ライフサイエンスコーパス: calpain

1 n sheaths prefigure retractions, mediated by calpain.

2 guidance through activation of the protease calpain.

3 s due to increase in proteolytic activity of calpain.

4 e expression of several proteases, including calpain.

5 activation of the calcium-dependent enzyme, calpain.

6 mpaired its ability to inhibit the protease, calpain.

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

8 We identified calpain 1 (CAPN1) as an exclusive rPhe508del interactor

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

10 tered compartmentalization increased nuclear calpain 1 activity.

11 a calmodulin- and actin-binding protein) and calpain 1 and 2 (calcium-dependent cysteine proteases th

12 of TRPC6) results in the mislocalization of calpain 1 and 2 and significant downregulation of calpai

13 Markers of proteolysis including calpain 1 and calpain 2 remained activated 10 days after

14 al bidirectional cross-talk between NFIB and calpain 1 in GBM cells.

15 cells, NFIB expression decreased the CAST-to-calpain 1 ratio in the cytoplasm.

16 ST localizing primarily to the cytoplasm and calpain 1 to the nucleus.

17 We also show that nuclear calpain 1, by cleaving and activating calcineurin, induc

18 Of note, knockdown of calpain 1, NFIB, or both increased GBM cell migration an

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

20 subcellular compartmentalization of CAST and calpain 1, with CAST localizing primarily to the cytopla

21 Here, we uncovered an NFIB-calpain 1-positive feedback loop mediated through CAST a

22 reased autolysis and activity of cytoplasmic calpain 1.

23 Furthermore, activity and protein levels of calpain-1 (CAPN-1) were significantly higher in aortas a

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

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

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

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

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

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

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

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

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

33 MJD context and if reduction or ablation of calpain-1 expression ameliorates the disease-associated

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

35 Lowering or removal of calpain-1 in cells or mice counteracted calpain system o

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

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

38 Moreover, calpain-1 knockout in YAC84Q mice alleviated excessive f

39 body weight loss and extended survival upon calpain-1 knockout.

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

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

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

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

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

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

46 vation of the calpain-2 isoform but not with calpain-1, suggesting differential roles for both calpai

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

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

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

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

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

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

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

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

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

56 Calpain 15 (CAPN15) is an intracellular cysteine proteas

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

58 tion of calcium-dependent cytosolic protease calpain 2 and cleavage of its important downstream subst

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

60 rkers of proteolysis including calpain 1 and calpain 2 remained activated 10 days after extubation wi

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

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

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

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

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

66 in activity coincided with activation of the calpain-2 isoform but not with calpain-1, suggesting dif

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

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

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

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

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

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

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

74 wn reproducibly low micromolar inhibition of calpain-2.

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

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

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

78 Calpain 3 expression in muscle, assessed by western blot

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

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

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

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

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

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

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

86 Calpains, a group of calcium-dependent cysteine protease

87 followed by cell death that was dependent on calpain activation and CSNK1A1 degradation(4,5).

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

89 Calpain activation and tau hyperphosphorylation have bee

90 Calpain activation induced by overexpression or Ca/A2318

91 Moreover, calpain activation inhibited VEGF-induced VEGFR2 phospho

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

93 in intracellular Ca(2+) Although effects of calpain activation were detected in the axon initial seg

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

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

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

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

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

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

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

101 Gaussian process models highlighted calpain activity as a key event during primary rod photo

102 these cells using motility, detachment, and calpain activity assays; immunofluorescence; confocal or

103 analysed MJD models, we detected an elevated calpain activity at baseline.

104 High calpain activity coincided with activation of the calpai

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

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

107 models, spatiotemporal pattern of increased calpain activity matched the progression of primary rod

108 harmacologic and genetic approaches lowering calpain activity showed beneficial effects on molecular

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

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

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

112 7-independent mechanism but was dependent on calpain activity.

113 ique, constitutive, functional extracellular calpain activity.

114 t with its phosphorylation and virus-induced calpain activity.

115 nflammasome activation was also dependent on calpain activity.

116 in 1 and 2 and significant downregulation of calpain activity; this leads to altered podocyte cytoske

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

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

119 n-classical small optic lobe (SOL) family of calpains, an important class of developmental proteins,

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

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

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

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

124 activation of the calcium-dependent protease calpain and degradation of the AJ proteins VE-cadherin,

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

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

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

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

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

130 ion of PERK also increases the activation of calpains and deregulates the gene expression of the memb

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

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

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

134 Calpains are a family of intracellular, calcium-dependen

135 Calpains are calcium-dependent neutral cysteine protease

136 Calpains are intracellular proteases that play a key rol

137 While calpains are invariably reported to be exclusively intra

138 In our study, we tested whether calpains are overactivated in the MJD context and if red

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

140 Calpains are ubiquitous pro-inflammatory proteases, whos

141 We here identified calpain as the driver of the up- and down-regulation of

142 findings emphasize the general potential of calpains as a therapeutic target in MJD and other neurod

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

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

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

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

147 gulatory cross-talk between NFI and the CAST/calpain/calcineurin signaling pathway in MG cells.

