serpin-3.

38 HP5 is inhibited by Manduca sexta serpin-4, serpin-1A, and serpin-1J to regulate its activ

39 vely, our data link abnormal accumulation of serpins, a hallmark of serpinopathies, with dominant-neg

40 In the inhibition reaction of serpins, a protease cleaves a peptide bond in a solvent-

41 ents, there were higher levels of unmodified serpin A1 and A3, but following treatments with redox ac

42 spectrometry analyses identified Cys(256) of serpin A1 and Cys(263) of serpin A3 as the S-glutathiony

43 elevated plasma levels of S-glutathionylated serpin A1 monomer, trimer and serpin A3 monomer in patie

44 There is potential for S-glutathionylated serpins A1 and A3 to act as pharmacodynamic biomarkers f

45 n the trial and levels of S-glutathionylated serpins A1 and A3 were assessed by immunoblotting.

46 es and mass spectrometry, we identified that serpins A1 and A3 were S-glutathionylated in a dose- and

47 eral adipose tissue-derived serpin (vaspin), serpin A12 of the serpin family, and its target protease

48 tified Cys(256) of serpin A1 and Cys(263) of serpin A3 as the S-glutathionylated residues.

49 utathionylated serpin A1 monomer, trimer and serpin A3 monomer in patient blood following radiation.

50 r results constitute an in vivo example of a Serpin acting as a suicide inhibitor in plants, reminisc

51 sampling algorithm, we simulated the entire serpin active-to-latent transition in all-atom detail wi

52 evealed an association between baseline anti-serpin activity and slower residual beta cell function d

53 istent with the hypothesis that anti-clade B serpin activity blocks the serpin from binding, exposure

54 The exact mechanism by which anti-serpin activity is protective remains unclear.

55 he interference of RCL-derived peptides with serpin activity may lead to new possibilities of "silenc

56 correction restores Z-alpha1AT secretion and serpin activity to a level 50% that observed for wild-ty

57 ble one, can kinetically trap the proteinase-serpin acylenzyme intermediate.

58 orresponding loop of the non-heparin-binding serpin alpha(1)-proteinase inhibitor (ZPI-D-helix(alpha1

59 g the ability of component peptides from the serpin alpha(1)PI to associate, we have now elucidated t

60 The human serine protease inhibitor (serpin) alpha-1 antitrypsin (alpha1-AT) protects tissues

61 n the active-to-latent transition of another serpin, alpha1-antitrypsin, which does not readily go la

62 cific fluorophore-labeled derivatives of the serpin, alpha1-protease inhibitor (alpha1PI), which repo

63 Compared with other Ser protease inhibitors (serpins), alpha2AP contains an ~50-residue-extended C-te

64 provide new insights into the nature of the serpin and protease conformational changes involved in t

65 tease inhibitor (alpha1PI), which report the serpin and protease conformational changes involved in t

66 es significant conformational change in both serpin and protease.

67 ccelerated by a heparin template between the serpin and thrombin exosite II.

68 For serpins and canonical inhibitors, we predicted their put

69 form amyloid fibres, with examples including serpins and cystatins.

70 mation of thrombin in its final complex with serpins and find that in addition to exosite I, exosite

71 ication of these computational approaches to serpins and other large proteins highlights the successe

72 m can be successfully targeted by engineered serpins and that administration of such agents is effect

73 o quantify patient plasma S-glutathionylated serpins and that these post-translationally modified pro

74 s, from plants to vertebrates, now show that serpins and their unique inhibitory mechanism and confor

75 nt-exposed reactive center loop (RCL) of the serpin, and the serpin undergoes a conformational change

76 tiproteases, including leupeptin, aprotinin, serpins, and alpha2-macroglobulin, suggesting the presen

77 Thus, miropin is unique among inhibitory serpins, and it has apparently evolved the ability to in

78 ory mechanism, the inherent metastability of serpins, and the high-affinity association of PAI-1 with

79 We conclude that anti-serpin antibodies prevent serpin B13 from neutralizing p

80 s, various biochemical assays, and the human serpin antithrombin III (ATIII) as a model, we explored

81 The serpin antithrombin III (ATIII) targets thrombin and oth

82 ycosaminoglycans allosterically activate the serpin, antithrombin, by binding through a specific pent

83 n allosteric activation of the anticoagulant serpin, antithrombin, is the release of the reactive cen

84 nalization and the intracellular role of the serpin are not well understood.

