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1 ase in expression of calpastatin (endogenous calpain inhibitor).
2 mined at high concentrations in vitro by the calpain inhibitor.
3 ng apoptosis was significantly retarded by a calpain inhibitor.
4 also significantly increased (P < 0.05) with calpain inhibitor.
5 vented by calpastatin, a naturally occurring calpain inhibitor.
6 overexpression of calpastatin, an endogenous calpain inhibitor.
7 select for resistance to this cell-permeant calpain inhibitor.
8 d 4) mechanical ventilation with a selective calpain inhibitor.
9 ceptors; both effects were also blocked by a calpain inhibitor.
10 spase inhibitor but not by the proteosome or calpain inhibitor.
11 slices was prevented by a membrane-permeable calpain inhibitor.
12 agmatic levels of calpastatin, an endogenous calpain inhibitor.
13 e intracellular Ca2+ chelator but not by the calpain inhibitor.
14 pha processing was blocked by proteasome and calpain inhibitors.
15 d preservation in the presence or absence of calpain inhibitors.
16 gn of cyclic peptides and peptidomimetics as calpain inhibitors.
17 Cleavage was inhibited by calpain inhibitors.
18 ely proteasome-independent, but sensitive to calpain inhibitors.
19 respectively) was limited with any of these calpain inhibitors.
20 eolysis occurs in a manner sensitive only to calpain inhibitors.
21 xide 1h (IC50 = 0.35 microM) are also potent calpain inhibitors.
22 ased by about 50%, an effect also blocked by calpain inhibitors.
23 ctivity as well as evaluating the effects of calpain inhibitors.
24 egulated by distinct doses of proteasome and calpain inhibitors.
25 nto smaller fragments was totally blocked by calpain inhibitors.
26 Activation is prevented by calpain inhibitors.
27 n be inhibited by calcium chelators and some calpain inhibitors.
28 D1 protein that was completely reversible by calpain inhibitors.
29 on, but this inhibition could be reversed by calpain inhibitors.
30 to classic electrophilic "warheads" in known calpain inhibitors.
31 st PPADS, the calcium chelator BAPTA-AM, and calpain inhibitors.
32 tive form required Ca(2+) and was blocked by calpain inhibitors.
33 lpain substrate, was modulated by Ca(2+) and calpain inhibitors.
34 dent on calpains, such that it is blocked by calpain inhibitors.
35 on, which was completely blocked by MAPK and calpain inhibitors.
36 ketoesters was synthesized and studied as mu-calpain inhibitors.
37 tenuated by buffering [Ca2+]i and blocked by calpain inhibitors.
38 rons, which was largely blocked by selective calpain inhibitors.
39 rs when added to osteoclasts pretreated with calpain inhibitors.
40 ells by up-regulating endogenous caspase and calpain inhibitors.
46 ies was substantially delayed by addition of calpain inhibitors after sublethal excitotoxic exposure.
47 n this study, we evaluated the effect of the calpain inhibitor AK295 [Z-Leu-aminobutyric acid-CONH(CH
48 of calpains with the peptide alpha-ketoamide calpain inhibitor AK295 can reduce the clinical and path
50 the cysteine protease inhibitor E-64 or the calpain inhibitor ALLN (N-acetyl-leucyl-leucyl-norleucin
52 ion-induced immobilization is prevented by a calpain inhibitor and by an allosteric LFA-1 inhibitor.
