ライフサイエンスコーパス: kallikrein

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

2 prekallikrein-HK autoactivation to generate kallikrein.

3 oxidants caused inactivation of both HK and kallikrein.

4 meet target levels for inhibition of plasma kallikrein.

5 ase 7 (KLK7) is a member of the human tissue kallikreins.

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

7 oup of endogenous proteolytic enzymes called kallikreins.

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

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

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

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

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

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

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

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

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

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

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

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

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

21 dapted influenza viruses by kallikrein 5 and kallikrein 12.

22 Here, we found that the protease kallikrein 13 (KLK13) was required for the infection of

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

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

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

26 d 8-fold increase versus the human glandular kallikrein 2 (hK2).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

46 Kallikrein 5 and kallikrein 12 were examined for their a

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

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

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

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

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

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

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

54 In VZV-infected skin, kallikrein 6 and the ubiquitin ligase MDM2 are upregulat

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

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

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

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

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

60 formation and growth by immunocytochemistry, kallikrein 8 (KLK8) mRNA by reverse transcription polyme

61 Previous work in our lab has identified Kallikrein-8 (KLK8) as a potential candidate since it sh

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

63 Similarly, purified kallikrein activated FIX in buffer and initiated TG in n

64 (SMTR/S and SLLR/S) strongly inhibit plasma kallikrein, activated FXII, and plasmin.

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

66 the classic FXIIa-FXI-FIX pathway and direct kallikrein activation of FIX.

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

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

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

70 that blocking the B2R and inhibiting plasma kallikrein activity might have an ameliorating effect on

71 sue swelling as a consequence of unregulated kallikrein activity or increased prekallikrein activatio

72 Kallikrein activity was inhibited while the renin-angiot

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

74 U-HAE moves through an unbalanced control of kallikrein activity, with bradykinin as most likely medi

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

76 Kallistatin is an inhibitor of tissue kallikrein and also inhibits the Wnt pathway.

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

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

79 e determined the relationship between plasma kallikrein and cardiovascular disease (CVD) outcomes as

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

86 Both kallikrein and plasmin activate factor XII; kallikrein i

87 is highly sensitive to activation by plasma kallikrein and plasmin, compared with FXII-WT or FXII-T3

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

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

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

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

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

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

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

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

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

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

100 Kallikreins belong to a family of serine proteases that

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

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

103 procal activation to the proteases FXIIa and kallikrein by a process that is enhanced by surfaces (co

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

105 ition of FXIIa by corn trypsin inhibitor and kallikrein by soybean trypsin inhibitor was necessary fo

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

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

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 tic efficiency ~1500-fold lower than that of kallikrein cleavage of HK.

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

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

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

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

117 Prostasin/kallikrein-cleaved gammaENaC was detected consistently o

118 Kallikrein cleaves high-molecular-weight kininogen (HK),

119 DHI also significantly increased serum kallikrein content in SHR.

120 d (2) a noncanonical pathway in which plasma kallikrein directly activates FIX, which ultimately resu

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

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

123 otensin, key RAS receptors, kinogen and many kallikrein enzymes that activate it, and both bradykinin

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

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

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

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

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

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

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

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

132 ubated in polystyrene plates and assayed for kallikrein formation.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

153 ) is an oral, once-daily inhibitor of plasma kallikrein in development for the prophylaxis of heredit

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

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

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

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

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

159 -induced TG in normal pooled plasma, whereas kallikrein inhibition alone was sufficient to abolish TG

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

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

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

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

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

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

166 main of TFPI1 had already yielded the potent kallikrein inhibitor, Kalbitor(R) (ecallantide), which i

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

168 alytic efficiency of deltaFXII activation by kallikrein is 15-fold greater than for full-length FXII.

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

170 Recent evidence suggests that the kallikrein-kinin and coagulation system might participat

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

200 ting a disturbed balance between the RAS and kallikrein-kinin systems.

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

202 Here, we identify plasma kallikrein (KK) as a specific direct modulator of BBB in

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

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

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

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

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

208 Kallikreins (KLK), a family of serine proteases with a d

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

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

211 zyme 2 (ACE-2), neprilysin (NEP), and plasma kallikrein (KLKB1) cleave and inactivate it, with the la

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

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

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

215 These novel findings indicate that plasma kallikrein level associates with the risk of any CVD and

216 The association between plasma kallikrein levels and the risk of any CVD remained signi

217 dels assessed the association between plasma kallikrein levels and the risk of CVD.

218 For MACE, higher plasma kallikrein levels were associated with higher risk in th

219 In unadjusted models, higher plasma kallikrein levels were associated with higher risk of an

220 Plasma kallikrein levels were measured longitudinally in 693 su

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

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

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

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

225 Levels of kallikrein markers were compared with biopsy outcome.

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

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

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

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

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

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

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

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

234 = 1.16 per 20 nmol/L higher levels of plasma kallikrein; P = 0.0177) as well as over the EDIC-only pe

235 Antagonizing the kallikrein pathway augmented disease, while agonists dam

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

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

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

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

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

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

242 recursor of the trypsin-like plasma protease kallikrein (PKa), which cleaves kininogens to release br

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

244 Plasma kallikrein (pKal) proteolytically cleaves high molecular

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

246 Kallikreins play a pivotal role in establishing prostate

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

248 oagulation involving factor XIIa (FXIIa) and kallikrein, promoting neutrophils to release the antimic

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

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

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

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

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

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

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

256 AR)-regulated prostate-specific enzyme human kallikrein-related peptidase 2 (hK2; KLK2).

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

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

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

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

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

262 reproductive system produced via cleavage by kallikrein-related peptidase 3 (KLK3), aka prostate-spec

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

264 pathway consisting of PRSS3/mesotrypsin and kallikrein-related peptidase 5 (KLK5) in lung adenocarci

265 cy or selectivity of existing inhibitors for kallikrein-related peptidase 5 and show that a variant w

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 Kallikrein-related peptidase 6 (KLK6) is a secreted seri

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

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

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

272 The serine protease kallikrein-related peptidase 7 (KLK7) is a member of the

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

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

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

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

277 5, 2 of the 15 serine proteases known as the kallikrein-related peptidases (KLKs).

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

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

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

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

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

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 e pathogenesis of severe COVID-19: the kinin-kallikrein system, resulting in acute lung inflammatory

288 cytokine and complement inhibitors, and the kallikrein system.

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

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

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

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

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

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

295 ct system leads to elevated levels of plasma kallikrein, which cleaves high molecular weight kininoge

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