ライフサイエンスコーパス: trypsinogen

1 utation of the catalytic Ser(200) residue in trypsinogen.

2 tivation peptide functions in human cationic trypsinogen.

3 eropeptidase, the physiological activator of trypsinogen.

4 cidic pH inhibited autoactivation of anionic trypsinogen.

5 ively than previously observed with cationic trypsinogen.

6 the cleavage of its physiological substrate, trypsinogen.

7 reatic hydrolases by cleaving and activating trypsinogen.

8 inogen appears to be less active than bovine trypsinogen.

9 t trypsin is 10(8)-fold more active than rat trypsinogen.

10 r, and acidic compartment where it activates trypsinogen.

11 increases the BPTI affinity and activity of trypsinogen.

12 reatic hydrolases by cleaving and activating trypsinogen.

13 also maintains the inactive conformation of trypsinogen.

14 inar cells and activation of CTSD, CTSB, and trypsinogen.

15 e protease domain is structurally similar to trypsinogen.

16 does not require intra-acinar activation of trypsinogen.

17 psin levels compared with wild-type cationic trypsinogen.

18 ergence from Thr-21 found in other mammalian trypsinogens.

19 leaved the calcium binding loop in all mouse trypsinogens.

20 mice for pancreatic gene products, including trypsinogen-2, amylase-2, elastase-1, elastase-2, and ch

21 correlated with promoter hypermethylation of trypsinogen-4 by bisulfite DNA sequence.

22 rains, including RIKEN cDNA 1810009J06 gene (trypsinogen 5), Ccl8, and Ccl6.

23 rom the pancreas of rats or mice (wild-type, trypsinogen 7, or cathepsin B-deleted) were stimulated w

24 We used novel trypsinogen-7 knock-out mice (T(-/-)), which lack intra-

25 ra-acinar activation of trypsinogen, such as trypsinogen-7-null (T(-/-)) and cathepsin B-null (CB(-/-

26 re containing ribonuclease A and alpha-chymo-trypsinogen A which exhibited very similar retention beh

27 ective displacer interacted with alpha-chymo-trypsinogen A, it had no interaction with ribonuclease A

28 ic adenocarcinomas (71%) also showed reduced trypsinogen accompanied by reduction in PAR2, a G protei

29 Trypsin-mediated trypsinogen activation (autoactivation) facilitates dige

30 in CP, study its pathogenesis in relation to trypsinogen activation (widely regarded as the key event

31 nduced pancreatitis, i.e., intra-acinar cell trypsinogen activation and acinar cell injury.

32 ulating concentration of cerulein results in trypsinogen activation and acinar cell injury.

33 cleavages lead to increased intrapancreatic trypsinogen activation and cause hereditary pancreatitis

34 The signaling mechanisms that regulate trypsinogen activation and inflammation in acute pancrea

35 he relative contributions of intrapancreatic trypsinogen activation and nuclear factor kappa B (NFkap

36 ivo enhanced cerulein-induced (50 microg/kg) trypsinogen activation and pancreatic edema.

37 trate that Itmap1 plays an essential role in trypsinogen activation and that both impaired and augmen

38 ht to play a central role in intrapancreatic trypsinogen activation and the onset of experimental pan

39 Trypsinogen activation and trypsin activity were measure

40 dependent alterations in cathepsin B-induced trypsinogen activation are not the cause of hereditary p

41 for the first time to observe, in real time, trypsinogen activation by caerulein in the pancreatic ca

42 ations do not lead to increased or decreased trypsinogen activation by cathepsin B.

43 kappa B degradation by Western blotting, and trypsinogen activation by fluorogenic assay.