53 l calcium sensor-1 (NCS1), or treatment with calpain inhibitor and ibudilast reversed deficits observ
56 rption in a manner similar to the effects of calpain inhibitors and had no further effect on these pa
57 d breast cancer cells that was reversible by calpain inhibitors and not by phenylmethylsulfonyl fluor
58 romolar range, rivaling other peptidomimetic calpain inhibitors and presenting an improved selectivit
59 sults indicate that MP acts as a proteinase (calpain) inhibitor and define a new mechanism for its ac
60 The mRNA levels of calpastatin (endogenous calpain inhibitor) and beta-actin (house-keeping) genes
61 bitors (peptidomimetic and natural product), calpain inhibitors, and anti-PgPM4 monoclonal antibodies
63 rs, including three GSK3beta inhibitors, two calpain inhibitors, and one adenylyl cyclase activator,
64 h is sensitive to wortmannin (IC50 7 nM) and calpain inhibitors, and the phosphorylation of PtdIns3P
67 e positive CD4(+) thymocytes, not only did a calpain inhibitor augment CD3-induced proliferation, but
68 protease inhibitor, and the highly specific calpain inhibitor BDA-410 restored normal synaptic funct
69 raperitoneal administration of the selective calpain inhibitor benzyloxycarbonyl-leucyl-leucinal (5 m
73 of C6 cells with calpeptin (a cell-permeable calpain inhibitor) blocked calpain overexpression, MAG d
75 etreatment of Jurkat cells with calpeptin, a calpain inhibitor, blocked PTP1B cleavage and inhibited
76 lencing; however, it could be prevented with calpain inhibitors, calcium-chelating agents, calpain kn
77 rt-term (4-h) exposure to the cell-permeable calpain inhibitors calpain inhibitor II and E-64-d incre
78 cular endothelial cell monolayers exposed to calpain inhibitors (calpain inhibitor III and calpastati
80 In contrast to proteasomal inhibitors, the calpain inhibitor calpastatin and the lysosomal inhibito
84 yR antagonists ryanodine and dantrolene, the calpain inhibitor calpastatin, and by a specific inhibit
85 calpeptin, overexpression of the endogenous calpain inhibitor calpastatin, or gene silencing of calp
89 lled by a marked depletion of the endogenous calpain inhibitor, calpastatin (CAST), from AD neurons,
91 on, whereas overexpression of the endogenous calpain inhibitor, calpastatin, attenuated Ox-LDL-induce
92 alpains and overexpression of the endogenous calpain inhibitor, calpastatin, prevent the production o
95 rn indicative of calpain activation, and the calpain inhibitor calpeptin abrogated SAHA-induced cell
98 retreatment of HL-60 cells with the specific calpain inhibitor calpeptin effectively blocked both dru
101 ected with AdPCSK9 and then treated with the calpain inhibitor calpeptin to inhibit FLNA cleavage.
104 died possible neuroprotective effects of the calpain inhibitors calpeptin and calpain inhibitor V.
107 received daily intraperitoneal injections of calpain inhibitor (calpeptin) or vehicle from day 1 unti
108 d by the PI3K inhibitor, wortmannin, and the calpain inhibitor, calpeptin, constituting the first evi
109 se hamster ovary cells were decreased by the calpain inhibitor, calpeptin, or the highly specific cal
112 d from this animal model of SCI suggest that calpain inhibitor can provide neuroprotection in patient
113 ssive depletion; we show here that selective calpain inhibitors can block this step, which suggests t
115 hesions or stress fibers) in the presence of calpain inhibitors; cells expressing constitutively acti
117 ing the EGFP-ataxin-3-84Q zebrafish with the calpain inhibitor compound calpeptin decreased levels of
118 und that treating the MJD zebrafish with the calpain inhibitor compound calpeptin produces complete r
119 findings indicate that Sarm1 and/or specific calpain inhibitors could be developed to prevent cisplat
122 cTnT-ND in myocardial ischemia reperfusion, calpain inhibitors decreased the level of cTnT-ND in Tri
123 Experimental treatments with caspase 3 or calpain inhibitors demonstrated that PV IgGs induced aca
124 ddition, I-benzyl-CH=C(SH)COOH (PD150606), a calpain inhibitor directed toward the calcium binding si
126 T3, prostate, and breast cancer cells with a calpain inhibitor dramatically increased the half-life o
128 ydrazine, KCl, quinine, merocyanine 540, the calpain inhibitor E-64d, and the scramblase inhibitor R5
129 pan-caspase inhibitor z-VAD-fmk, but not the calpain inhibitor E-64d, prevents Bid cleavage, Bax conf
131 he absence of calcium and in the presence of calpain inhibitors (E64c, PD 150606 and calpastatin).
133 knowledge, this study is the first to use a calpain inhibitor following brain trauma and suggests th
135 pastatin peptide and PD150606, two selective calpain inhibitors, had no effect on BRCA1 stability, wh
136 dysfunction, all of which were attenuated by calpain inhibitor I (10 mg/kg i.p.), administered 30 min
137 s completely inhibited by preincubation with calpain inhibitor I (N-acetyl-leucyl-leucyl-norleucinal
138 h ubiquitin-dependent proteasome inhibitors: calpain inhibitor I and lactacystin each prevented this
139 bited by the addition of protease inhibitors calpain inhibitor I and N-tosyl-phechloromethyl ketone a
140 by pharmacological inhibitors (calpeptin and calpain inhibitor I and PD98059, respectively) for EGF-i