85 Serpins are a family of serine protease inhibitors that

86 tion, an increasing number of non-inhibitory serpins are emerging as important elements within a dive

87 Interestingly, serpins are homologs of the well-known ovalbumin antigen

88 During folding, inhibitory serpins are kinetically trapped in a metastable state in

89 Serpins are remarkable and unique proteins in being able

90 Serine protease inhibitors, termed serpins, are key regulators in many biologic events.

91 Serine protease inhibitors, or serpins, are paradigms for this delicate balance between

92 we use conserpin, a synthetic, thermostable serpin, as a model protein with which to investigate the

93 ice with a monoclonal antibody (mAb) against serpin B13 also leads to fewer inflammatory cells in the

94 Human studies involved measuring anti-serpin B13 autoantibodies by Luminex.

95 Secretion of anti-serpin B13 autoantibodies in young diabetes-prone nonobe

96 enous anti-serpin B13 mAb or endogenous anti-serpin B13 autoantibodies resulted in cleavage of the su

97 conclude that anti-serpin antibodies prevent serpin B13 from neutralizing proteases, thereby impairin

98 We found that serpin B13 is expressed in the exocrine component of the

99 We also found that anti-serpin B13 mAb blocked the inhibitory activity of serpin

100 pin from binding, exposure to exogenous anti-serpin B13 mAb or endogenous anti-serpin B13 autoantibod

101 hy young Balb/c male mice were injected with serpin B13 mAb or IgG control and examined for the numbe

102 We found that injecting anti-serpin B13 monoclonal Ab enhanced beta cell proliferatio

103 n B13 mAb blocked the inhibitory activity of serpin B13, thereby allowing partial preservation of the

104 so documented the perivascular expression of Serpin B2 by angiotropic melanoma cells in the murine br

105 f anti-PA serpins, including neuroserpin and serpin B2, to prevent plasmin generation and its metasta

106 annexin V, heparanase, ERp57, kallekrein-14, serpin B6, tetranectin, and collagen VI showed a bias fo

107 ifferentially affected furin reactivity with serpin B8 and alpha1PDX in a manner that depended on the

108 inhibitor of furin, together with alpha1PDX-serpin B8 and furin-PC chimeras to identify determinants

109 p (RCL) sequences of alpha1PDX with those of serpin B8 demonstrated that both the P4-P1 RXXR recognit

110 te loops whose role in furin reactivity with serpin B8 was tested by engineering furin-PC loop chimer

111 Here, we characterize serpin B8, a natural inhibitor of furin, together with a

112 Modeling of the serpin B8-furin Michaelis complex identified serpin exos

113 (+) T cells and reduced TNFR2, IDO2, TDO and Serpin B9 expression levels.

114 To investigate how serpins balance function and folding, we used consensus

115 proteins, hereafter named biliverdin-binding serpins (BBS), have absorption spectra that mimic those

116 g the amino-terminal segment of the RCL into serpin beta-sheet A as a new strand.

117 n, chloride channel accessory 1 (CLCA1), and Serpin beta2 (SERPINB2) in airway epithelial brushings i

118 city by mutating the RCL to that of a target serpin, but the rules governing specificity are not unde

119 es (contact activation) and regulated by the serpin C1 inhibitor.

120 htly regulated in healthy individuals by the serpin C1-inhibitor, but individuals with hereditary ang

121 f action, these SPIs can be categorized into serpins, canonical inhibitors and alpha-2-macroglobulins

122 unexpected EPO action mode via an EPOR-Spi2A serpin-cathepsin axis in maturing erythroblasts, with ly

123 placentation: the prolactins (two clusters), serpins, cathepsins, and the natural killer (NK)/C-type

124 ulting in suppression of inhibitory protease-serpin complex formation.

