ライフサイエンスコーパス: kallikrein

1 prekallikrein-HK autoactivation to generate kallikrein.

2 oxidants caused inactivation of both HK and kallikrein.

3 t are selective either for or against plasma kallikrein.

4 onal views of the catalytic domain of plasma kallikrein.

5 for factor Xa relative to trypsin and plasma kallikrein.

6 meet target levels for inhibition of plasma kallikrein.

7 inin-forming cascade, namely factor XIIa and kallikrein.

8 s, beta-defensins, S100 family proteins, and kallikreins.

9 oup of endogenous proteolytic enzymes called kallikreins.

10 ipoprotein B/apolipoprotein A1 ratio (1.40), kallikrein (0.73), lipoprotein a (1.29), matrix metallop

11 Fabs against human tissue kallikrein 1 (hK1, KLK1 gene product) were discovered by

12 including zinc finger protein 94 and several kallikrein 1-related peptidases which could account for

13 Over-expression of tissue kallikrein-1 and modulation of the KKS shows beneficial

14 c promoter whose activation initiates murine kallikrein-1 expression within the kidneys.

15 c administration of recombinant human tissue kallikrein-1 protein (DM199) to non-obese diabetic mice

16 d and tested DM199, recombinant human tissue kallikrein-1 protein (rhKLK-1), as a potential novel the

17 he role of kallikreins, in particular tissue kallikrein-1, in type 1 diabetes mellitus (T1D).

18 s is well documented, but the role of tissue kallikrein-1, the protease that generates bradykinin in

19 ified by PCA were Mesothelin, Muc4, Muc5A/C, Kallikrein 10, Transglutaminase 2, Fascin, TMPRSS3 and s

20 ly unrecognized ones, such as uroplakins and kallikrein 11, both confirmed by immunohistochemistry.

21 resulted in activation of each zymogen, with kallikrein 12 being a more potent activator.

22 the H1 and H3 subtypes most efficiently and kallikrein 12 cleaving the H1 and H2 subtypes most effic

23 Kallikrein 5 and kallikrein 12 were examined for their ability to activat

24 dapted influenza viruses by kallikrein 5 and kallikrein 12.

25 Autoantibodies against kallikrein 13 were identified in serum from dry-eye mice

26 differentially overexpressed genes included kallikreins (13, 16, and 26), FKBP51, PI3K alpha regulat

27 ibition of kallikreins 5 and 7, and possibly kallikrein 14 and matriptase, (that initiates the kallik

28 y gland extract or recombinant mouse protein kallikrein 1b22 (Klk1b22) emulsified in complete Freund'

29 using three composite promoters called human kallikrein 2 (hK2)-E3/P, PSA-E2/P, and ARR2PB, derived f

30 -reactivity with a homologous protein (human Kallikrein 2) and low response to human serum albumin (H

31 mel during development, and mutations in the kallikrein 4 (KLK4) and enamelysin (MMP20) genes cause a

32 Kallikrein 4 (Klk4) is believed to play an essential rol

33 es, matrix metalloproteinase-20 (MMP-20) and kallikrein 4 (KLK4), are known to cleave amelogenin and

34 ses, matrix metalloproteinase 20 (MMP20) and kallikrein 4 (KLK4), have each been reported in a single

35 n of matrix metalloproteinase 20 (MMP20) and kallikrein 4 (KLK4).

36 sion of enamelin but decreased expression of kallikrein 4 (protease essential for removing enamel pro

37 g multiple forms of MMPs, cathepsin D and K, kallikrein 4 and proprotein convertases.

38 purified, and digested with MMP-20 or Klk4 (kallikrein 4).

39 tumor-related proteins enamelysin (MMP-20), kallikrein-4 (KLK-4), and odontogenic ameloblast-associa

40 secretory stage as the enamel thickens, and kallikrein-4 (KLK-4, EMSP1) is expressed later during th

41 Kallikrein-4 (KLK4) is a serine protease expressed durin

42 g by matrix metalloproteinase-20 (MMP20) and kallikrein-4 (KLK4) is critical for enamel formation, an

43 t pig MMP-20 (rpMMP20) and recombinant human kallikrein-4 (rhKLK4), respectively.