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

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

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

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

152 Calpain cleavage exposes a region that is recognized by

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

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

155 Blocking calpain cleavage of talin and FAK inhibits repulsive tur

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

157 , via two proteolytic fragments generated by calpain cleavage.

158 reover, we found that STAT3 interacts with a calpain-cleaved carboxyl-terminal fragment of FLNA.

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

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

161 Calpain conditional knockout mice were studied in the mo

162 roptosis and that sensitivity to rupture was calpain-dependent and linked with cleavage of vimentin a

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

164 cellular space to drive death receptor 6 and calpain-dependent catastrophic degeneration.

165 ctivation of Flna and chemical inhibition of calpain-dependent cleavage of FLNA impaired macrophage s

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

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

168 ERK signaling in turn caused calpain-dependent MPS degradation, providing a negative

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

170 0%) and membrane blebbing (-90%); 3) reduced calpain-dependent protein cleavage (-60%); and 4) modera

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

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

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

174 orylation at Ser-55 and Ser-83 and resisting calpain digestion.

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

176 nts constitutively overexpressing the active CALPAIN domain of DEK1.

177 ocalization appears to be independent of its calpain domain proteolytic activity.

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

179 Calpain exteriorization and TLR2 cleavage were critical

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

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

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

183 Calpain-I expression paralleled with a proteolysis of vo

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

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

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

187 , the physical interaction between TRPC6 and calpain in the podocyte is important for cell motility a

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

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

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

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

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

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

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

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

196 ess failure and edema formation secondary to calpain-induced disruption of VE-cadherin adhesion.

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

198 Calpains influence VSMC proliferation and collagen synth

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

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

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

202 Calpain inhibition by ritonavir may be a powerful tool f

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

204 Calpain inhibition has beneficial effects against TBI-in

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

206 Furthermore, calpain inhibition preserved BBB integrity/permeability

207 Calpain inhibition showed a transient improvement in glu

208 Furthermore, calpain inhibition suppressed macrophage migration to ad

209 Calpain inhibition via calpain inhibitor III and calpast

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

211 centrations within the therapeutic range for calpain inhibition.

212 Collectively, calpains inhibition plays crucial roles in vascular rest

213 Calpains inhibition protects against inflammaging, limit

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

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

216 Calpain inhibitor ALLN induced VEGFR2 activation, which

217 l calcium sensor-1 (NCS1), or treatment with calpain inhibitor and ibudilast reversed deficits observ

218 ected with AdPCSK9 and then treated with the calpain inhibitor calpeptin to inhibit FLNA cleavage.

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

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

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

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

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

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

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

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

227 findings indicate that Sarm1 and/or specific calpain inhibitors could be developed to prevent cisplat

228 gn of cyclic peptides and peptidomimetics as 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 Here we show that activation of calpains is required for both neurotoxicity and formatio

234 However, specifically targeting one of the calpain isoforms by genetic means has not yet been evalu

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

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

237 Different PKMs or calpain isoforms were blocked by overexpressing specific

238 in-1, suggesting differential roles for both calpain isoforms.

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

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

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

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

245 Inhibiting calpain-mediated FLNA cleavage with calpeptin in macroph

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

247 up- and down-regulating I(NaP) and KCC2, the calpain-mediated proteolysis of Nav and KCC2 drives the

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 The nitric oxide deficiency reduces neuronal calpain nitrosylation and results in enzyme activation,

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

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

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

256 Calpain overactivation has been implicated in a variety

257 Calpain-overexpressing plants also have increased levels

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

259 While calpains participate in these phenomena, very few studie

260 S216 results in Abi1 degradation through the calpain pathway.

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

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

263 Calcineurin is cleaved and activated by calpain proteases whose activity is, in turn, regulated

264 the activation pattern of Ca(2+) -dependent calpain proteases, generating spatiotemporal maps of the

265 cineurin is cleaved and thereby activated by calpain proteases, which are, in turn, inhibited by calp

266 Low-calcium conditions inhibited calpain proteases, which target ten-eleven translocated

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

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

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

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

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

272 Acute inhibition of calpains reduced this proteolysis, restored the motoneur

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

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

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

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

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

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

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

280 Deletion of Piezo1 in ECs or inhibition of calpain similarly prevented reduction in the AJ proteins

281 and LabCaS outperformed other predictors for calpain-specific cleavage sites.

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

283 l of calpain-1 in cells or mice counteracted calpain system overactivation and led to reduced cleavag

284 The relationships between MHC isoforms, calpain systems and meat quality characteristics of diff

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

286 ling after pathologic stress and disinhibits calpain through phosphorylation of calpastatin.

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

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

289 Inhibition of calpain using calpain knockout mice attenuated airway sm

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

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

292 an inhibitor of the Ca(2+)-dependent enzyme, calpain, we conclude that both effects were mediated by

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

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

297 n of Rb requires action by another protease, calpain, which cleaves Rb after Lys 810.

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