ライフサイエンスコーパス: calpain

1 s due to increase in proteolytic activity of calpain.

2 LTF is blocked by dn small optic lobe (SOL) calpain.

3 e expression of several proteases, including calpain.

4 ha dissociation and subsequent processing by calpain.

5 n sheaths prefigure retractions, mediated by calpain.

6 omotes its nuclear export and degradation by calpain.

7 guidance through activation of the protease calpain.

8 We demonstrate that selective inhibition of calpain 1 activation improves wound healing and normaliz

9 omolar inhibitory activity against the human calpain 1 protease.

10 This is secondary to increased activity of calpain 1, the primary enzyme responsible for focal adhe

11 mGluR-LTD was associated with calpain-1 activation following T-type calcium channel op

12 Calpain-1 activation is required for the induction of lo

13 These studies demonstrate that calpain-1 acts as a mediator of IL-1beta-induced loss of

14 We review recent studies indicating that calpain-1 and calpain-2 exhibit opposite functions in bo

15 the two major calpain isoforms in the brain, calpain-1 and calpain-2, play opposite functions in syna

16 the two major calpain isoforms in the brain, calpain-1 and calpain-2.

17 es, and for two highly homologous proteases, calpain-1 and calpain-2.

18 ite-directed mutagenesis, we identified that calpain-1 cleaves hERG at position Gly-603 in the S5-por

19 fically, we show that Gp91phox activation of calpain-1 degrades Erk5 in free fatty acid (FFA)-stresse

20 Here we determined the contribution of calpain-1 in another type of synaptic plasticity, the lo

21 Recent studies indicate that calpain-1 is required for the induction of long-term pot

22 In contrast, in hippocampal slices from calpain-1 knock-out (KO) mice, application of the mGluR

23 Furthermore, calpain-1 KO mice exhibited impairment in fear memory ex

24 Consistently, mGluR-LTD was impaired in calpain-1 KO mice, and the impairment could be rescued b

25 in-2 was involved in RhoA synthesis, whereas calpain-1 mediated RhoA degradation.

26 These results indicate that calpain-1 plays a critical role in mGluR-LTD and is invo

27 vention of Erk5 loss by blocking Gp91phox or calpain-1 rescues mitochondrial functions.

28 tor III and calpastatin) or transfected with calpain-1 siRNA demonstrated attenuation of IL-1beta-ind

29 Using cell biology approaches, we found that calpain-1 was actively released into the extracellular m

30 e the authors show that high fat diet causes calpain-1-dependent degradation of ERK5 leading to mitoc

31 sion kinase (FAK), and cortactin and reduced calpain-1-specific membrane localization, suggesting a r

32 ntaining proper localization and activity of calpain-1.

33 ollagen synthesis, and reduced expression of calpain-1/2 and MMP2/TGF-beta1.

34 ibited in transgenic mice, and expression of calpain-1/2 and MMP2/transforming growth factor-beta1 (T

35 e and specific small interfering RNA against calpain-1/2 were introduced.

36 nally, restenosis enhanced the expression of calpain-1/2, but reduced calpastatin content.

37 imaging, small interfering RNA knockdown of calpain 12 in skin from K14-H2B GFP mice led to signific

38 In summary, our results indicate that calpain 12 plays an essential role during epidermal onto

39 The calpain 12 protein was found to be expressed in both the

40 Thymic stromal lymphopoietin (TSLP) and calpain 14 (CAPN14) genetic variations contribute to EoE

41 food and associated with genetic variants in calpain 14 (CAPN14).

42 genous inhibitor of calpain, or knockdown of calpain 2 also decreased ablation.

43 l calpain or atypical small optic lobe (SOL) calpain 2 d after 5-HT treatment or paired stimuli did n

44 c-Abl pathway provides a direct link between calpain-2 activation and abnormal tau aggregation, which

45 Following TBI, calpain-2 activation cleaved PTPN13, activated c-Abl and

46 LTP) and is generally neuroprotective, while calpain-2 activation limits the extent of potentiation a

47 t to reduce cellular levels of NF-kappaB and calpain-2 and secreted levels of the proangiogenic prote

48 recent studies indicating that calpain-1 and calpain-2 exhibit opposite functions in both synaptic pl

49 gomers after TBI, as post-TBI injection of a calpain-2 selective inhibitor inhibited c-Abl activation

50 rmal growth factor receptor and the protease calpain-2 through a redox-dependent mechanism involving