44 ces of mRNA of the proteases, enamelysin and kallikrein-4) on days 0 and 1, persisted until day 3, an

45 The serine proteases kallikrein 5 (KLK5) and kallikrein 7 (KLK7) control enzy

46 d abundance and activity of cathelicidin and kallikrein 5 (KLK5), a predominant trypsin-like serine p

47 in conventionally housed NC/Tnd mice reduced kallikrein 5 activity and ameliorated the dermatitis.

48 hat alterations in skin pH directly modulate kallikrein 5 activity leading to skin barrier dysfunctio

49 in specific pathogen-free conditions induced kallikrein 5 and activated protease-activated receptor 2

50 Expression of the proteases kallikrein 5 and cathepsin D was dramatically reduced in

51 Kallikrein 5 and kallikrein 12 were examined for their a

52 the HA of human-adapted influenza viruses by kallikrein 5 and kallikrein 12.

53 ence for particular influenza subtypes, with kallikrein 5 cleaving the H1 and H3 subtypes most effici

54 e resulted in a calcium-dependent release of kallikrein 5 from keratinocytes, a critical protease inv

55 y investigations on skin sections from human kallikrein 5 transgenic mouse revealed significant reduc

56 teases stratum corneum tryptic enzyme (SCTE, kallikrein 5) and stratum corneum chymotryptic protease

57 r definitive (suicide type) or transient for kallikreins 5 and 14, and matriptase.

58 The inhibition of kallikreins 5 and 7, and possibly kallikrein 14 and matr

59 by trypsin-like serine proteases, including kallikrein-5 (KLK5), or by treatment with activating pep

60 Kallikrein 6 (K6, MSP) is a newly identified member of t

61 n identified, including p53, HER2/neu, IL-6, kallikrein 6, and claudin-4, some of which may be suscep

62 as alpha-fetoprotein in liver carcinoma, and kallikreins 6 and 10 in ovarian cancer, or therapeutic u

63 f the serpin family, and its target protease kallikrein 7 (KLK7) are heparin-binding proteins, and in

64 The serine proteases kallikrein 5 (KLK5) and kallikrein 7 (KLK7) control enzymatic processing of cath

65 onstrated direct interaction of miR-217 with kallikrein 7 (KLK7), encoding a putative oncogene not pr

66 A suicide mechanism was observed against kallikrein 7 whereas the inactivation was either definit

67 stratum corneum chymotryptic protease (SCCE, kallikrein 7) were shown to control activation of the hu

68 ssed proteins after FLG knockdown, including kallikrein-7 (KLK7; 2.2-fold), cyclophilin A (PPIA; 0.9-

69 a novel mechanism of bradykinin-independent kallikrein action that may contribute to the regulation

70 recruitment of EPCs in arthritis, acting via kallikrein activation and B2R-dependent mechanisms.

71 ved OSCS induced hypotension associated with kallikrein activation when administered by intravenous i

72 induced alkalinization of vitreous increased kallikrein activity and its generation of factor XIIa, r

73 kinase cascade via a mechanism that requires kallikrein activity but does not involve bradykinin rece

74 Here, we show increased activation of FXII, kallikrein activity, and HK cleavage in AD patient plasm

75 h a kallikrein gene polymorphism that lowers kallikrein activity, the brachial artery undergoes eutro

76 expression of the protease domain of plasma kallikrein, along with the purification and high resolut

77 d strong structure and order conservation of kallikreins among four mammalian species.

78 In patients with hereditary angioedema, kallikrein and bradykinin formation can occur without in

79 of the prekallikrein-HK complex to generate kallikrein and bradykinin.

80 C1-INH led to conversion of prekallikrein to kallikrein and cleavage of HK, as was seen in plasma fro

81 evidence for a broad link between the kinin-kallikrein and complement systems, and suggest a role of

82 e it activates matrix metalloproteinases and kallikrein and degrades fibronectin.

