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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.
41                                          The calpain inhibitor (2)-3-(4-iodophenyl)-2-mercapto-2-prop
42 nous protease which is inhibited by specific calpain inhibitors; 3.
43                                          The calpain inhibitor A-705253 (3-10 mg/kg) was tested in a
44  generation of p29 was Ca(2+)-dependent, and calpain inhibitors abolished p29 production.
45                                  Addition of calpain inhibitors after BDNF or TEA treatment maintaine
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
49                   Pretreatment with both the calpain inhibitor ALLN (N-acetyl-Leu-Leu-norleucinal) an
50  the cysteine protease inhibitor E-64 or the calpain inhibitor ALLN (N-acetyl-leucyl-leucyl-norleucin
51                                              Calpain inhibitor ALLN induced VEGFR2 activation, which
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
54              Data suggests CYGAK may be a P' calpain inhibitor and may achieve its specificity throug
55          (CYGAK)(2) is the first P' specific calpain inhibitor and will be a valuable tool to prevent
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
62 xazolyl-propionic acid receptor antagonists, calpain inhibitors, and cyclosporine A analogues.
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
65 om P3 rats were used to test the efficacy of calpain inhibitors as otoprotective molecules.
66      Greater sensitivity of HT-29 cells to a calpain inhibitor, as measured by IL-8 secretion, sugges
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
70                                    Moreover, calpain inhibitors blocked the ischaemia-induced depress
71                                              Calpain inhibitors blocked these changes.
72 e receptor into the cell culture medium, and calpain inhibitors blocked this effect.
73 of C6 cells with calpeptin (a cell-permeable calpain inhibitor) blocked calpain overexpression, MAG d
74                  Calpeptin, a cell-permeable calpain inhibitor, blocked both Erk1,2 activation and ne
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
79                                        Three calpain inhibitors, calpain inhibitor I, MDL-28170, and
80   In contrast to proteasomal inhibitors, the calpain inhibitor calpastatin and the lysosomal inhibito
81         Transient expression of the specific calpain inhibitor calpastatin blocked the loss of p107 p
82                  Transient expression of the calpain inhibitor calpastatin increased cyclin D1 protei
83                        Overexpression of the calpain inhibitor calpastatin or eIF4G1 resulted in incr
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
86 of either m- or mu-calpain or the endogenous calpain inhibitor calpastatin.
87  proteases and down-regulated the endogenous calpain inhibitor calpastatin.
88 regulated the caspase inhibitor FLIP and the calpain inhibitor calpastatin.
89 lled by a marked depletion of the endogenous calpain inhibitor, calpastatin (CAST), from AD neurons,
90 es showed increased levels of the endogenous calpain inhibitor, calpastatin (CAST).
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
93 lt of the marked depletion of the endogenous calpain inhibitor, calpastatin.
94 lation-induced degradation of the endogenous calpain inhibitor, calpastatin.
95 rn indicative of calpain activation, and the calpain inhibitor calpeptin abrogated SAHA-induced cell
96                                  Indeed, the calpain inhibitor calpeptin and the removal of the calpa
97                        Pretreatment with the calpain inhibitor calpeptin blocked calpain activation a
98 retreatment of HL-60 cells with the specific calpain inhibitor calpeptin effectively blocked both dru
99     Treatment of MEL cells with the specific calpain inhibitor calpeptin increased the levels of USF
100                                          The calpain inhibitor calpeptin increased WASP levels in act
101 ected with AdPCSK9 and then treated with the calpain inhibitor calpeptin to inhibit FLNA cleavage.
102            Interestingly, treatment with the calpain inhibitor calpeptin, overexpression of the endog
103 um-dependent and was blocked by the specific calpain inhibitor calpeptin.
104 died possible neuroprotective effects of the calpain inhibitors calpeptin and calpain inhibitor V.
105 ffect was much less than that exerted by the calpain inhibitors calpeptin and/or E64-d.
106                                 The peptidyl calpain inhibitors calpeptin, MDL 28,170 (MDL) and E64d
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
110          In addition, preincubation with the calpain inhibitor, calpeptin, suppressed the accumulatio
111 1 subunits were significantly reduced by the calpain inhibitor, calpeptin.
