ライフサイエンスコーパス: zymogen

1 allosterically preventing activation of its zymogen.

2 mediated non-proteolytic activation of FXIII zymogen.

3 when the activated protease cleaves its own zymogen.

4 iptase to activate the endogenous matriptase zymogen.

5 making this proenzyme a remarkably inactive zymogen.

6 ligomeric transmembrane sheddase, and of its zymogen.

7 rtue of its nonproteolytic activation of the zymogen.

8 MT1-MMP is synthesized as a zymogen.

9 tial mechanism for engineering an artificial zymogen.

10 metalloproteinase (TIMP)-free status of the zymogen.

11 hich depended on the TIMP-free status of the zymogen.

12 osegment of 176 amino acid residues from the zymogen.

13 minant of the structure and function of this zymogen.

14 hibit activation of the highly related MMP-2 zymogen.

15 biquitination of the unprocessed form of the zymogen.

16 bacterial subtilisin and are synthesized as zymogens.

17 ctly or indirectly by activating HA-cleaving zymogens.

18 y of proteases that are secreted as inactive zymogens.

19 tion of the blood coagulation and complement zymogens.

20 Mechanisms of zymogen activation - pathologic calcium signaling, pH ch

21 educed the sensitizing effects of low pHe on zymogen activation and cellular injury.

22 her insight into the roles and mechanisms of zymogen activation and inflammatory pathways in pancreat

23 ncreatic acinar cell to secretagogue-induced zymogen activation and injury and may increase the risk

24 in early secretagogue-induced pancreatitis (zymogen activation and injury) were examined in rats (1)

25 rom 7.6 to 6.8 enhanced secretagogue-induced zymogen activation and injury, but did not affect secret

26 nus of the heavy chain, which is formed upon zymogen activation and inserts into the protein core, is

27 tension and cardiac hypertrophy impair corin zymogen activation and natriuretic peptide processing ac

28 s novel and unexpected features of SKI-1/S1P zymogen activation and subcellular specificity of activi

29 ability of plasminogen to induce matriptase zymogen activation and the subsequent acceleration of pl

30 t matriptase and prostasin form a reciprocal zymogen activation complex with unique features.

31 Thus, cofactor and zymogen activation did not contribute to DHG inhibition

32 ifferentiation, we found elevated matriptase zymogen activation during early stages of epidermal diff

33 Zymogen activation imparts proteolytic activity to throm

34 Targeting zymogen activation in this manner may also allow for pha

35 vel class of matriptase inhibitors targeting zymogen activation is developed by a combination of the

36 or thrombin and prethrombin-2 indicates that zymogen activation is linked to a significant shift in t

37 We have reported that zymogen activation is mediated by the vacuolar ATPase (v

38 Zymogen activation of SKI-1/S1P involves sequential auto

39 Zymogen activation of SKI-1/S1P requires removal of an N

40 ty in T555I/Q568P variant and found that the zymogen activation of the corin variant was impaired sig

41 In addition, matriptase zymogen activation was predominantly detected in the bas

42 This study investigates the dynamics of zymogen activation when both extrinsic tenase and prothr

43 After matriptase zymogen activation, a proportion of active matriptase is

44 However, reduced pHe alone had no effect on zymogen activation, amylase secretion, or cell injury.

45 llular calcium transients, intra-acinar cell zymogen activation, and acinar cell injury.

46 Zymogen activation, observed within acini early during a

47 responsible for the induction of matriptase zymogen activation, was shown to be plasminogen.

48 ostasin, which is a co-factor for matriptase zymogen activation.

49 on that CTRC is a key regulator of digestive zymogen activation.

50 (100 nmol/L), blocked the low pHe effects on zymogen activation.

51 nduced phosphorylation of ERK1/2 or Akt is a zymogen activity, not an enzymatic event.