83 cis-pQTLs for kallikrein and F12 also show trans associations for prot

84 A proteolytic cascade involving kallikrein and Factor XII cleaves chromogranins to activ

85 ochemical and enzymatic properties of plasma kallikrein and paves the way for structure-based design

86 DHI treatment up-regulated the expression of kallikrein and plasma kallikrein B genes.

87 Both kallikrein and plasmin activate factor XII; kallikrein i

88 In addition, Desmolaris binds kallikrein and reduces bradykinin generation in plasma a

89 Multi-sensitization towards lipocalin, kallikrein and secretoglobin components is associated wi

90 e find that HGFA, matriptase, hepsin, plasma kallikrein and trypsin are potently inhibited, and use t

91 ins (uPAR, kininogen) known to be cleaved by kallikrein and with NTproBNP.

92 bitor-2 (TFPI-2) inhibits factor XIa, plasma kallikrein, and factor VIIa/tissue factor; accordingly,

93 ng revealed activation of factor XII, plasma kallikrein, and kininogen during the acute phase of anap

94 Collectively, these studies suggest that kallikreins are protective disease-associated genes in a

95 us was close to this threshold (rs4253311 in kallikrein B [KLKB1], P=5.5x10(-8)).

96 ated the expression of kallikrein and plasma kallikrein B genes.

97 raits; in a companion study, variants in the kallikrein B locus were associated with B-type natriuret

98 e identified 2 genetic loci (kininogen 1 and kallikrein B) influencing key components of the RAAS, co

99 A as a predictive marker and in the field of kallikrein-based tests: [-2] proPSA, the prostate health

100 allikrein is stoichiometrically converted to kallikrein because of release of heat shock protein-90 (

101 Kallikreins belong to a family of serine proteases that

102 ted factor XII (factor XIIa) or biotinylated kallikrein bound to avidin-coated plates.

103 ersion to the proteases alphaFXIIa and alpha-kallikrein by a process called contact activation.

104 Inhibition of plasma kallikrein by EPI-KAL2 and 13G11 significantly suppresse

105 ikrein activation and increased formation of kallikrein-C1 inhibitor complexes, without Factor XIa ac

106 of whether we measured factor XIIa-C1-INH or kallikrein-C1-INH complexes, and the two assays were in

107 iency of C1 inhibitor--a serpin inhibitor of kallikrein, C1r, C1s, factor XII, and plasmin.

108 We experimentally demonstrate that kallikrein can cleave proBNP (NTproBNP precursor) in vit

109 n assay to assess the amidolytic activity of kallikrein can supplement analytic tests to protect the

110 ously published finding that a panel of four kallikreins can predict the result of biopsy for prostat

111 mouse model by premature activation of a pro-kallikrein cascade.

112 after proteolytic cleavage at the prostasin/kallikrein cleavage site (K181-V182 and mAbprostasin) to

113 HK on cells such that MPO masked the plasma kallikrein cleavage site on HK, and MPO-generated oxidan

114 tors (PARs) 1 and 2, which possess consensus kallikrein cleavage sites, but not PAR4.

115 In vitro, kallikrein cleaved recombinant human CHGA to catestatin,

116 Prostasin/kallikrein-cleaved gammaENaC was detected consistently o

117 DHI also significantly increased serum kallikrein content in SHR.

118 ransfected HEK293 cells, we find that plasma kallikrein directly activates G protein-coupled protease

119 doses >/=400 mg q8 h met or exceeded plasma kallikrein EC50 values throughout the dosing interval.

120 e strains that upregulated renal and urinary kallikreins exhibited less evidence of disease.

121 ths and then were monitored for 8 months for kallikrein expression and disease.

122 Tamoxifen-induced up-regulation of renal kallikrein expression increased nitric oxide production

123 ly inhibitory domain, and it inhibits plasma kallikrein, factor XIa, and plasmin.

124 prekallikrein-HK leads to rapid formation of kallikrein; factor XII alone does not autoactivate.