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
114                                              Calpain inhibitors can protect against necrotic neuronal
115 hesions or stress fibers) in the presence of calpain inhibitors; cells expressing constitutively acti
116  were studied; subgroups were treated with a calpain inhibitor (CI).
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
120                          Previous work using calpain inhibitor CYLA in our laboratory showed signific
121  cell receptor-stimulated murine thymocytes, calpain inhibitors decreased cleavage of gammac.
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
125                                              Calpain inhibitors disrupted the podosome belt, blocked
126 T3, prostate, and breast cancer cells with a calpain inhibitor dramatically increased the half-life o
127 pain activity which can be attenuated by the calpain inhibitor E-64-d.
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
130                                          The calpain inhibitor E64-d or the lysosomal protease inhibi
131 he absence of calcium and in the presence of calpain inhibitors (E64c, PD 150606 and calpastatin).
132                                              Calpain inhibitors elicited effects at concentrations of
133  knowledge, this study is the first to use a calpain inhibitor following brain trauma and suggests th
134 pase-2 down-regulation by rottlerin, whereas calpain inhibitor had no effect.
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
143           Here we investigate the effects of calpain inhibitor I on the organ injury (kidney, liver,
144            As anticipated, pretreatment with calpain inhibitor I prevented the proteolytic degradatio
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
148                    Our results indicate that calpain inhibitor I, calpain inhibitor II, and leupeptin
149  addition of protease inhibitors, leupeptin, calpain inhibitor I, E-64, or pepstatin (0.5 mM each) to
150                            Sulfasalazine and calpain inhibitor I, inhibitors of NF-kappaB activation,
151                     The cell permeant agent, calpain inhibitor I, limited EGF-induced motility and de
152                    Three calpain inhibitors, calpain inhibitor I, MDL-28170, and PD150606, but not th
153 s as nifedipine, verapamil and diltiazem, by calpain inhibitor I, or by the intracellular calcium che
154                              Lactacystin and calpain inhibitor I, specific inhibitors of the 26S prot
155  which could be blocked by pretreatment with calpain inhibitor I.
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
158  in YY1 protein levels could be prevented by calpain inhibitor II and calpeptin.
159 scle strips and adipocytes, exposure to both calpain inhibitor II and E-64-d reduced insulin-mediated
160                                              Calpain inhibitor II similarly blocked formation of the
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
164                       Calpain inhibition via calpain inhibitor III and calpastatin decreased IL-1beta
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.
173                               Cell-permeable calpain inhibitors, including calpastatin and calpeptin,
174            Studies using specific caspase or calpain inhibitors indicate that the pattern of spectrin
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
177                                              Calpain inhibitors inhibited the cleavage of the beta3 c
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
184                                        These calpain inhibitors limited epidermal growth factor-induc
185                                              Calpain inhibitors may therefore be useful therapeutical
186 hich was attenuated by pretreatment with the calpain inhibitor MDL-28170 or by transgenic overexpress
187            These effects were blocked by the calpain inhibitor MDL-28170.
188 uct immunoreactivity could be blocked by the calpain inhibitor MDL28,170 and appeared in neuronal cel
189                              Addition of the calpain inhibitors MDL28,170, calpain inhibitors I and I
190 n of Akt in ASMCs, which were blocked by the calpain inhibitor MDL28170.
191                                          The calpain inhibitor, MDL28170, significantly improved the
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
195             Exposure of preadipocytes to the calpain inhibitor N-acetyl-Leu-Leu-norleucinal or overex
196                                          The calpain inhibitor N-acetyl-leucyl-leucyl-norleucinal (AL
197                                              Calpain inhibitor N-acetyl-leucyl-leucyl-norleucinal blo
198                                              Calpain inhibitors N-acetyl-leu-leu-norleucinal (ALLN) a
199                            We found that the calpain inhibitors N-acetyl-leu-leu-norleucinal (calpain
200 ocarbamate), Ca(2+) chelator (BAPTA-AM), and calpain inhibitor (N-acetyl-Leu-Leu-Met-H).
