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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 overexpression of calpastatin, an endogenous calpain inhibitor.
4 ng apoptosis was significantly retarded by a calpain inhibitor.
5 also significantly increased (P < 0.05) with calpain inhibitor.
6 vented by calpastatin, a naturally occurring 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 gn of cyclic peptides and peptidomimetics as calpain inhibitors.
15 pha processing was blocked by proteasome and calpain inhibitors.
16 d preservation in the presence or absence of 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 egulated by distinct doses of proteasome and calpain inhibitors.
21 eolysis occurs in a manner sensitive only to calpain inhibitors.
22 xide 1h (IC50 = 0.35 microM) are also potent calpain inhibitors.
23 ased by about 50%, an effect also blocked by calpain inhibitors.
24 ctivity as well as evaluating the effects of 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 to classic electrophilic "warheads" in known calpain inhibitors.
30 on, but this inhibition could be reversed by 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.
55 rption in a manner similar to the effects of calpain inhibitors and had no further effect on these pa
56 d breast cancer cells that was reversible by calpain inhibitors and not by phenylmethylsulfonyl fluor
57 romolar range, rivaling other peptidomimetic calpain inhibitors and presenting an improved selectivit
58 sults indicate that MP acts as a proteinase (calpain) inhibitor and define a new mechanism for its ac
59 The mRNA levels of calpastatin (endogenous calpain inhibitor) and beta-actin (house-keeping) genes
60 bitors (peptidomimetic and natural product), calpain inhibitors, and anti-PgPM4 monoclonal antibodies
62 rs, including three GSK3beta inhibitors, two calpain inhibitors, and one adenylyl cyclase activator,
63 h is sensitive to wortmannin (IC50 7 nM) and calpain inhibitors, and the phosphorylation of PtdIns3P
66 e positive CD4(+) thymocytes, not only did a calpain inhibitor augment CD3-induced proliferation, but
67 protease inhibitor, and the highly specific calpain inhibitor BDA-410 restored normal synaptic funct
68 raperitoneal administration of the selective calpain inhibitor benzyloxycarbonyl-leucyl-leucinal (5 m
72 of C6 cells with calpeptin (a cell-permeable calpain inhibitor) blocked calpain overexpression, MAG d
74 etreatment of Jurkat cells with calpeptin, a calpain inhibitor, blocked PTP1B cleavage and inhibited
75 lencing; however, it could be prevented with calpain inhibitors, calcium-chelating agents, calpain kn
76 rt-term (4-h) exposure to the cell-permeable calpain inhibitors calpain inhibitor II and E-64-d incre
77 cular endothelial cell monolayers exposed to calpain inhibitors (calpain inhibitor III and calpastati
79 In contrast to proteasomal inhibitors, the calpain inhibitor calpastatin and the lysosomal inhibito
83 yR antagonists ryanodine and dantrolene, the calpain inhibitor calpastatin, and by a specific inhibit
84 calpeptin, overexpression of the endogenous calpain inhibitor calpastatin, or gene silencing of calp
88 lled by a marked depletion of the endogenous calpain inhibitor, calpastatin (CAST), from AD neurons,
90 on, whereas overexpression of the endogenous calpain inhibitor, calpastatin, attenuated Ox-LDL-induce
91 alpains and overexpression of the endogenous calpain inhibitor, calpastatin, prevent the production o
94 rn indicative of calpain activation, and the calpain inhibitor calpeptin abrogated SAHA-induced cell
97 retreatment of HL-60 cells with the specific calpain inhibitor calpeptin effectively blocked both dru
102 died possible neuroprotective effects of the calpain inhibitors calpeptin and calpain inhibitor V.
105 received daily intraperitoneal injections of calpain inhibitor (calpeptin) or vehicle from day 1 unti
106 d by the PI3K inhibitor, wortmannin, and the calpain inhibitor, calpeptin, constituting the first evi
107 se hamster ovary cells were decreased by the calpain inhibitor, calpeptin, or the highly specific cal
110 d from this animal model of SCI suggest that calpain inhibitor can provide neuroprotection in patient
111 ssive depletion; we show here that selective calpain inhibitors can block this step, which suggests t
113 hesions or stress fibers) in the presence of calpain inhibitors; cells expressing constitutively acti
114 ing the EGFP-ataxin-3-84Q zebrafish with the calpain inhibitor compound calpeptin decreased levels of
115 und that treating the MJD zebrafish with the calpain inhibitor compound calpeptin produces complete r
118 cTnT-ND in myocardial ischemia reperfusion, calpain inhibitors decreased the level of cTnT-ND in Tri
119 Experimental treatments with caspase 3 or calpain inhibitors demonstrated that PV IgGs induced aca
120 ddition, I-benzyl-CH=C(SH)COOH (PD150606), a calpain inhibitor directed toward the calcium binding si
122 T3, prostate, and breast cancer cells with a calpain inhibitor dramatically increased the half-life o
124 ydrazine, KCl, quinine, merocyanine 540, the calpain inhibitor E-64d, and the scramblase inhibitor R5
125 pan-caspase inhibitor z-VAD-fmk, but not the calpain inhibitor E-64d, prevents Bid cleavage, Bax conf
127 he absence of calcium and in the presence of calpain inhibitors (E64c, PD 150606 and calpastatin).
