ライフサイエンスコーパス: zymogen

1 biquitination of the unprocessed form of the 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 hibit activation of the highly related MMP-2 zymogen.

10 allosterically preventing activation of its zymogen.

11 minant of the structure and function of this zymogen.

12 tion of the blood coagulation and complement zymogens.

13 fferent conformational plasticity of the two zymogens.

14 bacterial subtilisin and are synthesized as zymogens.

15 ctly or indirectly by activating HA-cleaving zymogens.

16 y of proteases that are secreted as inactive zymogens.

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

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

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

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

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

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

23 have been identified as regulators of early zymogen activation and thus modulators of the severity o

24 ncreatitis not by reducing intra-acinar cell zymogen activation but by reducing infiltration of neutr

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

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

27 ostasin co-immunoprecipitation and prostasin zymogen activation experiments identified prostasin as a

28 Zymogen activation imparts proteolytic activity to throm

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

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

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

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

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

34 of most SC(1-246) variants, consistent with zymogen activation through occupation of the specificity

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

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

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

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

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

40 causes mitochondrial dysfunction, premature zymogen activation, and necrosis, ultimately leading to

41 Zymogen activation, observed within acini early during a

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

43 tory effect of thrombomodulin on the rate of zymogen activation.

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

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

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

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

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

49 y the structures of the apo-AC enzyme in its zymogen and activated conformations are available.

50 competitive inhibitors that target both the zymogen and activated forms of matriptase.

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

52 aining granules resembling those of exocrine zymogen and endocrine hormone secreting cells; and (ii)

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

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

55 , which showed that PfClpP oligomerizes as a zymogen and is matured via transautocatalysis.

56 Colocalization of zymogen and lysosomal fraction occurs early after pancre

57 Under physiological conditions, both zymogen and protease adopt a conformation with all domai

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

62 MT2 is synthesized as a zymogen and undergoes autocleavage for activation.

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 that binds the catalytic domain of both FXI (zymogen) and activated FXI.

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

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

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

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

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

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

72 , biological mechanisms for processing these zymogens are uncertain.

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

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

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

76 Zymogen autoactivation is explained by conformational se

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

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

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

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

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

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

83 ased on the production of several complement zymogens by MCs and their activation by MC-released prot

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

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

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

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

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

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

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

91 teinase formation beyond simply reporting on zymogen cleavage.

92 d that its own proteolytic activity mediates zymogen cleavage.

93 Setting intraclot zymogen concentrations to plasma levels (and neglecting

94 the serine protease domain is locked in the zymogen conformation, we confirmed that the zymogen form

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

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

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

98 Prostasin zymogen conversion to active prostasin is dependent on m

99 n matriptase but does not require matriptase zymogen conversion.

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

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

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

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

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

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

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

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

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

109 zymogen conformation, we confirmed that the zymogen form of human matriptase has catalytic activity.

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

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

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

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

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

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

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

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

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

119 operties of trypsin-like proteases and their zymogen forms remain controversial because of a lack of

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

121 t that binds coagulation factor Xa (FXa) and zymogen FX, with formation of a quaternary tissue factor

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

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

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

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

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

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

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

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

130 0%) or rare (2/2, 50%) ducts and rare acinar zymogen granules (3/4, 75%).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

145 ypoplastic and individual acini produced few zymogen granules.

146 2 may mediate the sequestration of zinc into zymogen granules.

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

148 hat are predominantly associated with mature zymogen granules.

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

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

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

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

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

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

155 Both caspases exist as inactive zymogens in normal cells but are activated during apopto

156 The CpaAB organization was akin to zymogen inactivation, with CpaB serving as a prodomain t

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

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

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

160 Chymotrypsin zymogen is activated by proteolytic processing at the N

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

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

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

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

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

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

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

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

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

170 , it is unclear whether the free protease is zymogen-like and shifts to its mature form upon a ligand

171 s on recent hypotheses that free thrombin is zymogen-like and transitions to protease-like forms upon

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

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

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

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

176 traps FXI and activated FXI in an inactive, zymogen-like conformation, explaining its equally high b

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

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

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

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

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

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

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

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

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

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

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

188 providing no evidence that free thrombin is zymogen-like.

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

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

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

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

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

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

195 characterize the catalytic activity of human zymogen matriptase and to develop mAb inhibitors against

196 Inhibition of zymogen matriptase may therefore be a highly effective a

197 crystal structure of the catalytic domain of zymogen matriptase was solved to 2.5 angstrom resolution

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

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

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

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

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

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

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

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

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

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

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

209 Recent studies suggest that the zymogen of matriptase possesses enough catalytic activit

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

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

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

213 rage lesion-induced RBC-MVs to activate each zymogen of the intrinsic pathway was assessed in a buffe

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

215 to an active protease capable of activating zymogens of downstream coagulation proteases.

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

217 istent with the hypothesis that the putative zymogens of many trypsin-like proteases are actually act

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

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

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

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

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

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

224 formational properties of a protease and its zymogen precursor in the free form.

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

226 , or coagulation factor II, is a multidomain zymogen precursor of thrombin that undergoes an alloster

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

228 n is quite different from that of its direct zymogen precursor prethrombin-2 and more similar to that

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

230 rties that is generated by thrombin from the zymogen precursor protein C in a reaction greatly accele

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

232 rgeting specific cleavage sites within their zymogen precursors.

233 +/- 0.005 nM) but does not target either the zymogen (prekallikrein) or any other serine protease tes

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

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

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

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

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

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

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

241 Adult zymogen-producing (zymogenic) chief cells (ZCs) in the m

242 ne proteases, matriptase is synthesized as a zymogen (proform), requiring a cleavage event for full a

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

244 Neither MMP-3 zymogen (proMMP-3) nor the individual catalytic (Cat) an

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

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

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

248 Hence, the zymogen protein C likely interacts with the thrombin-thr

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

250 r pharmacologic reduction of the coagulation zymogen prothrombin in mice.

251 The zymogen prothrombin is composed of fragment 1 containing

252 The zymogen prothrombin is proteolytically converted by fact

253 coagulation cascade where conversion of the zymogen prothrombin to the protease meizothrombin by the

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

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

256 Granular, zymogen-rich pyramidal acinar cells in normal glands pre

257 ing an explanation for continuous pancreatic zymogen secretion in these species.

258 Zymogen secretory granules in pancreatic acinar cells ex

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

260 relationship of an anticoagulant targeting a zymogen serving as a scaffold for TF inhibition.

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 ana legumain isoform beta (AtLEGbeta) in its zymogen state.

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

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

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

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

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

270 MT2 is synthesized as a zymogen that undergoes autocleavage for activation and s

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

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

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

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

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

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

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

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

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 The zymogen to protease conversion of protein C involves rem

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