44 efore investigated the site of intracellular trypsinogen activation by using an established cellular

45 ivation and that both impaired and augmented trypsinogen activation can be associated with increased

46 Premature activation of trypsinogen activation can cause pancreatic injury and h

47 ts of Asp(19-22) had minimal or no effect on trypsinogen activation catalyzed by human enteropeptidas

48 he concentration of wortmannin that inhibits trypsinogen activation causes a 75% decrease in phosphat

49 It became clear that intra-acinar trypsinogen activation contributes to early acinar injur

50 entrations of caerulein that induced ex vivo trypsinogen activation do not significantly increase pho

51 previously shown to occur concurrently with trypsinogen activation during early stages of pancreatit

52 RECENT FINDINGS: Pathologic intra-acinar trypsinogen activation had been hypothesized to be the c

53 Trypsinogen activation has traditionally held the spotli

54 f note, the CTSD KO greatly reduced CTSB and trypsinogen activation in acinar cells, and CTSD directl

55 he relationship of ER stress to intra-acinar trypsinogen activation in pancreatic injury.

56 ate lipid accumulation in hepatic steatosis, trypsinogen activation in pancreatitis, and hepatitis vi

57 Absence of trypsinogen activation in T(-/-) mice led to near comple

58 onic pancreatitis developed independently of trypsinogen activation in the caerulein model.

59 The role of trypsinogen activation in the pathogenesis of acute panc

60 s depends on endocytic vacuole formation and trypsinogen activation in this compartment.

61 vation peptide 4-fold and causes accelerated trypsinogen activation in vitro.

62 tophagosomes results in cathepsin B-mediated trypsinogen activation induced by caerulein.

63 mediated apoptosis depends on intravesicular trypsinogen activation induced by CTSB, not CTSB activit

64 entification of the cellular compartment for trypsinogen activation is inconclusive.

65 Ex vivo, caerulein-induced trypsinogen activation is inhibited by wortmannin and LY

66 Although the mechanism of NFkappaB and trypsinogen activation is not entirely clear, further in

67 Intra-acinar trypsinogen activation leads to acinar death during earl

68 Intra-acinar trypsinogen activation leads to early pancreatic injury,

69 nt with the notion that cathepsin B-mediated trypsinogen activation might play a pathogenic role in h

70 Trypsinogen activation occurred in pancreatitis but not

71 calized with cleaved BZiPAR, indicating that trypsinogen activation occurred within endocytic vacuole

72 The cellular compartment in which trypsinogen activation occurs currently is unknown.

73 the identified genes have been connected to trypsinogen activation or trypsin inactivation.

74 A marker of trypsinogen activation partially localized to autophagic

75 We investigated the use of an assay of trypsinogen activation peptide (TAP).

76 y cleave the Phe18-Asp19 peptide bond in the trypsinogen activation peptide and remove the N-terminal

77 Finally, processing of the trypsinogen activation peptide at Phe-18 by CTRC inhibit

78 by wet/dry weight ratio, plasma amylase, and trypsinogen activation peptide in the pancreas.

79 There was no difference in trypsinogen activation peptide levels between caerulein-

80 Thus, cleavage of the trypsinogen activation peptide or the calcium binding lo

81 CTRC cleavage of the trypsinogen activation peptide stimulates autoactivation

82 the rate of autoactivation by processing the trypsinogen activation peptide to a shorter form.

83 after induction of necrotizing pancreatitis; trypsinogen activation peptide was measured to quantify

84 rved tetra-aspartate (Asp19-22) motif in the trypsinogen activation peptide.

85 esidues of peptidyl substrates that resemble trypsinogen activation peptides such as Val-(Asp)4-Lys.

86 tion; while at pH 5.0, inhibition of anionic trypsinogen activation resulted in lower trypsin yields.

87 he idea that a very early event is premature trypsinogen activation triggered by lysosomal cathepsin

88 s protein degradation, but these depended on trypsinogen activation via CTSB.