51 m-selective calpain inhibitors revealed that calpain-2 was involved in RhoA synthesis, whereas calpai

52 Competitive and mixed inhibition against calpain-2 was observed, and an allosteric inhibition sit

53 calpain isoforms in the brain, calpain-1 and calpain-2, play opposite functions in synaptic plasticit

54 and the expression profiles of caspase-3 and calpain-2, the major enzymes involved in the degradation

55 PTPN13 is cleaved by calpain-2, which inactivates its phosphatase activity an

56 Thus, the calpain-2-PTPN13-c-Abl pathway provides a direct link be

57 atase PTPN13 as a key PDZ binding partner of calpain-2.

58 wn reproducibly low micromolar inhibition of calpain-2.

59 calpain isoforms in the brain, calpain-1 and calpain-2.

60 o highly homologous proteases, calpain-1 and calpain-2.

61 is due to loss-of-function mutations in the Calpain 3 (CAPN3) gene.

62 e encoding the muscle-specific family member calpain 3 (CAPN3) underlie limb-girdle muscular dystroph

63 This renders patients deficient in calpain 3 as in limb girdle muscular dystrophy type 2A,

64 Calpain 3 expression in muscle, assessed by western blot

65 , patients carrying a single mutation in the calpain 3 gene (CAPN3) are reported.

66 h a loss-of-function mechanism affecting the calpain 3 homodimer.

67 ssion of mutated mRNA and the severe loss of calpain 3 on western blotting, suggest a dominant negati

68 opathic changes on muscle biopsy and loss of calpain 3 protein on western blotting.

69 ce an unconventional nonproteolytic calpain, calpain-6 (CAPN6), which associates with the essential E

70 ization of a free Cactus pool induced by the Calpain A protease.

71 tatin is an endogenous specific inhibitor of calpain, a calcium-dependent cysteine protease.

72 uggest that Tpr is an example of a bacterial calpain, a calcium-responsive peptidase that may generat

73 n levels by synergistically increasing micro-calpain, a proteolytic enzyme that targets E-cadherin.

74 oxygen species from mitochondria, leading to calpain activation and high levels of IL-1alpha, which f

75 navirus infection in mice is associated with calpain activation and is the result of neuronal death t

76 Calpain activation and tau hyperphosphorylation have bee

77 t increased mitochondrial ROS production and calpain activation are significant contributors to the d

78 HHcy potentiated HG-induced calpain activation in aortic endothelial cells isolated

79 scued HHcy/HG-induced ED in mouse aortas and calpain activation in cultured HAECs.

80 ed HHcy/HG-induced ED in the mouse aorta and calpain activation in human aortic endothelial cells (HA

81 Calpain activation induced by overexpression or Ca/A2318

82 Moreover, calpain activation inhibited VEGF-induced VEGFR2 phospho

83 heart and skeletal muscles and, importantly, calpain activation is a major contributor to DOX-induced

84 letion of GPR68 or inhibition of calcium and calpain activation suppressed LEN-induced cytotoxicity.

85 cytoplasmic calcium release responsible for calpain activation underlying IL-1alpha release.

86 Moderate HHcy- and HG-induced mu-calpain activation was potentiated by a combination of H

87 ith IBD were both characterized by increased calpain activation, beclin 1 and ATG5 cleavage, and inte

88 species (ROS)-dependent RyR1 fragmentation, calpain activation, increased SR Ca(2+) leak at rest, an

89 Hyperosmotic shock induces early calpain activation, Smac/DIABLO release from the mitocho

90 ontaining NMDA receptors, Ca(2+) influx, and calpain activation.

91 Finally, changing one of the three calpain active-site amino acid residues results in the s

92 GTPases, RhoA and Rac1, and Ca(2+)-dependent Calpain activites, but seem to be independent of intrace

93 Modulation of local PTP1B and/or calpain activities may prove beneficial in the treatment

94 gical blockade of NMDA-R, calcium influx, or calpain activity abolished SSC and glutamate neurotoxici

95 Elevated micro-calpain activity and a higher p25/p35 ratio in the corte

96 HO-1 depletion inhibited VEGF-induced calpain activity and vimentin cleavage, while vimentin s

97 Furthermore, pharmacologic inhibition of calpain activity following glomerular injury substantial

98 It has been observed that mu-calpain activity in breast and thigh muscles declined ve

99 Ritonavir treatment significantly reduced calpain activity in the hippocampus, protected hippocamp

100 Functional studies demonstrated that calpain activity is essential for the P2X purinoceptor 7

101 I and calpastatin decreased IL-1beta-induced calpain activity significantly (p < 0.05).

102 Living parasites exhibit surface calpain activity that is blocked in the absence of calci

103 tathione level, thioltransferase activity, m-calpain activity, and m-calpain level (as assessed by We

104 elevated transcription of p35 nor disrupted calpain activity, but rather to the slower degradation o

105 ique, constitutive, functional extracellular calpain activity.