125 epend on the regions of thrombin unfolded by serpin complexation.

126 levels of fXII, and reduced levels of fXIIa-serpin complexes, consistent with fXII being a substrate

127 Serpins compose the largest superfamily of peptidase inh

128 SERPINS comprise a large and functionally diverse family

129 r inhibition of proteinases, so that massive serpin conformational change, driven by the favorable en

130 through a unique mechanism in which a major serpin conformational change, resulting in a 70-A transl

131 ion and movement of the protease and coupled serpin conformational changes involving the F helix-shee

132 fficacy in plasminogen activator inhibitor-1 serpin-deficient transplants.

133 mmatory cytokines, such as CD31, BDNF, TFF3, Serpin E-1, VCAM-1, Vitamin D BP, and PDGF-AA, were sign

134 nhibition, demonstrating an up-regulation of Serpin E1 signal.

135 ude a unique profile of cytokines, including Serpin E1, which is not generated by other T cells, MIF,

136 ave now elucidated the pathway by which this serpin efficiently folds into its metastable state.

137 eaving aside antithrombin, a closely related serpin, essentially unactivated.

138 Serpins exist in a metastable state that undergoes a maj

139 serpin B8-furin Michaelis complex identified serpin exosites in strand 3C close to the 298-300 loop w

140 nant human PEDF (rhuPEDF) was cleaved at its serpin-exposed loop by limited chymotrypsin proteolysis.

141 ions also help elucidate why some inhibitory serpin families are more conformationally labile than ot

142 tichymotrypsin (alpha1-ACT), a member of the serpin family (SERPINA3), is an acute-phase protein secr

143 a nonsynonymous single-nucleotide variant in serpin family A member 1 (SERPINA1) encoding alpha-1 ant

144 actor 4 alpha [HNF4A], fucosyltransferase 2, serpin family A member 1 [SERPINA1], jumonji domain cont

145 nstrated that the concentration of SERPINA1 (serpin family A member 1) in small HDL was also lower in

146 Here we report that serpin family B member 1 (SERPINB1) limited the activity

147 ibitor Portland (alpha1PDX) is an engineered serpin family inhibitor of the proprotein convertase (PC

148 The serpin family of metastable protease inhibitors uses lar

149 redicts a 45-kDa protein that belongs to the serpin family of protease inhibitors.

150 giotensinogen-a non-inhibitory member of the serpin family of protease inhibitors.

151 a antigens 1 and 2 (SCCA1/2), members of the Serpin family of serine/cysteine protease inhibitors, ar

152 he same mechanism-the presence of a class of serpin family proteins that bind biliverdin.

153 tivator inhibitor-2 (PAI-2), a member of the serpin family with known antiapoptotic activity.

154 e-derived serpin (vaspin), serpin A12 of the serpin family, and its target protease kallikrein 7 (KLK

155 Like other members of the serpin family, neuroserpin undergoes a large conformatio

156 e other thrombin inhibitors belonging to the serpin family, PN1 is not synthesized in the liver and d

157 potential inhibitors from the intracellular serpin family.

158 ogenous inhibitors of APC are members of the serpin family: protein C inhibitor (PCI) and alpha1-anti

159 ny members of the serine protease inhibitor (serpin) family are activated by glycosaminoglycans (GAGs

160 ectin 1 (FN1) and serine protease inhibitor (serpin) family E member 2 (SERPINE2) are essential for V

161 s a member of the serine protease inhibitor (serpin) family of proteins, whose target proteases inclu

162 s a member of the serine protease inhibitor (serpin) family.

163 een shown that the formation of the thrombin-serpin final complex disorders the active site and exosi

164 wever, conformational lability of the native serpin fold renders them susceptible to misfolding and a

165 ever, conformational labiality of the native serpin fold renders them susceptible to misfolding, whic

166 How serpins fold into such a metastable state is unknown.

167 potentially explains the affinity of this ov-serpin for heparin, as opposed to ovalbumin.