89 In contrast, rates of trypsinogen activation were markedly reduced with increa

90 The Ca(2+) signal and trypsinogen activation were similarly reduced in acini i

91 They suggest that the HSP acts by preventing trypsinogen activation within acinar cells.

92 ated early in acinar cells, independently of trypsinogen activation, and might be responsible for pro

93 d macrophage inflammatory protein 2 (CXCL2), trypsinogen activation, and tissue damage in the pancrea

94 eatic diseases does not affect physiological trypsinogen activation, but significantly limits trypsin

95 urolithocholic acid 3-sulfate responded with trypsinogen activation, decreased cell viability, organe

96 NFATc3 regulates trypsinogen activation, inflammation, and pancreatic tis

97 which occurs parallel to but independent of trypsinogen activation, may be crucial in pancreatitis.

98 dministration of trehalose largely prevented trypsinogen activation, necrosis, and other parameters o

99 ed by trypsin, and chymotrypsin C stimulates trypsinogen activation, these reactions establish a posi

100 k-out mice (T(-/-)), which lack intra-acinar trypsinogen activation, to clarify the relationship of E

101 of the duodenum, chymotrypsin C facilitates trypsinogen activation, whereas in the lower intestines,

102 systemic inflammation in AP does not require trypsinogen activation.

103 ough an antiapoptotic effect, rather than by trypsinogen activation.

104 of this disease are vacuole accumulation and trypsinogen activation.

105 tially fatal disease caused by intracellular trypsinogen activation.

106 dihydrochloride (BZiPAR) was used to detect trypsinogen activation.

107 activity of trypsin, rather than by reducing trypsinogen activation.

108 ities, but similar percentages of pancreatic trypsinogen activation.

109 (NF-kappa B), abnormal Ca(2+) responses, and trypsinogen activation.

110 potential sites of pathological intra-acinar trypsinogen activation.

111 nhibitor, prevents cerulein-induced in vitro trypsinogen activation.

112 thereby curtailing harmful intra-pancreatic trypsinogen activation.

113 pathologic calcium signaling independent of trypsinogen activation.

114 mechanism that can mitigate intrapancreatic trypsinogen activation.

115 athepsin B activity and consequently reduced trypsinogen activation.

116 mouse model lacking pathologic intra-acinar trypsinogen activation.

117 and intrapancreatic digestive enzyme (i.e., trypsinogen) activation.

118 noteworthy that the well known pathological trypsinogen activator cathepsin B exhibited a preference

119 Significant stabilization of anionic trypsinogen against degradation was achieved by simultan

120 by CTRC inhibited autoactivation of anionic trypsinogen, although cationic trypsinogen was strongly

121 In mixtures of cationic and anionic trypsinogen, an increase in the proportion of the anioni

122 cathepsin B are both secreted together with trypsinogen and active trypsin into the pancreatic juice

123 A synergetic anti-tumour effect for Trypsinogen and Chymotrypsinogen A was determined at a r

124 present a combination of the two pro-enzymes Trypsinogen and Chymotrypsinogen A with potent in vitro

125 ow conformational changes upon activation of trypsinogen and formation of noncovalent complexes betwe

126 lein-induced pancreatitis, concentrations of trypsinogen and its activation peptide TAP were measured

127 gen-active enzyme pairs of chymotrypsinogen, trypsinogen and prethrombin-2 showed a similar distribut

128 r the natural CTRC substrates human cationic trypsinogen and procarboxypeptidase A1.

129 necessary for intrapancreatic activation of trypsinogen and regulating the severity of acute pancrea

130 ) protects against pancreatitis by degrading trypsinogen and thereby curtailing harmful intra-pancrea

131 at pH 8.0, selective degradation of anionic trypsinogen and trypsin caused diminished trypsin produc

132 imary structure, we found that human anionic trypsinogen and trypsin exhibited a significantly increa

133 th an imbalance between CatL, which degrades trypsinogen and trypsin, and CatB, which converts trypsi

134 ocatalytic degradation, relative to cationic trypsinogen and trypsin.

135 in activity by promoting degradation of both trypsinogen and trypsin.