52 )-S195A, but not other procoagulant protease zymogens, also results in initiation of protective intra

53 d in two forms in the epidermis: a one-chain zymogen and a two-chain proteolytically active form, gen

54 nd to the so-called activation domain of the zymogen and changed the conformation of mature PR3, resu

55 factor X activation under flow showing that zymogen and enzyme membrane binding events further regul

56 otease, prostasin, to activate the prostasin zymogen and initiate a proteolytic cascade that is requi

57 In addition, zymogen and neck cell markers were coexpressed in the sa

58 Both the zymogen and protease undergo a pre-existing equilibrium

59 compound that inhibited activation of MMP-9 zymogen and subsequent generation of catalytically activ

60 Then, the structures of both caspase-6 zymogen and the Ac-VEID-CHO peptide inhibitor complex de

61 inhibitor of metalloproteinases (TIMP)-free zymogen and the catalytic activity of the activated enzy

62 otein that were thought to be dynamic in the zymogen and to become rigid upon activation, in particul

63 glycoprotein that circulates in plasma as a zymogen and when converted to proteolytically active pla

64 n-like proteases are synthesized as inactive zymogens and convert to the mature form upon activation

65 e (TACE or ADAM17), ADAM10 is expressed as a zymogen, and removal of the prodomain results in its act

66 r their ability to activate the thrombolytic zymogens, and both resulted in activation of each zymoge

67 ients, intracellular activation of digestive zymogens, and cell injury when these responses are induc

68 s that reveal the active conformation of the zymogens, and the structure of a partially matured C7:P7

69 s caspase-7, are stored as inactive protease zymogens, and when activated, lead to a fate-determining

70 sible equilibration of meizothrombin between zymogen- and proteinase-like states provides new insight

71 nversions of thrombin between a continuum of zymogen- and proteinase-like states.

72 Human alpha- and beta-protryptase zymogens are abundantly and selectively produced by mast

73 be parked on the hub, when an odd number of zymogens are bound.

74 , biological mechanisms for processing these zymogens are uncertain.

75 ified procaspase-8 (procasp8), the caspase-8 zymogen, as a cytosolic target for Lyn in B-CLL cells, t

76 fluorescence microscopy, we observed the Mpl zymogen associated with the bacterium at physiological p

77 a) activates factor IX (FIX) by cleaving the zymogen at Arg(145)-Ala(146) and Arg(180)-Val(181) bonds

78 Zymogen autoactivation is explained by conformational se

79 The zymogen autoactivation rate of MASP-1 is approximately 3

80 for the facile production of enzymes through zymogen autoactivation that is broadly applicable to try

81 oactivation of MASPs occurs in two steps: 1) zymogen autoactivation, when one proenzyme cleaves anoth

82 VesB is likely produced as a zymogen because sequence alignment with trypsinogen iden

83 parently counteracted the negative effect of zymogen binding; a small impact was observed at endogeno

84 report propeptide processing of the ADAMTS15 zymogen by furin activity, identifying RAKR(212) downwar

85 is, we determined the crystal structure of a zymogen C1s construct (comprising two complement control

86 se and C3 convertase, as well as the unbound zymogen C2 obtained by small angle x-ray scattering anal

87 omain of c-FLIP(L) alone and in complex with zymogen C8 identify the unique determinants that favor h

88 zation, and induce the latent active site of zymogen C8 into a productive conformation.

89 her vitamin K-dependent coagulation protease zymogens can modulate PAR-dependent signaling responses

90 We show that these intein "zymogens" can be used to create protein sensors and actu

91 indicating disrupted differentiation of the zymogen cell lineage from the mucous neck cells in the s

92 nd reductions in the numbers of parietal and zymogen cells in Slc26a9(-/-) stomach.

93 h controls, numbers of total mucous neck and zymogen cells were significantly decreased in stomachs o

94 dependent activity than purified recombinant zymogen cFVII.

95 The pancreatic zymogen, chymotrypsin C, can degrade pathologically acti

96 structural pocket in proximity to the MMP-9 zymogen cleavage site near Arg-106, which is distinct fr

97 teinase formation beyond simply reporting on zymogen cleavage.

98 d that its own proteolytic activity mediates zymogen cleavage.

99 stribution of CTSD from the lysosomal to the zymogen-containing subcellular compartment of acinar cel

100 ed prostasin in hair follicles, dependent on zymogen conversion by matriptase.

101 iptase activation requires neither prostasin zymogen conversion nor prostasin catalytic activity.

102 Prostasin zymogen conversion to active prostasin is dependent on m

103 n matriptase but does not require matriptase zymogen conversion.