129 knowledge, this study is the first to use a calpain inhibitor following brain trauma and suggests th
131 pastatin peptide and PD150606, two selective calpain inhibitors, had no effect on BRCA1 stability, wh
132 dysfunction, all of which were attenuated by calpain inhibitor I (10 mg/kg i.p.), administered 30 min
133 s completely inhibited by preincubation with calpain inhibitor I (N-acetyl-leucyl-leucyl-norleucinal
134 h ubiquitin-dependent proteasome inhibitors: calpain inhibitor I and lactacystin each prevented this
135 bited by the addition of protease inhibitors calpain inhibitor I and N-tosyl-phechloromethyl ketone a
136 by pharmacological inhibitors (calpeptin and calpain inhibitor I and PD98059, respectively) for EGF-i
137 muscle cells (activated with endotoxin) with calpain inhibitor I attenuated the binding of activated
138 whereas complete inhibition is observed with calpain inhibitor I but not with the proteasome inhibito
141 rovide evidence that the mechanisms by which calpain inhibitor I reduces the circulatory failure as w
142 ain inhibitors N-acetyl-leu-leu-norleucinal (calpain inhibitor I) and carbenzoxy-val-phe-H (MDL 28,17
143 and N-acetyl-leucinyl-leucinyl-norleucinal (calpain inhibitor I) were found to inhibit the CL activi
145 addition of protease inhibitors, leupeptin, calpain inhibitor I, E-64, or pepstatin (0.5 mM each) to
149 s as nifedipine, verapamil and diltiazem, by calpain inhibitor I, or by the intracellular calcium che
152 e activity, in NIH3T3 cells was inhibited by calpain inhibitors I and II or the p38 MAP kinase inhibi
153 ddition of the calpain inhibitors MDL28,170, calpain inhibitors I and II, and leupeptin (all 1-100 mi
155 scle strips and adipocytes, exposure to both calpain inhibitor II and E-64-d reduced insulin-mediated
157 y TCDD, whereas the protease inhibitors EST, calpain inhibitor II, and chloroquine do not affect this
158 r results indicate that calpain inhibitor I, calpain inhibitor II, and leupeptin all provided signifi
160 ll monolayers exposed to calpain inhibitors (calpain inhibitor III and calpastatin) or transfected wi
161 eridine propranol and were partly blocked by calpain inhibitor III but were not affected by the NR2A-
162 murine L cells, treatment with calpeptin or calpain inhibitor III increased Abeta42, but not Abeta40
163 and Abeta42 prompted us to determine how the calpain inhibitor III MDL 28170 influences these three c
164 inhibitor of calcium/calmodulin kinase, and calpain inhibitor III, a calpain inhibitor, inhibited NM
165 ibiting the activation of calpain by a novel calpain inhibitor in aged 3xTgAD mice with well-establis
166 overexpress human calpastatin, an endogenous calpain inhibitor, in skeletal muscle were produced.
167 nase (CaMK) type IV, which was attenuated by calpain inhibitors, in GCs supplemented with 20 mm KCl.
170 Studies with a selective membrane permeable calpain inhibitor indicated that tTG is likely to be an
171 illomavirus E6 protein was unaffected by the calpain inhibitor, indicating that the stabilization did
173 modulin kinase, and calpain inhibitor III, a calpain inhibitor, inhibited NMDA-induced potentiation a
174 , indicating that inhibition of apoptosis by calpain inhibitors is independent of effects on viral re
175 apoptosis, indicating that the effect of the calpain inhibitors is not due to cross-inhibition of lys
176 nsulin secretion with short-term exposure to calpain inhibitors is not mediated by increased response
177 vage is inhibited by calpeptin, calpastatin, calpain inhibitor IV, and E-64d, but not by caspase 3 in
178 of p107 protein which was reversible by the calpain inhibitor leucyl-leucyl-norleucinal but not by t
181 hich was attenuated by pretreatment with the calpain inhibitor MDL-28170 or by transgenic overexpress
183 uct immunoreactivity could be blocked by the calpain inhibitor MDL28,170 and appeared in neuronal cel
187 Here, we report that treatment with the calpain inhibitor N-[N-(N-acetyl-l-leucyl)-l-leucyl]-l-n
188 uced NF-kappaB activation was blocked by the calpain inhibitor N-Ac-Leu-Leu-norleucinal, suggesting t
195 lator, 3,4,5-trimethoxybenzoic acid, and the calpain inhibitor, N-acetyl-Leu-Leu-norleucinal, both bl
198 ressing calpastatin, the specific endogenous calpain inhibitor, on the activity of the two proteolyti
202 microM), a potent calmodulin inhibitor, and calpain inhibitor peptide (CIP, 10 microM) protected neu
208 lines were established that overexpress the calpain inhibitor protein, calpastatin, under control of
213 calpain-knockout mice or rats treated with a calpain inhibitor resulted in prevention of increased ri
216 In contrast, animals pretreated with the calpain inhibitor showed minimal evidence of apoptosis.
218 e-3 and could be completely inhibited by the calpain inhibitor SJA6017, implicating both calpain and
222 ketophosphonates 1c,e,f are much less potent calpain inhibitors than dimethyl alpha-ketophosphonate 1
225 Intraperitoneal injection of a short term calpain inhibitor to timed pregnant female mice abrogate
226 otoxins (e.g., cisplatin, CDDP), the role of calpain inhibitors under these conditions was examined i
228 vo treatment with the calpastatin peptide, a calpain inhibitor, was strongly neuroprotective in mice
231 4 as a lead, three successive generations of calpain inhibitors were developed using computationally
236 product identified as a potent nonselective, calpain inhibitor, with demonstrated efficacy in animal
238 therefore hypothesized that treatment with a calpain inhibitor would protect neurons from immune-medi
239 e inhibited by the dipeptide alpha-ketoamide calpain inhibitor Z-Leu-aminobutyric acid-CONH(CH(2))3-m
241 itor), N-acetyl-leucyl-leucyl-norleucinal (a calpain inhibitor), z-VAD-fmk (a pan-caspase inhibitor),
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