125 K6, MSP) is a newly identified member of the Kallikrein family of serine proteases that is preferenti

126 elated peptidase 6 (KLK6) is a member of the kallikrein family of serine-type proteases, characterize

127 A), a serine protease belonging to the human kallikrein family, is best known as a prostate cancer bi

128 le-chain FXII initiates alphaFXIIa and alpha-kallikrein formation on a surface.

129 ubated in polystyrene plates and assayed for kallikrein formation.

130 was assessed by using a chromogenic assay of kallikrein formation.

131 using pro-phe-arg-p-nitroanilide reflecting kallikrein formation.

132 invoking factor XII activation, although the kallikrein formed can rapidly activate factor XII if it

133 We previously reported that a panel of four kallikrein forms in blood-total, free, and intact prosta

134 erum scuPAR levels identified a human plasma kallikrein gene (KLKB1) promoter polymorphism (rs4253238

135 we investigated the protective role of local kallikrein gene delivery in ischemia/reperfusion-induced

136 Kallikrein gene delivery markedly reduced reperfusion-in

137 of the underexpressed genes belonged to the kallikrein gene family,which encodes serine esterases.

138 Delivery of the kallikrein gene increased phosphorylation of Src, Akt, g

139 I, Azizi et al. report that in humans with a kallikrein gene polymorphism that lowers kallikrein acti

140 AC clone-derived physical map of the porcine kallikrein gene region and have fully sequenced a BAC cl

141 Adenovirus carrying the human tissue kallikrein gene was delivered locally into the heart usi

142 Radiation hybrid mapping assigns this kallikrein-gene-rich region to porcine chromosome 6.

143 lling episodes caused by uncontrolled plasma kallikrein generation and excessive bradykinin release r

144 Notably, variants in kinin-kallikrein genes KNG1, F12, KLKB1, and ACE were associat

145 g mice with a genetic interval harboring the kallikrein genes onto a disease-resistant background.

146 ve fully sequenced a BAC clone containing 13 kallikrein genes, 11 of which are novel.

147 s nephritis were found to be associated with kallikrein genes, particularly KLK1 and the KLK3 promote

148 ymus being the only tissue expressing all 13 kallikrein genes.

149 ition, nephritis-sensitive mouse strains had kallikrein haplotypes that were distinct from those of c

150 The production of BK from HK by plasma kallikrein has been implicated in the pathogenesis of in

151 Although plasma kallikrein has been purified for 40 years, its structure

152 zymogens plasminogen, urokinase, and plasma kallikrein have all been shown to cleave and activate in

153 The 15 human and 24 mouse kallikreins have been implicated in pathophysiology of b

154 armacologic inhibition of factor XII, plasma kallikrein, high-molecular-weight kininogen, or the brad

155 We also assessed human glandular kallikrein (hK2) expression in a subset of 164 patients.

156 n 90 leads to conversion of prekallikrein to kallikrein in a zinc-dependent reaction.

157 Similarly, kinin or transduction of kallikrein in cultured cardiomyocytes promoted cell viab

158 trate that prekallikrein-HK will activate to kallikrein in phosphate-containing buffers and that the

159 ession and localization of recombinant human kallikrein in rat myocardium after gene transfer were de

160 ferences in the rate of cleavage by purified kallikrein in the 3 strains in the absence of N-glycosyl

161 A critical role for plasma kallikrein in the pathogenesis of autoantibody-induced a

162 rption by parathyroid hormones or the tissue kallikrein in vivo.

163 pathway: factor XIa, factor XIIa, and plasma kallikrein, in the presence and absence of high molecula

164 owever, much less is known about the role of kallikreins, in particular tissue kallikrein-1, in type

165 cultured in the presence of tunicamycin, the kallikrein-induced cleavage rate of Lewis HK was not inc

166 le of plasma KKS was examined using a plasma kallikrein inhibitor (EPI-KAL2) and an antikallikrein an

167 Kunitz plant inhibitor SbTI, the recombinant kallikrein inhibitor (rBbKIm) led to prostate cancer cel

168 llowing treatment with ecallantide, a plasma kallikrein inhibitor approved for HAE attack treatment.