201 lator, 3,4,5-trimethoxybenzoic acid, and the calpain inhibitor, N-acetyl-Leu-Leu-norleucinal, both bl
202                                          The calpain inhibitor, N-acetyl-leucyl-leucyl-methional, or
203         Surprisingly, calpeptin was the only calpain inhibitor of several tested with the ability to
204 ressing calpastatin, the specific endogenous calpain inhibitor, on the activity of the two proteolyti
205                            Studies utilizing Calpain inhibitors or Calpain-deficient cells confirm th
206 S activity in HAECs, which were prevented by calpain inhibitors or mu-calpsiRNA.
207 k but were blocked fully by the irreversible calpain inhibitor PD150606.
208  microM), a potent calmodulin inhibitor, and calpain inhibitor peptide (CIP, 10 microM) protected neu
209                Treating diabetic mice with a calpain inhibitor prevented loss of platelet dicer as we
210                                          The calpain inhibitor prevented proteoglycan loss, but the p
211                      Calpastatin, a specific calpain inhibitor prevented the effects of calpain I on
212                                              Calpain inhibitors prevented cleavage of Bid as well as
213                               Cell-permeable calpain inhibitors prevented E-cad(100) induction by ion
214  lines were established that overexpress the calpain inhibitor protein, calpastatin, under control of
215 inhibitor, calpeptin, or the highly specific calpain inhibitor protein, calpastatin.
216                                              Calpain inhibitors reduced IL-1alpha release and MCP-1 u
217 ated AR, and treatment of these cells with a calpain inhibitor reduces truncated AR expression.
218                                              Calpain inhibitors rescued HHcy- and HHcy/HG-induced ED
219 calpain-knockout mice or rats treated with a calpain inhibitor resulted in prevention of increased ri
220                            Co-treatment with calpain inhibitors resulted in preservation of titin, re
221        Finally, the use of isoform-selective calpain inhibitors revealed that calpain-2 was involved
222     In contrast, animals pretreated with the calpain inhibitor showed minimal evidence of apoptosis.
223                                              Calpain inhibitor SJA6017 may have potential for testing
224 e-3 and could be completely inhibited by the calpain inhibitor SJA6017, implicating both calpain and
225 ted calpain, and reduction of cell damage by calpain inhibitor SJA6017.
226 he retinal cells treated with 10 and 100 muM calpain inhibitor SNJ-1945.
227                                              Calpain inhibitors suppressed NF-kappaB activation via i
228 ketophosphonates 1c,e,f are much less potent calpain inhibitors than dimethyl alpha-ketophosphonate 1
229           Both aLLN and PD150606, a specific calpain inhibitor that interacts with the calcium-bindin
230                         In the presence of a calpain inhibitor, the apoptosis-inducing activity of PS
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
233 ects of the calpain inhibitors calpeptin and calpain inhibitor V.
234 vo treatment with the calpastatin peptide, a calpain inhibitor, was strongly neuroprotective in mice
235                         Using proteasome and calpain inhibitors, we determined that the basal activit
236              These beneficial effects of the calpain inhibitors were associated with restoration of n
237 4 as a lead, three successive generations of calpain inhibitors were developed using computationally
238 Rac or Rho, respectively, occurred even when calpain inhibitors were present.
239 ations of calpastatin, a naturally occurring calpain inhibitor, were protective.
240         This effect was also seen with other calpain inhibitors with different mechanisms of action b
241                                 As nanomolar calpain inhibitors with promising selectivity and low to
242 product identified as a potent nonselective, calpain inhibitor, with demonstrated efficacy in animal
243             Some compounds acted as specific calpain inhibitors, with comparable activity on both cal
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
246                Six animals were administered calpain inhibitor (Z-Leu-Leu-Tyr-fluoromethyl ketone; 1
247 itor), N-acetyl-leucyl-leucyl-norleucinal (a calpain inhibitor), z-VAD-fmk (a pan-caspase inhibitor),
248                                              Calpain inhibitors ZLLYCHN2, MDL 28170, and PD 150606 bl

 
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