106 nflammasome activation was also dependent on calpain activity.

107 cological inhibitor was exploited to inhibit calpain activity.

108 7-independent mechanism but was dependent on calpain activity.

109 he P23H dominant mutations activate both the calpain-Aif cell death pathway and ER-stress responses t

110 A receptors or pharmacological inhibition of calpain also led to increased KCC2 expression and defect

111 The concentrations of mu-, m-calpain and calpastatin detected in the extracts of bloo

112 ytical method for accurate identification of calpain and calpastatin from chicken blood and muscle sa

113 the method standardized for the detection of calpain and calpastatin has the potential to be applied

114 ination, expression of Atrogin-1 and Murf-1, calpain and caspase-3 activities, autophagy, and protein

115 es for the intracellular cysteine proteases, calpain and caspase.

116 and salubrinal suggests co-activation of the calpain and ER-stress death pathways in mice bearing dom

117 Similar to the calpain and MEM domains, the Linker is highly conserved

118 However, the link between calpain and tau phosphorylation has not been fully ident

119 p) mutant sap2456 and S. oralis increased mu-calpain and triggered mucosal invasion and systemic diss

120 f function is characterized by activation of calpains and apoptosis-inducing factor (Aif) in dying ph

121 SSC treatment activated the protease calpain, and calpain-dependent degradation of the inhibi

122 the pro-apoptotic calcium-dependent enzyme, calpain, and partly suppress beta cell death in INS1E ce

123 the non-apoptotic activities of caspase and calpain are demonstrated to be important, but the substr

124 sion and activation of the cysteine protease calpain are required for DOX-induced myopathy in rat car

125 Calpains are a family of intracellular, calcium-dependen

126 Calpains are broadly distributed, calcium-dependent enzy

127 Calpains are calcium-dependent neutral cysteine protease

128 Calpains are intracellular proteases that play a key rol

129 While calpains are invariably reported to be exclusively intra

130 loped transgenic mice in which extracellular calpains are specifically inactivated, we provide eviden

131 Calpains are ubiquitous pro-inflammatory proteases, whos

132 r, these findings identify calcium-activated calpains as powerful modulators of cellular sumoylation

133 nal Linker subsegment containing a potential calpain autolytic site severely disturbs gametophore dev

134 Our previously reported structures of calpain bound to its endogenous inhibitor calpastatin ha

135 the DEK1 MEM-Linker complex inactivates the calpain by forcing apart the two calpain subunits carryi

136 g from stimulation of NMDAR is activation of calpains-calcium-dependent cysteine proteases.

137 ines induce an unconventional nonproteolytic calpain, calpain-6 (CAPN6), which associates with the es

138 levels and activation of a calcium-dependent calpain, CAPN1, which were requisite steps for induction

139 In comparison with other human calpains, CAPN14 has a unique expression pattern, with t

140 calmodulin-dependent protein kinase and the calpain-caspase pathway, ultimately inducing striatal ne

141 PP1c-binding sites were separated (mimicking calpain cleavage of NCX1).

142 In addition, blocking calpain cleavage of talin and FAK in vivo promotes Rohon

143 Blocking calpain cleavage of talin and FAK inhibits repulsive tur

144 C-terminal region of JP2 as the predominant calpain cleavage site.

145 ination of computational analysis to predict calpain cleavage sites and in vitro calpain proteolysis

146 lysis reactions, we identified four putative calpain cleavage sites within JP2 with three N-terminal

147 utively active isoforms of PKCs generated by calpain cleavage, in the sensory neuron and L7 are requi

148 , via two proteolytic fragments generated by calpain cleavage.

149 3) C-terminal four-C2 domain module; and 4) calpain-cleaved mini-dysferlinC72, which is particularly

150 y in a calcium-dependent manner, involving a calpain clp-4.