169 Ecallantide (a kallikrein inhibitor approved for use in the United Stat

170 lstat is a potent small-molecule oral plasma kallikrein inhibitor under development for treatment of

171 ) and (2) those receiving aprotinin (2x10(6) kallikrein inhibitor units [KIU] in pump prime, 2x10(6)

172 oup (n=7) was administered aprotinin (40,000 kallikrein inhibitor units [KIU]/kg loading dose, 40,000

173 Lanadelumab (DX-2930) is a new kallikrein inhibitor with the potential for prophylactic

174 KIm is the recombinant Bauhinia bauhinioides kallikreins inhibitor that was modified to include the R

175 New agents such as recombinant C1 inhibitor, kallikrein inhibitors, and bradykinin inhibitors may off

176 kallikrein and plasmin activate factor XII; kallikrein is 20 times more potent on a molar basis.

177 Plasma kallikrein is a serine protease that has many important

178 agulation and activation of the inflammatory kallikrein-kinin and complement systems.

179 trinsic coagulation pathway and triggers the kallikrein-kinin and the complement systems.

180 Complement and the kallikrein-kinin cascade system are both activated in in

181 in mediating the inflammatory effects of the kallikrein-kinin pathway.

182 cessive activation of the bradykinin-forming kallikrein-kinin pathway.

183 The kallikrein-kinin system (KKS) comprises a cascade of pro

184 The plasma kallikrein-kinin system (KKS) consists of serine proteas

185 Modulation of the kallikrein-kinin system (KKS) has been shown to have ben

186 This study examines the role of the kallikrein-kinin system (KKS) in RIHD by investigating t

187 monoclonal antibody C11C1 attenuates plasma kallikrein-kinin system activation, local and systemic i

188 se the intriguing possibility that decreased kallikrein-kinin system activity may play an important r

189 nd anti-inflammatory pathways, including the kallikrein-kinin system and leukocyte activity.

190 ent with the close interrelation between the kallikrein-kinin system and the RAAS.

191 s also been reported that alterations of the kallikrein-kinin system are associated with formation of

192 The opposing effects of the kallikrein-kinin system are mediated by bradykinin actin

193 The principal effectors of the kallikrein-kinin system are plasma and tissue kallikrein

194 vascular remodeling and the up-regulation of Kallikrein-kinin system contribute, at least in part, to

195 Previous findings underline the role of the kallikrein-kinin system in angiogenesis.

196 To explore the role of the kallikrein-kinin system in relation to ischemia/reperfus

197 r angiotensin II levels, suggesting that the kallikrein-kinin system partly mediates the effects of t

198 between MPO and the components of the plasma kallikrein-kinin system resulted in decreased bradykinin

199 The kallikrein-kinin system, along with the interlocking ren

200 Hemodialysis activates the kallikrein-kinin system, increasing bradykinin.

201 important role in the assembly of the plasma kallikrein-kinin system.

202 at plays a central role in activation of the kallikrein-kinin system.

203 ng cascade, the fibrinolytic system, and the kallikrein-kinin system.

204 or the assembly of the vasoregulatory plasma kallikrein-kinin system; thus we explored whether MPO an

205 The renin-angiotensin and kallikrein-kinin systems are key regulators of vascular

206 The renin-angiotensin and kallikrein-kinin systems engage in cross-talk at multipl

207 opposing roles of the renin-angiotensin and kallikrein-kinin systems in vivo, the distinct propertie

208 ole in the renin-angiotensin-aldosterone and kallikrein-kinin systems.

209 een GPCR that link the renin-angiotensin and kallikrein-kinin systems.

210 for thrombosis risk reduction via the plasma kallikrein/kinin and renin angiotensin systems.