136 ombinantly expressed and purified both human trypsinogens and documented characteristics of autoactiv

137 that regulates activation and degradation of trypsinogens and procarboxypeptidases by targeting speci

138 alues of kcat/Km and BPTI affinity of mutant trypsinogens and trypsins.

139 e cathepsin B (CTSB) is a known activator of trypsinogen, and its deletion reduces disease severity i

140 cellular Ca(2+) mobilization, Ca(2+) influx, trypsinogen, and NF-kappa B activation were all diminish

141 Rat trypsinogen appears to be less active than bovine trypsi

142 gogue-induced pancreatitis, large amounts of trypsinogen are present in the interstitium and drain vi

143 Even though the two trypsinogens are approximately 90% identical in their pr

144 nique attributes of the lamprey and tunicate trypsinogens are noted.

145 70s when the potential of the immunoreactive trypsinogen assay for early identification of infants wi

146 3 microM and kcat = 0.1 s-1); HL-BEK cleaved trypsinogen at pH 5.6 with 520-fold greater catalytic ef

147 ypsin C (CTRC) is a proteolytic regulator of trypsinogen autoactivation in humans.

148 by CTRC-dependent dysregulation of cationic trypsinogen autoactivation, which results in elevated tr

149 .D19A, p.D22G, and p.K23R strongly stimulate trypsinogen autoactivation.

150 c reversal of the isoform ratio, and anionic trypsinogen becomes the predominant zymogen secreted.

151 procedure, we expressed (15)N-labeled S195A trypsinogens, both on a wild-type and on a D189S backgro

152 ing event is the intracellular activation of trypsinogen by cathepsin B (CTSB), which can be induced

153 Activation of trypsinogen by secretagogues in acinar cells was prevent

154 ze the regulation of autoactivation of mouse trypsinogens by mouse Ctrc.

155 anscripts for mast cell protease 1, cationic trypsinogen, carboxypeptidase A, IL-5, and phospholipase

156 ach other by hypoacetylated and inaccessible trypsinogen chromatin.

157 tion suggests that BPTI binds to an "active" trypsinogen conformation that is not kinetically accessi

158 e activation peptide stabilizes the inactive trypsinogen conformation.

159 The activation peptide of vertebrate trypsinogens contains a highly conserved tetra-aspartate

160 Deletion of T7 reduced the total trypsinogen content by 60% but did not affect physiologi

161 y chymotrypsin C (CTRC) resulting in reduced trypsinogen degradation and increased autoactivation.

162 The observations suggest that autocatalytic trypsinogen degradation may be an important defense mech

163 leavage of the calcium binding loop promotes trypsinogen degradation.

164 appears identical to enzyme Y, the enigmatic trypsinogen-degrading activity described by Heinrich Rin

165 igher in Ca(2+) than in EDTA, while [Thr(21)]trypsinogen demonstrated inverse characteristics.

166 the presence and absence of Ca(2+), [Ile(21)]trypsinogen exhibited significantly higher stability aga

167 This unique biochemical property of anionic trypsinogen explains the lack of association of PRSS2 mu

168 We investigated trypsinogen expression at the RNA level in 49 esophageal

169 nd 9 of 13 ESCC cell lines were silenced for trypsinogen expression.

170 activation of wild type and all three mutant trypsinogen forms was essentially identical under a wide

171 icle for speculation on the evolution of the trypsinogen gene family as well as the general modes of

172 utations have been described in the cationic trypsinogen gene in patients with hereditary pancreatiti

173 fied a single R117H mutation in the cationic trypsinogen gene in several kindreds with an inherited f

174 Neither mutations in the cationic trypsinogen gene nor mutations of the cystic fibrosis co

175 and in codons 16, 22, and 23 of the cationic trypsinogen gene) and act as disease modifiers.

176 e interval extending from Prss2 (the most 3' trypsinogen gene) to D(beta)1.

