ライフサイエンスコーパス: trypsinogen

1 psin levels compared with wild-type cationic trypsinogen.

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

3 positive for the exocrine enzymes lipase and trypsinogen.

4 tivation peptide functions in human cationic trypsinogen.

5 eropeptidase, the physiological activator of trypsinogen.

6 cidic pH inhibited autoactivation of anionic trypsinogen.

7 the cleavage of its physiological substrate, trypsinogen.

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

9 reatic hydrolases by cleaving and activating trypsinogen.

10 inogen appears to be less active than bovine trypsinogen.

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

12 ively than previously observed with cationic trypsinogen.

13 r, and acidic compartment where it activates trypsinogen.

14 e protease domain is structurally similar to trypsinogen.

15 does not require intra-acinar activation of trypsinogen.

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

17 leaved the calcium binding loop in all mouse trypsinogens.

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

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

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

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

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

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

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

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

26 , which alters the activation site Lys in T7 trypsinogen, abolished autoactivation while activation b

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

28 Trypsin-mediated trypsinogen activation (autoactivation) facilitates dige

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

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

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

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

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

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

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

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

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

38 Trypsinogen activation and trypsin activity were measure

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

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

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

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

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

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

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

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

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

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

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

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

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

52 Trypsinogen activation has traditionally held the spotli

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

69 Trypsinogen activation occurred in pancreatitis but not

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

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

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

73 A marker of trypsinogen activation partially localized to autophagic

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

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

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

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

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

79 CTRC cleavage of the trypsinogen activation peptide stimulates autoactivation

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

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

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

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

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

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

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

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

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

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

90 her through autoactivation (trypsin-mediated trypsinogen activation) or by the lysosomal protease cat

91 We tested the effects of CM4620 on SOCE, trypsinogen activation, acinar cell death, activation of

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 Trypsinogen activation, increased cathepsin B activity a

97 NFATc3 regulates trypsinogen activation, inflammation, and pancreatic tis

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

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

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

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

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

103 athepsin B activity and consequently reduced trypsinogen activation.

104 mouse model lacking pathologic intra-acinar trypsinogen activation.

105 systemic inflammation in AP does not require trypsinogen activation.

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

107 of this disease are vacuole accumulation and trypsinogen activation.

108 tially fatal disease caused by intracellular trypsinogen activation.

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

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

111 ities, but similar percentages of pancreatic trypsinogen activation.

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

113 potential sites of pathological intra-acinar trypsinogen activation.

114 thereby curtailing harmful intra-pancreatic trypsinogen activation.

115 pathologic calcium signaling independent of trypsinogen activation.

116 mechanism that can mitigate intrapancreatic 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 to inappropriate intracellular activation of trypsinogen and inflammatory pathways.

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

128 tions had increased pancreatic activation of trypsinogen and more edema, infiltration of lung and pan

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

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

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

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

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

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

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

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

137 ocatalytic degradation, relative to cationic trypsinogen and trypsin.

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

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

140 mouse enzymes demonstrated that CTRL cleaved trypsinogens and suppressed trypsin activation.

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

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

143 Rat trypsinogen appears to be less active than bovine trypsi

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

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

146 70s when the potential of the immunoreactive trypsinogen assay for early identification of infants wi

147 3 microM and kcat = 0.1 s-1); HL-BEK cleaved trypsinogen at pH 5.6 with 520-fold greater catalytic ef

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

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

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

151 We investigated whether trypsinogen becomes pathogenic only when its activation

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

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

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

155 Activation of trypsinogen by secretagogues in acinar cells was prevent

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

157 Trypsinogen can be activated to trypsin either through a

158 tease 1 gene (PRSS1), which encodes cationic trypsinogen, can accelerate its autoactivation and cause

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

160 ach other by hypoacetylated and inaccessible trypsinogen chromatin.

161 ntrations increased and serum immunoreactive trypsinogen concentrations decreased), and growth parame

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

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

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

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

166 leavage of the calcium binding loop promotes trypsinogen degradation.

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

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

169 in PRSS1 increases pancreatic activation of trypsinogen during secretagogue-induced pancreatitis.

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

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

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

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

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

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

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

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

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

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

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

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

182 bility by altering expression of the primary trypsinogen gene.

183 er associated with mutations in the cationic trypsinogen gene.

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

185 (2)=0.58, P=2 x 10(-)(5)) and immunoreactive trypsinogen (h(2)=0.52, P=3 x 10(-)(9)) also have a stro

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

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

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

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

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

191 d amylase, insulin, glucagon, lipase, and/or trypsinogen in 78 organ donor pancreata from birth throu

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

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

194 isruption of the locus that encodes cationic trypsinogen in mice (T7) causes loss of expression of th

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

196 Cathepsin B activates trypsinogen in these colocalized organelles.

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

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

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

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

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

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

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

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

205 Intracellular activation of trypsinogen is currently believed to initiate pancreatit

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

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

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

209 Autoactivation of cationic trypsinogen is proteolytically regulated by chymotrypsin

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

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

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

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

214 biochemical studies on novel mouse cationic trypsinogen (isoform T7) mutants engineered for selectiv

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

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

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

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

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

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

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

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

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

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

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

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

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

228 467.4 kbp) containing tandem AFGP, two TLP (trypsinogen-like protease), and surprisingly three chime

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

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

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

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

233 e that we successfully engineered a mouse T7 trypsinogen mutant (D22A,K24G), which is robustly activa

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

235 ion of mutations D22A and K24G resulted in a trypsinogen mutant that exhibited 14-fold increased acti

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

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

238 on the autoactivation of clinically relevant trypsinogen mutants.

239 Since the discovery of the first trypsinogen mutation in families with hereditary pancrea

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

241 Trypsinogen mutations that alter these regulatory cleava

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

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

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

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

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

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

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

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

250 Trypsinogen, procathepsin B, and IL-6 concentrations as

251 yme mixture composed of Chymotrypsinogen and Trypsinogen (PRP) on CSCs derived from a human pancreati

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

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

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

255 itary pancreatitis, associated with cationic trypsinogen (PRSS1) gene mutations.

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

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

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

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

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

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

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

263 A trypsinogen sample comprising several modifications was

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

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

266 le through knocking in mutations that render trypsinogen sensitive to CTSB but resistant to trypsin.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

283 The interacting trypsinogen variants showed similar affinity toward apro

284 The trypsinogen variants were separated and could be assigne

285 For most trypsinogen variants, shifts in electrophoretic mobility

286 Trypsinogen was activated efficiently by purified entero

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

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

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

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

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

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

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

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

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

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

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

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

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

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