211 In conclusion, kallikrein/kinin protects against cardiomyocyte apoptosi

212 Most of the cellular actions of kallikrein (KK) are thought to be mediated by bradykinin

213 t cell tryptase, trypsin, tissue factor, and kallikrein (KLK) 5 and KLK14, were assessed in bronchoal

214 in conventionally housed NC/Tnd mice reduced kallikrein (KLK) 5activity and ameliorated the dermatiti

215 Strikingly, six kallikrein (KLK)-related peptidase genes, namely KLK5, K

216 The human kallikrein (KLK)-related peptidases are the largest fami

217 t expression of a panel of serine proteinase kallikreins (KLK 5, 7, 8, and 10) is correlated with for

218 TSLP), cathelicidin, proteases, that is, the kallikreins (KLK)-5 and KLK-7, were observed as compared

219 hese regions include the proteolytic enzymes kallikrein (KLKB1) and Factor XII (F12).

220 Upregulation of kallikreins (KLKs) including KLK5 has been reported in a

221 ncided with increased expression of mRNA for kallikreins (KLKs), with KLK6, 13, and 14 showing the gr

222 ase (PRCP) activates prekallikrein to plasma kallikrein, leading to bradykinin liberation, and degrad

223 In contrast to the adjacent conserved kallikrein-like genes, the CD33rSiglec genes showed exte

224 emic pathologies through the deregulation of kallikrein-like proteinase (KLK) family members.

225 ne acetylation were also observed at another kallikrein locus (KLK2), at a third AR target locus (TMP

226 al" KLKs 1-3, which share an extended 99- or kallikrein loop near their non-primed substrate binding

227 Evidence implies that a panel of kallikrein markers improves the specificity and reduces

228 Levels of kallikrein markers were compared with biopsy outcome.

229 e prostate health index, and a panel of four kallikrein markers.

230 PSA testing intervals and reflex-testing of kallikrein-markers for men with modestly increased PSA v

231 Statistical models based on kallikrein-markers in blood improve the specificity at m

232 luding to some of the pathways through which kallikreins may be operating within the kidneys.

233 lasma protein factor XII (FXII) and leads to kallikrein-mediated cleavage of high molecular-weight ki

234 Inhibition of extracellular CA-I and kallikrein-mediated innate inflammation could provide ne

235 The protective effect of kallikrein on apoptosis and its signaling mediators was

236 The effect of kallikrein on cardiomyocyte survival was blocked by domi

237 prekallikrein (PK), the proenzyme of plasma kallikrein, on vascular endothelial cells is not fully d

238 KD1-L17R did not inhibit factor XIa, plasma kallikrein, or factor VIIa/tissue factor.

239 Antagonizing the kallikrein pathway augmented disease, while agonists dam

240 rence standard, directly activated the kinin-kallikrein pathway in human plasma, which can lead to th

241 results uncover a pathogenic matriptase-pro-kallikrein pathway that could operate in several human s

242 Plasma kallikrein (PK) cleaves high-molecular-weight kininogen

243 Plasma kallikrein (PK) has been identified in vitreous fluid ob

244 augmented expansion is ameliorated by plasma kallikrein (PK) inhibition or deficiency.

245 treal injections of autologous blood, plasma kallikrein (PK), bradykinin, and collagenase were perfor

246 Although plasma kallikrein (PKal) has been implicated in contributing to

247 Plasma kallikrein (pKal) proteolytically cleaves high molecular

248 type plasminogen activator (tPA), and plasma kallikrein (PKal).

249 Kallikreins play a pivotal role in establishing prostate

250 ancer is the most common type of cancer, and kallikreins play an important role in the establishment

251 Moreover, kallikrein promoted Bad.14-3-3 complex formation and inh

252 allikrein-kinin system are plasma and tissue kallikreins, proteases that cleave high molecular weight

253 r previous study has shown that human tissue kallikrein protected against ischemia/reperfusion-induce

254 h-molecular-weight kininogen, but not plasma kallikrein, protected mice from prostasome-induced letha

255 krein 14 and matriptase, (that initiates the kallikrein proteolytic cascade) constitutes an innovativ

256 (nMus m 1, rEqu c 1, Fel d 4, rCan f 1, 2), kallikrein (rCan f 5) and secretoglobin (rFel d 1)--was

257 ins encoded by two androgen-regulated genes, kallikrein related peptidase 4 (KLK4) and promyelocytic