177 tations at codons 29 and 122 of the cationic trypsinogen gene), whereas others have a low penetrance

178 s in understanding mutations in the cationic trypsinogen gene, the pancreatic secretory trypsin inhib

179 itment of the 5' and 3' ends of an ancestral trypsinogen gene, which provided the secretory signal an

180 er associated with mutations in the cationic trypsinogen gene.

181 bility by altering expression of the primary trypsinogen gene.

182 chromatin containing Tcrb gene segments and trypsinogen genes, respectively.

183 zation and analyses of notothenioid AFGP and trypsinogen genes.

184 (2)=0.58, P=2 x 10(-)(5)) and immunoreactive trypsinogen (h(2)=0.52, P=3 x 10(-)(9)) also have a stro

185 in the activation peptide of human cationic trypsinogen have been found in patients with chronic pan

186 AIP against pancreas-specific antigens like trypsinogens I and II, pancreatic secretory trypsin inhi

187 rg(117) --> His and Asn(21) --> Ile in human trypsinogen-I have been recently associated with heredit

188 as a zymogen because sequence alignment with trypsinogen identified a putative cleavage site for acti

189 tation, Thr(21) in the highly homologous rat trypsinogen-II was replaced with Asn or Ile, and the rec

190 site was also delayed in trypsin relative to trypsinogen in a calcium-dependent manner, but for this

191 ibe here the high-level expression of bovine trypsinogen in E. coli, its refolding and activation to

192 tions indicate that up-regulation of anionic trypsinogen in pancreatic diseases does not affect physi

193 ls, and CTSD directly activated CTSB but not trypsinogen in vitro During pancreatitis in pancreas-spe

194 eatitis-associated mutation A16V in cationic trypsinogen increases the rate of chymotrypsin C-mediate

195 Expression of PACE-trypsinogen induced apoptosis of HEK293 cells and pancre

196 Activation of this extracellular trypsinogen induces hemorrhagic necrosis in a setting of

197 inogen and trypsin, and CatB, which converts trypsinogen into trypsin, resulting in intra-acinar accu

198 Circulating immunoreactive trypsinogen (IRT), a biomarker of exocrine pancreatic di

199 acellular activation of the digestive enzyme trypsinogen is considered to be the initiating event in

200 the observations indicate that human anionic trypsinogen is controlled by CTRC in a manner that indiv

201 Intracellular activation of trypsinogen is currently believed to initiate pancreatit

202 ation of digestive enzyme zymogens including trypsinogen is generally believed to be an early and cri

203 Autoactivation of human cationic trypsinogen is inhibited by a repulsive electrostatic in

204 In pancreatitis, when trypsinogen is prematurely activated, PAR-2-mediated duc

205 Autoactivation of cationic trypsinogen is proteolytically regulated by chymotrypsin

206 ctivation of N-terminally truncated cationic trypsinogen is stimulated approximately 3-fold, and this

207 DeltaI16V17 trypsinogen is the lone outlier; its BPTI affinity is hi

208 We conclude that autoactivation of mouse trypsinogens is under the control of mouse Ctrc with som

209 tide bond of human cationic trypsin, but not trypsinogen, is thermodynamically stable, such that clea

210 We generated and characterized mice lacking trypsinogen isoform 7 (T7) gene (T(-/-)).

211 psin C also rapidly degrades all three human trypsinogen isoforms and appears identical to enzyme Y,

212 found that the mouse pancreas expresses four trypsinogen isoforms to high levels, T7, T8, T9, and T20

213 uman pancreatic secretions contain two major trypsinogen isoforms, cationic and anionic trypsinogen,

214 The human pancreas expresses two major trypsinogen isoforms, cationic trypsinogen (PRSS1) and a

215 vation of mesotrypsinogen of all three human trypsinogen isoforms, suggesting a biochemical mechanism

216 idase reduced the apparent molecular mass of trypsinogen IV from 36 to 30 kDa and generated enzymatic