168 ntitrypsin propose therapeutic uses of these serpins for the management of coagulation and contact sy

169 Serpins form an enormous superfamily of 40-60-kDa protei

170 SmSrpQ, one of two S. mansoni serpins found in larval secretions, is only expressed du

171 that anti-clade B serpin activity blocks the serpin from binding, exposure to exogenous anti-serpin B

172 Although serpins from animals, plants, and viruses have been wide

173 combination of techniques, we purified these serpins from several species of nonmodel treefrogs and d

174 s for potent and selective modulation of the serpin function, especially for inhibiting the initiatio

175 suggest a novel framework for understanding serpin function, especially with respect to thrombin inh

176 y with respect to thrombin inhibition, where serpins functionally "rezymogenize" proteases to ensure

177 pe (ATM) or Z mutant form (ATZ) of the human serpin fused to GFP.

178 ons reveal the evolutionary pathway of seven serpin genes in group C.

179 icroorganisms, and only very few prokaryotic serpins have been investigated from a mechanistic standp

180 posure to proteases within the cell, clade B serpins help to maintain homeostasis by inducing protect

181 Inactivation of thrombin (T) by the serpins heparin cofactor II (HCII) and antithrombin (AT)

182 le inactivation of alpha-thrombin (T) by the serpin, heparin cofactor II (HCII), is accelerated by te

183 tor region-specific folding of the canonical serpin human alpha(1)-antitrypsin (alpha(1)-AT).

184 All prokaryotic genes encoding putative serpins identified to date are found in environmental an

185 Our findings reveal a new role for the anti-serpin immunological response in promoting adaptive chan

186 pe-1 (PAI-1) is a serine protease inhibitor (serpin) implicated in numerous pathological processes, i

187 ering, indicating a functional role for this SERPIN in the dual-growth factor model of induced motili

188 n, and plasminogen activator (PA) inhibitory serpins in cancer cells as a shield against this defense

189 est that elevated circulating antiangiogenic serpins in diabetic patients may contribute to impaired

190 glutathionylated serine protease inhibitors (serpins) in blood could be used as biomarkers of exposur

191 breast cancer express high levels of anti-PA serpins, including neuroserpin and serpin B2, to prevent

192 revealed a patchy distribution of bacterial serpins incompatible with a vertical descent model.

193 It is not known whether these serpins influence immunological tolerance and the risk f

194 asminogen activator inhibitor 1 (PAI-1) is a serpin inhibitor of the plasminogen activators urokinase

195 hat, contrary to this view, the FXa-specific serpin inhibitor, protein Z-dependent protease inhibitor

196 inhibitor (ZPI) are among two physiological serpin inhibitors in plasma that are involved in the reg

197 PN-1 mutated in the serpin inhibitory domain, the reactive center loop, fail

198 However, the complexity of the serpin inhibitory mechanism, the inherent metastability

199 ted acceleration of fXIa inhibition by these serpins is incompletely understood, as heparin appears t

200 The misfolding of serpins is linked to several genetic disorders including

201 oop docking site to the opposite pole of the serpin, kinetically traps the acyl-intermediate complex.

202 ovel EPO-triggered pathway involving a Spi2A serpin-lysosome-cathepsin cascade that is initiated thro

203 Both serpins markedly reduce arterial inflammation and plaque

204 rpins similar to known functional inhibitory serpins may participate in immune responses.

205 lding and function required by the exquisite serpin mechanism of action.