151 Calpain conditional knockout mice were studied in the mo

152 ced activation of an intracellular caspase-1/calpain cysteine protease cascade degraded filamin, ther

153 mpal cultures demonstrate that menin and its calpain-dependent C-terminal fragment (C-menin) regulate

154 reatment activated the protease calpain, and calpain-dependent degradation of the inhibitory synaptic

155 t high glutamate loads, they undergo a rapid calpain-dependent endocytosis that likely represents an

156 in MDS and AML that depend on a calcium- and calpain-dependent pathway.

157 0%) and membrane blebbing (-90%); 3) reduced calpain-dependent protein cleavage (-60%); and 4) modera

158 ecent studies from our group have implicated calpain-dependent proteolytic fragments of menin, the pr

159 These results suggest that TRPV1/Ca(2+)/calpain-dependent signaling plays a dominant role in cap

160 er, we found that the activation of specific calpains depends on the features of the stimuli evoking

161 n inhibitor of the Ca(2+)-dependent protease calpain, diminished ablation.

162 nts constitutively overexpressing the active CALPAIN domain of DEK1.

163 ch form of LTF is sensitive to a distinct dn calpain expressed in the postsynaptic neuron.

164 Calpain exteriorization and TLR2 cleavage were critical

165 Thus, this study identifies calpain exteriorization as a potential target for immune

166 ed, we provide evidence for the relevance of calpain externalization in vivo in regulating IL-17A exp

167 ity to cysteine peptidases of the papain and calpain families.

168 reveals that two proteases belonging to the calpain family (SmCalp1 and SmCalp2) are expressed in th

169 We show here that calpain-generated natural C-terminal fragments of protei

170 minus and correlated with over-activation of calpain I in AD brain.

171 ggest that truncation of GSK-3beta by Ca(2+)/calpain I markedly increases its activity and involvemen

172 Calpain I proteolyzed GSK-3beta in vitro at C-terminus,

173 However, the role of calpain in airway smooth muscle remodelling remains unkn

174 To investigate the role of calpain in asthmatic airway remodelling as well as the u

175 ndrial ROS emission are required to activate calpain in heart and skeletal muscles and, importantly,

176 e have previously discovered a novel role of calpain in mediating VEGF-induced PI3K/AMPK/Akt/eNOS act

177 esion kinase (FAK) as proteolytic targets of calpain in Xenopus laevis spinal cord neurons both in vi

178 these results demonstrate the involvement of calpains in alcohol-seeking and relapse and present a ra

179 e of this study was to determine the role of calpains in mediating BBB dysfunction and hyperpermeabil

180 resent study demonstrates a pivotal role for calpains in mediating HFD-induced adipose tissue remodel

181 uman macrophages and show a pivotal role for calpains in the activation of the inflammatory response

182 However, the roles of calpastatin and calpains in vascular restenosis remain unclear.

183 rons both in vivo and in vitro Inhibition of calpain increases the localization of endogenous adhesio

184 ain injury increased lesion volume, enhanced calpain-induced alphaII-spectrin cleavage, and increased

185 this effect is mainly mediated by a calcium/calpain-induced cleavage of the SUMO E1 enzyme SAE2, thu

186 To define whether activated calpains influence diet-induced obesity and adipose tiss

187 Calpains influence VSMC proliferation and collagen synth

188 paired stimuli, however, blocking classical calpain inhibited the expression of persistent associati

189 rsistent associative LTF, while blocking SOL calpain inhibited the expression of persistent nonassoci

190 In turn, extracellular calpains inhibited IL-17A expression.

191 Calpain inhibition by ritonavir may be a powerful tool f

192 important role in the protective effects of calpain inhibition for the treatment of MJD.

193 Calpain inhibition has beneficial effects against TBI-in

194 Calpain inhibition led to protection against IL-1beta-in

195 Thus, calpain inhibition may be one means of normalizing plate

196 hyperpermeability and to test the effect of calpain inhibition on the BBB following traumatic insult

197 Furthermore, calpain inhibition preserved BBB integrity/permeability

198 Calpain inhibition showed a transient improvement in glu

199 Furthermore, calpain inhibition suppressed macrophage migration to ad

200 Calpain inhibition via calpain inhibitor III and calpast

201 We hypothesized that specific calpain inhibition would protect against aging-related l

202 centrations within the therapeutic range for calpain inhibition.