258 al proteases are overactive in NS, including kallikrein-related peptidase (KLK) 5, KLK7, and elastase

259 d intact prostate-specific antigen (PSA) and kallikrein-related peptidase 2 (hK2)-can reduce unnecess

260 Human kallikrein-related peptidase 2 (KLK2) is a key serine pr

261 Human kallikrein-related peptidase 2 (KLK2) is a tryptic serin

262 Free human kallikrein-related peptidase 2 was targeted in prostate

263 onal antibody that is specific to free human kallikrein-related peptidase 2, an antigen abundant in m

264 enes coordinately expressed with WT1 was the kallikrein-related peptidase 3 (KLK3) gene commonly know

265 Kallikrein-related peptidase 3 (KLK3), which codes for p

266 t the secreted, extracellular protease KLK5 (kallikrein-related peptidase 5) is efficient in promotin

267 Human kallikrein-related peptidase 6 (KLK6) is a member of the

268 Human kallikrein-related peptidase 6 (KLK6) is highly expresse

269 forms are resistant to direct proteolysis by kallikrein-related peptidase 6 (KLK6), an extracellular

270 The cleavage preferences of Kallikrein-related peptidase 7 (KLK7) have previously be

271 on pave the way to a deeper understanding of kallikrein-related peptidase biology and pathology.

272 expressed during the secretory stage, while kallikrein-related peptidase-4 (Klk4) is predominantly e

273 Kallikrein-related peptidases (KLKs) are a group of seri

274 We hypothesized that kallikrein-related peptidases (KLKs), previously known t

275 5, 2 of the 15 serine proteases known as the kallikrein-related peptidases (KLKs).

276 In this study, we have determined that the kallikrein-related peptidases 5 and 12 are secreted from

277 Auto-activation of pro-inflammatory pro-kallikrein-related peptidases that are associated with s

278 trypsin, matriptase, plasmin, thrombin, four kallikrein-related peptidases, and several clotting fact

279 se inhibition of fluid-phase Factor XIIa and kallikrein requires lower C1INH levels than inhibition o

280 Cleavage of HK by plasma kallikrein results in release of the nonapeptide bradyki

281 evere asthmatics positive to fewer lipocalin/kallikrein/secretoglobin components.

282 and identified peptidylarginine deiminases, kallikreins, serine proteinase inhibitor family members,

283 eaction-based expression analysis of porcine kallikreins showed a complex expression pattern across d

284 ated with cleavage at the putative prostasin/kallikrein site and removal of the inhibitory tract with

285 alphaFXIIa, with support from alpha-kallikrein, subsequently accelerates contact activation

286 esults highlight the importance of the kinin-kallikrein system in the regulation of serum peptide lev

287 cytokine and complement inhibitors, and the kallikrein system.

288 ened against four serine proteases: plasmin, kallikrein, thrombin, and trypsin.

289 so possible to activate factor XII either by kallikrein, thus formed, or by plasmin.

290 cific protease inhibitors showed that tissue kallikrein (TK) processed pro-EGF in response to X/XO.

291 weight kininogen can be hydrolysed by plasma kallikrein to bradykinin and cleaved high-molecular-weig

292 oteases (thrombin, tPA, FXa, plasmin, plasma kallikrein, trypsin, FVIIa).

293 Elevated expression of kallikrein was detected in the kidney and urine of tamox

294 Inhibition of plasma kallikrein was observed at all doses, and the degree of

295 of the prekallikrein-HK complex to generate kallikrein was seen with each agonist that releases Hsp9

296 Activated factor XII generates plasma kallikrein, which proteolyzes kininogen, leading to the

297 ively open active site of plasmin and plasma kallikrein, while it is rejected from sterically demandi

298 le derivative 10 inhibits plasmin and plasma kallikrein with K(i) of 0.77 and 2.4 nM, respectively, w

299 bition of PRCP with Z-Pro-Prolinal or plasma kallikrein with soybean trypsin inhibitor, Pro-Phe-Arg-c

300 Local expression of kallikreins within the kidney has the capacity to dampen