104 Pepsin, a zymogen-derived enzyme, without its prosegment (PS), is

105 e to proteolytically activate the matriptase zymogen directly but induces matriptase activation indir

106 Central to this paradigm is that the zymogen does not convert spontaneously to the mature enz

107 mplications for the transport of coagulation zymogens/enzymes in the interstitial spaces during clot

108 etition of activated factor VII (FVIIa) with zymogen factor VII (FVII) for tissue factor (TF) and loa

109 RNA(11F7t) binds equivalently to the zymogen factor X as well as derivatives lacking gamma-ca

110 The serine protease zymogen factor X is converted to its catalytically activ

111 Interestingly, zymogen factor XI bound SPGG with high affinity, suggest

112 The plasma zymogens factor XII (fXII) and factor XI (fXI) contribut

113 The zymogen, factor XI, and the enzyme, factor XIa, interact

114 ssing includes proteolytic activation of the zymogen for lysyl oxidase.

115 overcome competition between FVIIa and FVII zymogen for tissue factor (TF) binding, and (2) a high-d

116 Based on plasma-clotting assays, the target zymogen for VWbp may be ProT, but this has not been veri

117 a domain is not required for F12 to bind the zymogen form more favorably.

118 ree and PS-bound states, and pepsinogen, the zymogen form of pepsin.

119 te and trapped a conformation similar to the zymogen form of the enzyme.

120 ct, we determined the 2.6-A structure of the zymogen form of the G666E mutant of MASP-3.

121 These findings suggest that the zymogen form of thrombin possesses conformational plasti

122 The cleavage site for the conversion of the zymogen form to active enzyme was also identified betwee

123 It is synthesized in the zymogen form, prothrombin, and its activation at the end

124 h in turn does not feed back to activate its zymogen form.

125 otein was detected predominantly as inactive zymogen forms as part of an array of multiple noncovalen

126 ans in arthritis, in part, by activating the zymogen forms of MMP-3 and MMP-13, which are constitutiv

127 s access to the active site and protects the zymogen from autoproteolytic conversion to thrombin.

128 ecent availability of crystal structures for zymogen FXI and the FXIa catalytic domain have enhanced

129 increased contact-mediated autoactivation of zymogen FXII, resulting in excessive activation of the b

130 Whereas zymogen FXIII was not readily cleaved by plasmin, FXIIIa

131 ave identified the lectin-like protein ZG16 (zymogen granulae protein 16) as an abundant mucus compon

132 We performed single zymogen granule (ZG) exocytosis assays, Ca(2+) imaging s

133 the Ca(2+)-sensitive regulatory pathway for zymogen granule exocytosis.

134 The small GTPase Rab27B localizes to the zymogen granule membranes and plays an important role in

135 f these v-SNARE proteins are associated with zymogen granule membranes in pancreatic acinar cells.

136 granules, but only Rap1 was integral to the zymogen granule membranes.

137 as significant keratin overexpression alters zymogen granule organization and causes aging-associated

138 in increased cytoplasmic zinc and decreased zymogen granule zinc that further demonstrated that ZnT2

139 Acinar cell zymogen granules (ZG) express 2 isoforms of the vesicle-

140 ar cells contain two distinct populations of zymogen granules (ZGs) expressing either VAMP 2 or VAMP

141 treated) exhibit normal apical exocytosis of zymogen granules (ZGs) in response to physiologic stimul

142 lated amylase release and an accumulation of zymogen granules (ZGs).

143 The acinar cells lose their zymogen granules and approximately 75% of their RNA.

144 ansporter ZnT2 (Slc30a2) is localized to the zymogen granules and that dietary zinc restriction in mi

145 in mice decreased the zinc concentration of zymogen granules and ZnT2 expression.

146 Zymogen granules in K8/K18 pancreata were 50% smaller an

147 g disruption of retinal cell layers, lack of zymogen granules in the pancreas, and dilated Golgi in i

148 oad that results from the exocytic fusion of zymogen granules is significantly blunted by HCO3 (-) bu

149 he pancreatic pro-enzymes, packaged into the zymogen granules of acinar cells, become activated and c

150 rticipates in zinc transport into pancreatic zymogen granules through a glucocorticoid pathway requir

151 ed with disorganized and dilated ER, loss of zymogen granules, accumulation of autophagic vacuoles, a

152 as degeneration of exocrine cells, decreased zymogen granules, and alterations in the endoplasmic ret

153 Pancreatic acini are completely devoid of zymogen granules, and the ER is severely distended.

154 h Rap1 and Epac1 colocalized with amylase in zymogen granules, but only Rap1 was integral to the zymo

155 ish apical-basal polarity, properly position zymogen granules, or communicate with adjacent cells, di

156 pical-basal polarity, increasing the size of zymogen granules, reorganizing the cytoskeletal network,

157 ypoplastic and individual acini produced few zymogen granules.