203 Collectively, calpains inhibition plays crucial roles in vascular rest

204 Calpains inhibition protects against inflammaging, limit

205 ated with PDGF-BB, calpastatin induction and calpains inhibition suppressed the proliferation and mig

206 The calpain inhibitor A-705253 (3-10 mg/kg) was tested in a

207 Calpain inhibitor ALLN induced VEGFR2 activation, which

208 ing the EGFP-ataxin-3-84Q zebrafish with the calpain inhibitor compound calpeptin decreased levels of

209 und that treating the MJD zebrafish with the calpain inhibitor compound calpeptin produces complete r

210 Calpain inhibition via calpain inhibitor III and calpastatin decreased IL-1beta

211 ll monolayers exposed to calpain inhibitors (calpain inhibitor III and calpastatin) or transfected wi

212 hich was attenuated by pretreatment with the calpain inhibitor MDL-28170 or by transgenic overexpress

213 n of Akt in ASMCs, which were blocked by the calpain inhibitor MDL28170.

214 Treating diabetic mice with a calpain inhibitor prevented loss of platelet dicer as we

215 therefore hypothesized that treatment with a calpain inhibitor would protect neurons from immune-medi

216 vo treatment with the calpastatin peptide, a calpain inhibitor, was strongly neuroprotective in mice

217 overexpression of calpastatin, an endogenous calpain inhibitor.

218 cular endothelial cell monolayers exposed to calpain inhibitors (calpain inhibitor III and calpastati

219 he absence of calcium and in the presence of calpain inhibitors (E64c, PD 150606 and calpastatin).

220 Addition of calpain inhibitors after BDNF or TEA treatment maintaine

221 romolar range, rivaling other peptidomimetic calpain inhibitors and presenting an improved selectivit

222 S activity in HAECs, which were prevented by calpain inhibitors or mu-calpsiRNA.

223 Calpain inhibitors rescued HHcy- and HHcy/HG-induced ED

224 Finally, the use of isoform-selective calpain inhibitors revealed that calpain-2 was involved

225 As nanomolar calpain inhibitors with promising selectivity and low to

226 gn of cyclic peptides and peptidomimetics as calpain inhibitors.

227 egulated by distinct doses of proteasome and calpain inhibitors.

228 to classic electrophilic "warheads" in known calpain inhibitors.

229 talin (L432G) and FAK (V744G), we find that calpain inhibits paxillin-based adhesion assembly throug

230 IP3R1 can be cleaved by caspase or calpain into at least two receptor fragments.

231 The DEFECTIVE KERNEL1 (DEK1) calpain is a conserved 240-kD key regulator of three-dim

232 Calpain is a family of calcium-dependent endopeptidases,

233 80, the large subunit of Schistosoma mansoni calpain, is a leading antigen candidate for a schistosom

234 We recently discovered that the two major calpain isoforms in the brain, calpain-1 and calpain-2,

235 luated the respective roles of the two major calpain isoforms in the brain, calpain-1 and calpain-2.

236 Different PKMs or calpain isoforms were blocked by overexpressing specific

237 Inhibition of calpain using calpain knockout mice attenuated airway smooth muscle re

238 nsferase activity, m-calpain activity, and m-calpain level (as assessed by Western blot) were all sig

239 Damage of hERG mediated by proteases such as calpain may contribute to ischemia-associated QT prolong

240 he autophagy proteins beclin 1 and ATG5 from calpain-mediated cleavage during inflammation.

241 d that HMGB1 protects beclin 1 and ATG5 from calpain-mediated cleavage events that generate proapopto

242 ifferent PKM isoforms generated from PKCs by calpain-mediated cleavage maintain two forms of persiste

243 Although both PKMs are formed from calpain-mediated cleavage of protein kinase C (PKC) isof

244 te that ezrin-depleted cells display reduced calpain-mediated cleavage of the FA and invadopodia-asso

245 s myofilament calcium sensitivity and alters calpain-mediated cTnI proteolysis.

246 at of Kalirin, increasing its sensitivity to calpain-mediated degradation.

247 ce sustained integrin activation by limiting calpain-mediated integrin inactivation.

248 Our results indicate that calpain mediates cytokine-induced collagen-I synthesis a

249 sis indicators by suppressing the HIF-1alpha/calpains/MMP2/TGF-beta1 pathway.

250 Structurally, CAPN14 has classical calpain motifs, including a cysteine protease core.

251 hod was applied to determine the activity of calpains (mu and m) in eighty postmortem muscle samples.