217 Trypsinogen IV was cloned from PC-3 cells and expressed

218 Immunoreactive trypsinogen IV was detected in vesicles in these cells.

219 We expressed trypsinogen IV with an N-terminal Igkappa signal peptide

220 lasminogen activator, factor XII, protein C, trypsinogen IV, and a protease that we refer to as membr

221 lonic mucosa expressed mRNA encoding PAR(2), trypsinogen IV, and enteropeptidase, which activates the

222 In cerulein pancreatitis, trypsinogen levels increased prominently and were highes

223 espite a 4.5-fold increase in total cellular trypsinogen levels, are fully protected from intracellul

224 467.4 kbp) containing tandem AFGP, two TLP (trypsinogen-like protease), and surprisingly three chime

225 Ile16 from trypsin is expected to produce a trypsinogen-like protein since the Ile16-Asp194 salt bri

226 lassical proteolytic activation mechanism of trypsinogen-like serine proteinase zymogens, insertion o

227 tion, specific trypsinogen mutations lead to trypsinogen misfolding, endoplasmic reticulum stress, an

228 y suppressed autoactivation of human anionic trypsinogen more effectively than previously observed wi

229 Strikingly, a tetra-Ala(19-22) trypsinogen mutant devoid of acidic residues in the acti

230 We found that in the presence of CTRC, trypsinogen mutants associated with classic hereditary p

231 Increased intrapancreatic autoactivation of trypsinogen mutants has been hypothesized to initiate th

232 on the autoactivation of clinically relevant trypsinogen mutants.

233 In addition, specific trypsinogen mutations lead to trypsinogen misfolding, en

234 Trypsinogen mutations that alter these regulatory cleava

235 e, myeloperoxidase, and CXCL2; activation of trypsinogen; necrosis of acinar cells; edema; leukocyte

236 r trypsinogen isoforms, cationic and anionic trypsinogen, normally at a ratio of 2 : 1.

237 We expand the already large number of known trypsinogen nucleotide and amino acid sequences by prese

238 ts were screened by measuring immunoreactive trypsinogen on dried blood spots (from April 1985 throug

239 ride, specifically prevented the cleavage of trypsinogen or Gly-(Asp)4-Lys-beta-naphthylamide and red

240 pancreatic cancer involve germline cationic trypsinogen or PRSS1 mutations (hereditary pancreatitis)

241 In the current study, a mutant trypsinogen (paired basic amino acid cleaving enzyme (PA

242 Primary endpoints were urine trypsinogen positive days and overall complications (Cla

243 Human cationic trypsinogen, precursor of the digestive enzyme trypsin,

244 f a 9-nt Thr-Ala-Ala coding element from the trypsinogen progenitor to create a new protein coding re

245 Missense mutations in human cationic trypsinogen PRSS1 are frequently detected in patients wi

246 ses two major trypsinogen isoforms, cationic trypsinogen (PRSS1) and anionic trypsinogen (PRSS2).

247 Mutations in human cationic trypsinogen (PRSS1) cause autosomal dominant hereditary

248 /or chronic pancreatitis, including cationic trypsinogen (PRSS1), anionic trypsinogen (PRSS2), serine

249 enes encoding a trypsin inhibitor (PSTI) and trypsinogen (PRSS1).

250 luding cationic trypsinogen (PRSS1), anionic trypsinogen (PRSS2), serine protease inhibitor Kazal 1 (

251 ms, cationic trypsinogen (PRSS1) and anionic trypsinogen (PRSS2).

252 In contrast to this striking difference in trypsinogen recognition, the small synthetic substrate G

253 Hydrocortisone treatment did not alter trypsinogen release (2 or more positive days 46% vs 50%)

254 nd 2.6-fold increase in cellular amylase and trypsinogen, respectively.

255 gamma differs from those for the Ca(2+) and trypsinogen responses.

256 A trypsinogen sample comprising several modifications was

257 on intracellularly, which leads to decreased trypsinogen secretion and eventual acinar cell death.