158 2 may mediate the sequestration of zinc into zymogen granules.

159 creatic cancer cell line, MIA PaCa-2 without zymogen granules.

160 hat are predominantly associated with mature zymogen granules.

161 ding proteins and is localized on pancreatic zymogen granules.

162 mechanism of prothrombin activation and the zymogen --> protease conversion in trypsin-like protease

163 talytic moiety and the pro-domain within the zymogen, i.e. both complexes are mutually exclusive.

164 vorable thermodynamic constants when it is a zymogen in comparison to proteinase.

165 al transitions are genuine properties of the zymogen in solution.

166 f the trypsin fold for both the protease and zymogen in terms of a pre-existing equilibrium between c

167 ex formation among human pancreatic protease zymogens in a systematic manner, we performed binding ex

168 s proteolytic gingipains (Kgp and RgpA/B) as zymogens inhibited by a pro-domain that is removed durin

169 hanism of trypsinogen-like serine proteinase zymogens, insertion of the first 2 residues of SC into t

170 other proplasmepsins, the propeptide of the zymogen interacts with the C-terminal domain of the enzy

171 In contrast, the zymogen intermediate P2, formed following cleavage at Ar

172 f these tactics, such as the activation of a zymogen, involve the direct manipulation of a material b

173 Chymotrypsin zymogen is activated by proteolytic processing at the N

174 DJ-1 protease zymogen is activated by the removal of a 15-amino acid p

175 h the endo-lysosomal environment because the zymogen is autoactivated and remains optimally active in

176 fects ligand recognition by the protease and zymogen is poorly understood in quantitative terms.

177 ex formation among human pancreatic protease zymogens is limited to a subset of proelastases and proc

178 The conversion is started by the zymogen itself, which is capable of binding ligands at t

179 DNA extraction was done using Zymogen Kit according to its manufacturer's instructions

180 on the inactive precursor human cathepsin A (zymogen) led to a two-stage model for activation, where

181 he enzyme, are instead shown to be variously zymogen-like and can be made proteinase-like by active-s

182 stribution between the two forms, designated zymogen-like and proteinase-like, is affected by Na(+),

183 omain in favor of zymogen, thereby enforcing zymogen-like character in the proteinase.

184 with the ability of the propiece to enforce zymogen-like character in the proteinase.

185 The extent of zymogen-like character, including resistance to antithro

186 n meizothrombin imbues it with exceptionally zymogen-like character.

187 Previously, we found that a novel zymogen-like factor Xa variant (FXa-I16L) was effective

188 s with prothrombinase, we also show that the zymogen-like form is produced following the initial clea

189 converted proteinase-like thrombin to a more zymogen-like form.

190 , and mechanism of action suggest that novel zymogen-like forms of factor Xa might prove useful as ne

191 The active site of the SP domain is in a zymogen-like inactive conformation.

192 of the Arg(494)-Val(495) peptide bond in the zymogen-like pro-HGF results in allosteric activation of

193 Here we show that factor Xa mutants with zymogen-like properties (FXa(I16L) and FXa(V17A)) circum

194 Active-site ligands transitioned a zymogen-like state to a proteinase-like state.

195 d the mutational framework to tune the FX(a) zymogen-like state.

196 ating the transition from active to inactive zymogen-like states.

197 iologic function, including that of the most zymogen-like variant (FXa-I16T), was greatly enhanced wh

198 pending on the treatment situation, the more zymogen-like variants (V17S and I16T) were most useful w

199 actor VIIa (FVIIa) predominantly exists in a zymogen-like, catalytically incompetent state.

200 n site cleavage, that can be mediated by the zymogen-locked version of prostasin and a proteolysis-de

201 ing only activation site cleavage-resistant (zymogen-locked) endogenous prostasin.

202 ted isoforms lacking ER-localizing (pre) and zymogen-maintaining (pro) sequences, yet retain essentia

203 ition molecules leading to the activation of zymogen mannan-binding lectin-associated serine protease

204 .MASP complexes, and in the proenzymic phase zymogen MASP-1 controls the process.