252 Blocking either classical calpain or atypical small optic lobe (SOL) calpain 2 d a

253 n of calpastatin, an endogenous inhibitor of calpain, or knockdown of calpain 2 also decreased ablati

254 otency and specificity of inhibition against calpain over other cysteine proteases.

255 Calpain overactivation has been implicated in a variety

256 Calpain-overexpressing plants also have increased levels

257 Importantly, PTP1B inhibition and/or calpain overexpression significantly accelerated wound h

258 While calpains participate in these phenomena, very few studie

259 the primary signaling pathway of VEGF/VEGFR2/calpain/PI3K/AMPK/Akt/eNOS.

260 ted by the combination of HHcy and HG via mu-calpain/PKCbeta2 activation-induced eNOS-pThr497/495 and

261 Inhibition of calpain prevented the KA-induced changes.

262 itro activity assays, the mutation increased calpain protease activity and made it far more active at

263 The activity of the cytosolic C-terminal calpain protease is regulated by the membrane-anchored D

264 lcium flux, and activating calcium-dependent calpain proteases.

265 entified in CAPN12, encoding a member of the calpain proteases: a paternal missense mutation (c.1511C

266 n axon outgrowth and guidance is mediated by calpain proteolysis of the adhesion proteins talin and f

267 predict calpain cleavage sites and in vitro calpain proteolysis reactions, we identified four putati

268 These data implicate calpain/PTP1B negative feedback regulation of VEGFR2, in

269 n, our data for the first time demonstrate a calpain/PTP1B/VEGFR2 negative feedback loop in the regul

270 However, how calpain regulates growth cone motility remains unclear.

271 regulate axon outgrowth and guidance through calpain regulation of adhesion dynamics through specific

272 ings provide mechanistic insight into Ca(2+)/calpain regulation of growth cone motility and axon guid

273 the identified secreted proteins showed that calpain-related pathways were overrepresented in the sec

274 secretion and the functions of exteriorized calpains remain poorly understood.

275 h and 24 h, respectively while activity of m-calpain remained stable.

276 s relevant to AD suggests that inhibition of calpain represents an attractive approach with potential

277 Using live cell microscopy and specific calpain-resistant point-mutants of talin (L432G) and FAK

278 attributed to the cleavage of the enzyme by calpain, resulting in loss of function.

279 calpastatin forms a broad interaction around calpain's active site cysteine, we have constructed and

280 urated carbonyl moiety to the thiol group of calpain's catalytic Cys115 residue by a Michael 1,4-addi

281 mu-Calpain small interfering RNA (mu-calpsiRNA) prevented H

282 tivates the calpain by forcing apart the two calpain subunits carrying the three amino acids of the a

283 st that different stimuli activate different calpains that generate specific sets of PKMs in each neu

284 In homology modeling with other calpains, this R243L CAPN5 mutation was situated in a mo

285 nd that mouse and human lymphocytes secreted calpains through an ABCA1-driven process.

286 P35 is converted by calpain to p25, which, along with an extended t(1/2), pr

287 d activity requires cleavage of IL-1alpha by calpain to the more active mature form.

288 processing of Nrf1 by the proteasome and/or calpains to generate a cleaved active 85-kDa Nrf1 or a d

289 vide evidence that VE-cadherin is cleaved by calpain upon entry into clathrin-enriched domains.

290 Inhibition of calpain using calpain knockout mice attenuated airway sm

291 fy possible feedback regulation of VEGFR2 by calpain via its substrate protein phosphotyrosine phosph

292 anchored DEK1 MEM, which is connected to the calpain via the 600-amino acid residue Linker.

293 d on the conserved nature of animal and DEK1 calpains, we propose that the DEK1 MEM-Linker complex in

294 Casein zymography and Western blot of m-calpain were performed using the water soluble fraction

295 rotein and a 75-kDa NCX1 fragment along with calpain were up-regulated in aortic stenosis patients an

296 tatin (CAST Tg), the endogenous inhibitor of calpains were fed with high (60% kcal) fat diet for 16 w

297 Associative LTF is blocked by dn classical calpain, whereas non-associative LTF is blocked by dn sm

298 In accordance with this, calpains, which are calcium-dependent nonlysosomal cyste

299 mides as potent and reversible inhibitors of calpain with high selectivity versus related cysteine pr

300 Here we studied whether inhibition of calpains would produce therapeutic-like effects of NMDAR