258 We found that relative to wild-type trypsinogen, secretion of the mutants from transfected c

259 mino acid sequences by presenting additional trypsinogen sequences from the tunicate (Boltenia villos

260 The current array of known trypsinogen sequences now spans the entire vertebrate ph

261 are unable to verify this role for His40 in trypsinogen since the mutation of His40 to Phe appears t

262 sive trypsin generation in the pancreas, and trypsinogen stabilization by the Asn(21) --> Ile mutatio

263 Mice that lack intra-acinar activation of trypsinogen, such as trypsinogen-7-null (T(-/-)) and cat

264 autolysis loop and the activation peptide in trypsinogen, suggesting the cleaved autolysis loop may d

265 Likewise, trypsinogen template DNA-coated magnetic beads (2.8 mum

266 1985 through June 1991) or by combining the trypsinogen test with DNA analysis (from July 1991 throu

267 uent amino acid change found in the cationic trypsinogen (Tg) of patients with hereditary pancreatiti

268 lfide bond formation of a secretory protein, trypsinogen (TG), that behaves in vitro as a stringent,

269 Mutation Asn-21 --> Ile in human cationic trypsinogen (Tg-1) has been associated with hereditary p

270 f BPTI association is slower for DeltaI16V17 trypsinogen than for a mutant trypsinogen with a similar

271 can reduce the intrapancreatic activation of trypsinogen that occurs during two dissimilar experiment

272 e results demonstrate that in human cationic trypsinogen the Asp(19-22) motif per se is not required

273 ation, enteropeptidase cleaves and activates trypsinogen, thereby initiating the activation of other

274 increases the BPTI affinity and activity of trypsinogen to an even greater extent; thus, removal of

275 Increased sensitivity of anionic trypsinogen to CTRC-mediated degradation was due to an a

276 Our results reveal that the trypsinogen to trypsin conformational switch modulates c

277 The prototypical trypsinogen-trypsin system is an example of a minimally

278 ly reduced with increasing ratios of anionic trypsinogen under conditions that were typical of potent

279 activation peptide mutants of human cationic trypsinogen undergo autoactivation intracellularly, whic

280 The interacting trypsinogen variants showed similar affinity toward apro

281 The trypsinogen variants were separated and could be assigne

282 For most trypsinogen variants, shifts in electrophoretic mobility

283 Trypsinogen was activated efficiently by purified entero

284 The expression of the mutant trypsinogen was assessed by immunohistochemical staining

285 We found that PACE-trypsinogen was expressed in the secretory pathway and w

286 Activation of extracellular trypsinogen was induced by intravenous infusion of enter

287 on of anionic trypsinogen, although cationic trypsinogen was strongly stimulated.

288 nding of the protease inhibitor aprotinin to trypsinogen was used as protein-protein affinity model.

289 se, serine (PRSS) 3, a major extrapancreatic trypsinogen, was optimum at pH 8.0, and predominantly de

290 of aprotinin, both free and aprotinin-bound trypsinogen were detected revealing a 1:1 binding stoich

291 The effects of pathologic activation of trypsinogen were studied in these mice during induction

292 mogen degradation in [Asn(21)]- and [Ile(21)]trypsinogens were higher in Ca(2+) than in EDTA, while [

293 This stands in stark contrast to cationic trypsinogen where single mutations of either Leu-81 or A

294 present work identifies several features of trypsinogen which govern its activity.

295 ired basic amino acid cleaving enzyme (PACE)-trypsinogen), which is activated intracellularly by the

296 have higher activity and BPTI affinity than trypsinogen, which indicates that the activation peptide

297 The intracellular activation of trypsinogen, which is both pH- and calcium-dependent, is

298 T(-/-) mice lacked pathologic activation of trypsinogen, which occurs within acinar cells during ear

299 or DeltaI16V17 trypsinogen than for a mutant trypsinogen with a similar BPTI affinity.

300 zed activation of recombinant human cationic trypsinogen with hereditary pancreatitis-associated muta