206 Herein, we characterized a novel serpin (miropin) from the human pathogen Tannerella fors

207 In contrast to other serpins, miropin efficiently inhibited a broad range of

208 However, the serpin mutant inhibited chymotrypsin with an efficiency

209 The accumulation of serpin oligomers and polymers within the endoplasmic ret

210 miniscent of the activity of animal or viral serpins on immune/cell death regulators, including caspa

211 c colonization, suggesting that mutations in serpins or other members of the coagulation cascade can

212 However, like other serpins, PAI-1 has a labile structure, making it a diffi

213 ks centred on apolipoprotein E, jun, leptin, serpin peptidase inhibitor E type 1 and peroxisome proli

214 and potentially interdependent induction of serpin peptidase inhibitor, clade A member 3 (SERPINA3)

215 gene encoding alpha-1 antitrypsin, SERPINA1 (serpin peptidase inhibitor, clade A, member 1), in deter

216 Cela1 was covalently bound to serpin peptidase inhibitor, clade A, member 1, resulting

217 ed chloride channel regulator 1 (CLCA1), and serpin peptidase inhibitor, clade B (SERPINB2).

218 ltiple mutations were found in the SERPINF1 (Serpin Peptidase Inhibitor, Clade F) gene which encodes

219 n-like-8 (MTRNRL8), interleukin-8 (IL8), and serpin peptidase inhibitor, clade H (SERPINH1) and chemo

220 ental data for the latency transition of the serpin plasminogen activator inhibitor-1 (PAI-1).

221 These results suggest that the silkworm serpins play regulatory roles in defense responses.

222 se and respond to the accumulation of mutant serpin polymers in the endoplasmic reticulum (ER).

223 Standard serpins possess a single target bond and inhibit selecte

224 ely target heparin cofactor II (HCII), a key serpin present in human plasma, remain unknown.

225 strated that plasminogen activator inhibitor serpins promote brain metastatic colonization, suggestin

226 ously identified KCs as a rich source of the serpin protease inhibitor vaspin (serpinA12), originally

227 Intracellular (clade B) OVA-serpin protease inhibitors play an important role in tis

228 sed on a proteomic screen, we identified the serpin protease nexin-1 (PN-1) as a potential target of

229 d by vacuolar collapse and the appearance of serpin-protease complex.

230 in trapping the acyl-intermediate complex in serpin-protease reactions and support a previously propo

231 cally significant rate enhancements of other serpin-protease reactions.

232 nter loop scissile P1-P1' bond, resulting in serpin-protease suicide-inhibitory complexes.

233 Serpin protein protease inhibitors inactivate their targ

234 actor (PEDF) is a serine protease inhibitor (serpin) protein with well established neuroprotective an

235 The anticoagulant serpin, protein Z-dependent protease inhibitor (ZPI), is

236 ls and fostering vascular co-option, anti-PA serpins provide a unifying mechanism for the initiation

237 d alpha1PDX in a manner that depended on the serpin RCL-primed sequence.

238 n reactivity depending on the furin loop and serpin RCL-primed sequences.

239 observed in the reactions, ascribable to (i) serpin reactive center loop insertion into sheet A with

240 Target proteases cleave the serpin reactive center loop scissile P1-P1' bond, result

241 n(298-300) loop are critical determinants of serpin reactivity with furin, which may be exploited in

242 ithrombin reactivity and Arg(150) for native serpin reactivity.

243 Serpins regulate coagulation and inflammation, binding s

244 proteases cleaving the bait they offer (e.g. serpins, regulating cell death, and alpha-macroglobulins

245 Protease inhibition by serpins requires a large conformational transition from

246 This inhibition requires a near full-length serpin sequence.

247 active center loop residues of the prototype serpin, SERPINA1, with the P4-P5' residues of Sb9 contai

248 oci at genome-wide significance, the clade B serpin (SERPINB) gene cluster at 18q21.3, the cytokine g

249 nt and phylogenetic tree indicated that some serpins similar to known functional inhibitory serpins m

250 urin-PC chimeras to identify determinants of serpin specificity and selectivity for furin inhibition.

251 ith which to investigate the determinants of serpin specificity by engineering its RCL.

252 1'-P5' sequence are critical determinants of serpin specificity for furin.