205 loped against active MASP-1, indicating that zymogen MASP-1 fluctuates between an inactive and an act

206 oteases that depend on their propeptides for zymogen maturation and activation.

207 required as an intramolecular chaperone for zymogen maturation and secretion of SBT3 in vivo Secreti

208 Activation of the thrombolytic zymogens may therefore allow for both direct and indirec

209 tion from natural activatable materials like zymogens, membrane proteins, and metabolites, whereby st

210 GuSCN) Method, Wizard Method, Qiagen Method, Zymogen Method and Genespin Method were examined to dete

211 the crystal structures of mature SplB and a zymogen mimic show no rearrangement at the active site w

212 Synthesized as zymogens, MMPs become active after removal of their prod

213 P-9 indicated that in vivo activation of the zymogen occurred during the first 24 h after grafting.

214 Factor XI is the zymogen of a dimeric plasma protease, factor XIa, with t

215 Factor XI (FXI) is the zymogen of an enzyme (FXIa) that contributes to hemostas

216 ase-1 and -3 (MASP1/3(-/-)) express only the zymogen of factor D (pro-factor D [pro-Df]), a necessary

217 Factor XI (FXI) is the zymogen of FXIa, which cleaves FIX in the intrinsic path

218 Crystal structures of the truncated zymogen of HAP and of the complex of the mature enzyme w

219 kinase (SK) binding to plasminogen (Pg), the zymogen of plasmin (Pm).

220 Evidence implicating plasminogen (Plg), the zymogen of plasmin, in phagocytosis is extremely limited

221 (SK) conformationally activates the central zymogen of the fibrinolytic system, plasminogen (Pg).

222 Activation of plasminogen, the zymogen of the primary thrombolytic enzyme, plasmin, is

223 FXII, Hageman factor, EC = 3.4.21.38) is the zymogen of the serine protease, factor XIIa (FXIIa).

224 g residues 34p-38p in the prosegments of the zymogens of gastric aspartic proteases; a corresponding

225 Zymogens of the chymotrypsin-like serine protease family

226 We determined the crystal structures of the zymogens of two of these (Pyrococcus abyssi proabylysin

227 ite tethering of the substrate in either the zymogen or proteinase conformation dictates which cleava

228 s inactive plasmin (Pm) but normal levels of zymogen Pg (PAI-1(-/-)/Pg(S743A/S743A)).

229 Specifically, uPA cleaves the zymogen plasminogen into the active form (plasmin), whic

230 Additionally, the thrombolytic zymogens plasminogen, urokinase, and plasma kallikrein h

231 In the absence of dATP or ATP, Dronc zymogen potently induces formation of the Dark apoptosom

232 cascade, which results in processing of the zymogen PPO to PO.

233 Prothrombin is the zymogen precursor of the clotting enzyme thrombin, which

234 ntrol ligand recognition by thrombin and its zymogen precursor prethrombin-2 and have direct relevanc

235 Using the clotting protease thrombin and its zymogen precursor prethrombin-2 as relevant models we re

236 ion vector synthesis and purification of the zymogen/precursor yielded an active, mature-length prote

237 rgeting specific cleavage sites within their zymogen precursors.

238 +/- 0.005 nM) but does not target either the zymogen (prekallikrein) or any other serine protease tes

239 ) MMP is the physiological activator for the zymogen pro-MMP2.

240 In the endoplasmic reticulum, the zymogen pro-PCSK9 is first autocatalytically cleaved at

241 Unlike most precursor proteins, the ADAMTS9 zymogen (pro-ADAMTS9) is resistant to intracellular proc

242 KLK4 is secreted as an inactive zymogen (pro-KLK4), and identification of its activator

243 at the RgpA-Kgp complex cleaves the inactive zymogens, pro-uPA (at consensus sites Lys(158)-Ile(159)

244 omplex comprises a sensor, an adaptor, and a zymogen procaspase-1.

245 entral to apoptosis is the activation of the zymogen procaspase-3 to caspase-3.

246 dramatically promotes the maturation of the zymogen, procaspase-3, to its mature form, caspase-3.

247 coordinated dimerization and cleavage of the zymogen produce efficient activation in vitro and apopto

248 Biochemical analysis using HP14 zymogen (proHP14), betaGRP2, and the recombinant protein

249 tributed to their matrix metalloproteinase-9 zymogen (proMMP-9).