141 muscle cells (activated with endotoxin) with calpain inhibitor I attenuated the binding of activated
142 whereas complete inhibition is observed with calpain inhibitor I but not with the proteasome inhibito
145 rovide evidence that the mechanisms by which calpain inhibitor I reduces the circulatory failure as w
146 ain inhibitors N-acetyl-leu-leu-norleucinal (calpain inhibitor I) and carbenzoxy-val-phe-H (MDL 28,17
147 and N-acetyl-leucinyl-leucinyl-norleucinal (calpain inhibitor I) were found to inhibit the CL activi
149 addition of protease inhibitors, leupeptin, calpain inhibitor I, E-64, or pepstatin (0.5 mM each) to
153 s as nifedipine, verapamil and diltiazem, by calpain inhibitor I, or by the intracellular calcium che
156 e activity, in NIH3T3 cells was inhibited by calpain inhibitors I and II or the p38 MAP kinase inhibi
157 ddition of the calpain inhibitors MDL28,170, calpain inhibitors I and II, and leupeptin (all 1-100 mi
159 scle strips and adipocytes, exposure to both calpain inhibitor II and E-64-d reduced insulin-mediated
161 y TCDD, whereas the protease inhibitors EST, calpain inhibitor II, and chloroquine do not affect this
162 r results indicate that calpain inhibitor I, calpain inhibitor II, and leupeptin all provided signifi
163 viral activity, including GC376, boceprevir, calpain inhibitors II, and XII, with each containing a r
165 ll monolayers exposed to calpain inhibitors (calpain inhibitor III and calpastatin) or transfected wi
166 eridine propranol and were partly blocked by calpain inhibitor III but were not affected by the NR2A-
167 murine L cells, treatment with calpeptin or calpain inhibitor III increased Abeta42, but not Abeta40
168 and Abeta42 prompted us to determine how the calpain inhibitor III MDL 28170 influences these three c
169 inhibitor of calcium/calmodulin kinase, and calpain inhibitor III, a calpain inhibitor, inhibited NM
170 ibiting the activation of calpain by a novel calpain inhibitor in aged 3xTgAD mice with well-establis
171 overexpress human calpastatin, an endogenous calpain inhibitor, in skeletal muscle were produced.
172 nase (CaMK) type IV, which was attenuated by calpain inhibitors, in GCs supplemented with 20 mm KCl.
175 Studies with a selective membrane permeable calpain inhibitor indicated that tTG is likely to be an
176 illomavirus E6 protein was unaffected by the calpain inhibitor, indicating that the stabilization did
178 modulin kinase, and calpain inhibitor III, a calpain inhibitor, inhibited NMDA-induced potentiation a
179 , indicating that inhibition of apoptosis by calpain inhibitors is independent of effects on viral re
180 apoptosis, indicating that the effect of the calpain inhibitors is not due to cross-inhibition of lys
181 nsulin secretion with short-term exposure to calpain inhibitors is not mediated by increased response
182 vage is inhibited by calpeptin, calpastatin, calpain inhibitor IV, and E-64d, but not by caspase 3 in
183 of p107 protein which was reversible by the calpain inhibitor leucyl-leucyl-norleucinal but not by t
186 hich was attenuated by pretreatment with the calpain inhibitor MDL-28170 or by transgenic overexpress
188 uct immunoreactivity could be blocked by the calpain inhibitor MDL28,170 and appeared in neuronal cel
192 y of globupain led to the discovery that the calpain inhibitors MG101 and leupeptin inactivate globup
193 Here, we report that treatment with the calpain inhibitor N-[N-(N-acetyl-l-leucyl)-l-leucyl]-l-n
194 uced NF-kappaB activation was blocked by the calpain inhibitor N-Ac-Leu-Leu-norleucinal, suggesting t
201 lator, 3,4,5-trimethoxybenzoic acid, and the calpain inhibitor, N-acetyl-Leu-Leu-norleucinal, both bl
204 ressing calpastatin, the specific endogenous calpain inhibitor, on the activity of the two proteolyti
208 microM), a potent calmodulin inhibitor, and calpain inhibitor peptide (CIP, 10 microM) protected neu
214 lines were established that overexpress the calpain inhibitor protein, calpastatin, under control of
219 calpain-knockout mice or rats treated with a calpain inhibitor resulted in prevention of increased ri
222 In contrast, animals pretreated with the calpain inhibitor showed minimal evidence of apoptosis.
224 e-3 and could be completely inhibited by the calpain inhibitor SJA6017, implicating both calpain and
228 ketophosphonates 1c,e,f are much less potent calpain inhibitors than dimethyl alpha-ketophosphonate 1
231 Intraperitoneal injection of a short term calpain inhibitor to timed pregnant female mice abrogate
232 otoxins (e.g., cisplatin, CDDP), the role of calpain inhibitors under these conditions was examined i
234 vo treatment with the calpastatin peptide, a calpain inhibitor, was strongly neuroprotective in mice
237 4 as a lead, three successive generations of calpain inhibitors were developed using computationally
242 product identified as a potent nonselective, calpain inhibitor, with demonstrated efficacy in animal
244 therefore hypothesized that treatment with a calpain inhibitor would protect neurons from immune-medi
245 e inhibited by the dipeptide alpha-ketoamide calpain inhibitor Z-Leu-aminobutyric acid-CONH(CH(2))3-m
247 itor), N-acetyl-leucyl-leucyl-norleucinal (a calpain inhibitor), z-VAD-fmk (a pan-caspase inhibitor),