253 Engineering serpin specificity is therefore substantially more compl

254 Serpin specificity towards its protease target is dictat

255 The Serpins Spi2A in mice and SERPINB3 and SERPINB4 in aller

256 In this study, we characterized the serpin (SRPN) gene family in the mosquito Anopheles gamb

257 Unlike other serpins such as alpha(1)-antitrypsin, wild-type neuroser

258 A similar pocket is present on other serpins, suggesting that this site could be a common tar

259 clinically relevant role for a member of the serpin superfamily and a leukocyte elastase and crosstal

260 (ZPI) is a recently identified member of the serpin superfamily that functions as a cofactor-dependen

261 and introduce a function for a member of the serpin superfamily, the largest and most ubiquitous grou

262 presses miropin, a protease inhibitor in the serpin superfamily.

263 a serine protease inhibitor belonging to the serpin superfamily.

264 s a member of the serine protease inhibitor (serpin) superfamily and displays tumor-suppressing activ

265 a member of the serine proteinase inhibitor (SERPIN) superfamily with antiangiogenic activities, were

266 nsus design to create conserpin, a synthetic serpin that folds reversibly, is functional, thermostabl

267 otic and antifibrinolytic properties of this serpin that have heretofore gone unrecognized.

268 r human or mouse Sb9 results in a functional serpin that inhibits GzmB and resists ROS inactivation.

269 Antithrombin (AT) is an anticoagulant serpin that irreversibly inactivates the clotting protei

270 Protease nexin-1 (PN-1) is a serpin that is barely detectable in plasma but found in

271 ently identified a novel antibody to clade B serpin that reduces islet-associated T cell accumulation

272 tease inhibitor 9 (PI-9) is an intracellular serpin that specifically inhibits granzyme B, a cytotoxi

273 Alboserpin emerges as an atypical serpin that targets FXa and displays unique phospholipid

274 Here, using serpins that inhibit proteases as an example, we review

275 ibril association and covalent attachment of serpins that regulate clot dissolution.

276 a non-inhibitory serine protease inhibitor (serpin) that influences many cellular functions includin

277 or-1 (PAI-1) is a serine protease inhibitor (serpin) that regulates fibrinolysis, cell adhesion and c

278 igh affinity (K(D) = 30nM) and activated the serpin to rapidly (k(ass) approximately 10(6)M(-1)s(-1))

279 When they inhibit target proteases, serpins transition to a stable state in which the reacti

280 robial competitors, T. forsythia possesses a serpin-type proteinase inhibitor called miropin.

281 Here we show that miropin uses the serpin-type suicidal mechanism.

282 Serine proteinase inhibitors (serpins), typically fold to a metastable native state an

283 ive center loop (RCL) of the serpin, and the serpin undergoes a conformational change, incorporating

284 Visceral adipose tissue-derived serpin (vaspin), serpin A12 of the serpin family, and it

285 This tailor-made serpin was shown to form covalent complexes with all NSP

286 drugs, relative S-glutathionylation of these serpins was higher in plasma from normal individuals.

287 cting the allosteric activation state of the serpin were inconsistent with a two-state model of allos

288 increased levels of these S-glutathionylated serpins were correlated with increased duration of radio

289 Many of the A. gambiae serpins were expressed during all life stages.

290 ls of both unmodified and S-glutathionylated serpins were similar in each group.

291 in 1 (STC1), and serine protease inhibitors (SERPINs), which significantly correlated with age in pla

292 physiological inhibitors of thrombin are all serpins, whose mechanism involves significant conformati

293 Protein C inhibitor (PCI) is a serpin with broad protease reactivity.

294 tes the exosite-dependent interaction of the serpin with factors IXa (FIXa) and Xa (FXa), thereby imp

295 in an irreversible inhibitory complex of the serpin with the protease.

296 1-P1' bond in PCI and alpha1AT, resulting in serpins with the desired specificity profile.

297 o new possibilities of "silencing" arthropod serpins with unknown functions for investigation of thei

298 d HAI-2/SPINT2, as well as major circulating serpins) would determine the infection rate of host cell

299 In contrast, relative abundance of serpins Z1C and 1-Cys peroxiredoxin was increased at e[C

300 The serpin ZPI is a protein Z (PZ)-dependent specific inhibi