250 Secreted as a zymogen, proMMP-9 can be irreversibly converted to a mat

251 In contrast to other zymogen proprotein convertases, all incompletely matured

252 thesized in liver hepatocytes as an inactive zymogen (proprotein C).

253 We found that the 55-kDa Tpr inactive zymogen proteolytically processes itself into active for

254 The zymogen prothrombin is composed of fragment 1 containing

255 The zymogen prothrombin is proteolytically converted by fact

256 In the blood, the zymogens prothrombin and prethrombin-2 require the proth

257 rmational activator of the blood coagulation zymogen, prothrombin (ProT).

258 nd activation of prostasin by the matriptase zymogen provides a tentative mechanistic explanation for

259 Zymogen secretory granules in pancreatic acinar cells ex

260 that two loops (492-499 and 573-580) in the zymogen serine protease domain adopt a conformation that

261 inkers, and particularly Lnk2, confer on the zymogen significant flexibility in solution and enable p

262 f procarboxypeptidases and thereby increases zymogen stability and controls activation.

263 Thus, the active rather than the zymogen state is default in lectin.MASP complexes and mu

264 tions led to the formation of an unprocessed zymogen that acted as a dominant negative retaining the

265 Factor B is a zymogen that carries the catalytic site of the complemen

266 oxic ribonuclease barnase into an artificial zymogen that is activated by HIV-1 protease.

267 It is synthesized as a zymogen that is activated by proteolytic cleavage.

268 Factor XI (fXI) is a homodimeric zymogen that is converted to a protease with 1 (1/2-fXIa

269 tase was also found to activate thrombolytic zymogens that have been shown to cleave and activate the

270 ses are expressed as inactive precursors, or zymogens, that become activated by limited proteolysis.

271 the other MMPs, MT1-MMP is synthesized as a zymogen, the latency of which is maintained by its inhib

272 MT1-MMP is synthesized as a zymogen, the latency of which is maintained by its prodo

273 o bind the (pro)catalytic domain in favor of zymogen, thereby enforcing zymogen-like character in the

274 Maturation of the single-chain caspase-9 zymogen through autoproteolytic processing is mediated b

275 ediated conversion of the prothrombin (ProT) zymogen to active alpha-thrombin (alphaT).

276 The transition from zymogen to active C1s repositions both loops such that t

277 directly escort the transition of MASP from zymogen to active enzyme in the PRM/MASP complex; rather

278 collagen converts the surface-bound proMMP-1 zymogen to active MMP-1, which promotes aggregation thro

279 inactive by a defect in the transition from zymogen to active protease.

280 w parasite proteases mature from an inactive zymogen to an active enzyme is expected to inform new st

281 ed with maturation of SpeB from the inactive zymogen to its active form and identify the residues req

282 has the potential to unleash activity in the zymogen to produce autoactivation.

283 brillin-1, but innate resistance of ADAMTS10 zymogen to propeptide excision by furin was observed, su

284 d regulation in addition to the irreversible zymogen to protease conversion and points to new therape

285 lecular activation of factor X following the zymogen to protease transition not only drives catalytic

286 ombin species poised along the transition of zymogen to proteinase.

287 ance, we show that the transition of the C1s zymogen to the active form is essential for C1s binding

288 the irreversible transition from an inactive zymogen to the active protease form enables productive i

289 relies on recruitment of inactive monomeric zymogens to activated receptor complexes, where they pro

290 es within the activation domain causes these zymogens to spontaneously convert to thrombin.

291 minogen (the native, circulating form of the zymogen) to cells results in enhancement of its activati

292 e 8 vector delivery of a canine FVII (cFVII) zymogen transgene.

293 Enhanced binding to zymogen versus proteinase correlates with the ability of

294 Recently, it was shown that zymogen vesicles are transported on actin "superhighways

295 The zymogen was present in small amounts under all condition

296 riminate between mature PR3 and its inactive zymogen, which have different conformations, we generate

297 the SpeB protein is secreted as an inactive zymogen, which is autocatalytically processed through a

298 hat DJ-1 is synthesized as a latent protease zymogen with low-intrinsic proteolytic activity.

299 ens, and both resulted in activation of each zymogen, with kallikrein 12 being a more potent activato

300 is the crystal structure of the procaspase-1 zymogen without its caspase recruitment domain solved to