PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 15093730-5 2004 The activation of the caspase-3 was also inhibited by NMDA, and the neurons were more resistant towards death caused by high concentrations of glutamate and staurosporine. Glutamic Acid 143-152 caspase 3 Homo sapiens 22-31 14567692-2 2003 We show that replacement of valine 266, the residue at the center of the procaspase-3 dimer interface, with glutamate resulted in an increase in enzyme activity of approximately 60-fold, representing a pseudoactivation of the procaspase. Glutamic Acid 108-117 caspase 3 Homo sapiens 73-85 15042585-2 2004 We previously demonstrated that glutamate induces caspase-3 activation and death of the late oligodendrocyte progenitor known as the pro-oligodendroblast (pro-OL) via activation of the AMPA/kainate glutamate receptors. Glutamic Acid 32-41 caspase 3 Homo sapiens 50-59 15042585-8 2004 Moreover, IGF-I prevented caspase-3 activation in pro-OLs as long as 8 h after exposure of the cells to glutamate, suggesting that delayed activation of IGF-I-mediated survival pathways can block glutamate-mediated apoptosis in pro-OLs. Glutamic Acid 104-113 caspase 3 Homo sapiens 26-35 15042585-8 2004 Moreover, IGF-I prevented caspase-3 activation in pro-OLs as long as 8 h after exposure of the cells to glutamate, suggesting that delayed activation of IGF-I-mediated survival pathways can block glutamate-mediated apoptosis in pro-OLs. Glutamic Acid 196-205 caspase 3 Homo sapiens 26-35 13130505-0 2003 Cystamine inhibits transglutaminase and caspase-3 cleavage in glutamate-exposed astroglial cells. Glutamic Acid 62-71 caspase 3 Homo sapiens 40-49 13130505-7 2003 Glutamate exposure also promoted an increase in caspase-3 compared with control cultures. Glutamic Acid 0-9 caspase 3 Homo sapiens 48-57 13130505-10 2003 These results suggest that glutamate increased both TG and caspase-3 in astroglial cells early in the excitotoxin-induced events. Glutamic Acid 27-36 caspase 3 Homo sapiens 59-68 12929750-5 2003 Inhibition of caspase-8 by Lle-Glu (OMe)-Thr-Asp(OMe)-fluoromethyl ketone completely blocked caspase-3 cleavage and apoptosis in UVA-treated cells, suggesting that apoptosis was initiated by the Fas pathway. Glutamic Acid 31-34 caspase 3 Homo sapiens 93-102 12139923-3 2002 Glutamate induced time- and dose-dependent DNA fragmentation and caspase-3 activation in pro-OLs. Glutamic Acid 0-9 caspase 3 Homo sapiens 65-74 12660222-5 2003 The caspase-3 and caspase-9 inhibitors Z-Asp(OCH(3))-Glu(OCH(3))-Val-Asp(OCH(3))-fluoromethylketone (FMK) and Z-Leu-Glu(OCH(3))-His-Asp(OCH(3))-FMK reduced apoptotic bodies to 25-30% of the control cells. Glutamic Acid 53-56 caspase 3 Homo sapiens 4-13 11007881-4 2000 These findings extend previous in vitro observations and are the first to implicate the involvement of glutamate-mediated calcineurin activation and BAD dephosphorylation as upstream, premitochondrial signaling events leading to caspase-3 activation in traumatic spinal cord injury. Glutamic Acid 103-112 caspase 3 Homo sapiens 229-238 12829403-7 2002 Both LIGA20 and BDNF blocked glutamate-mediated activation of caspase-3 and consequently apoptosis; however, the anticaspase-3 activity was seen only when these compounds were added to the cultures several hours before glutamate, suggesting that LIGA20 and BDNF share an identical molecular mechanism. Glutamic Acid 29-38 caspase 3 Homo sapiens 62-71 11479221-6 2001 Helenalin led to a time-dependent (0-24 h) cleavage of the specific caspase-3-like substrate Asp-Glu-Val-Asp-7-amino-4-trifluoromethylcoumarin as well as to the proteolytic processing of procaspase-3 and -8. Glutamic Acid 97-100 caspase 3 Homo sapiens 187-206 11209755-6 2000 The architecture of the substrate binding site of granzyme B appears to be designed to accommodate and cleave hexapeptides such as the sequence Ile-Glu-Thr-Asp-/Ser-Gly present in the activation site of pro-caspase-3, a proven physiological substrate of granzyme B. Glutamic Acid 148-151 caspase 3 Homo sapiens 203-216 10037682-8 1999 Lithium pretreatment blocks glutamate-induced cytochrome c release and cleavage of lamin B1, a nuclear substrate for caspase-3. Glutamic Acid 28-37 caspase 3 Homo sapiens 117-126 10975859-4 2000 Both caspase-3 inhibitor Z-Asp(OCH3)-Glu(OCH3)-Val-Asp(OCH3)-CH2F and caspase-9 inhibitor Z-Leu-Glu(OCH3)-His-Asp(OCH3)-CH2F prevented the chondrocyte death. Glutamic Acid 37-40 caspase 3 Homo sapiens 5-14 10748267-4 2000 Moreover, r-hCTGF-induced apoptosis was significantly inhibited by an antibody to CTGF and a caspase-3 inhibitor, Z-Asp(Ome)-Glu-(Ome)Val-Asp(Ome)-FMK. Glutamic Acid 125-128 caspase 3 Homo sapiens 93-102 10724120-0 2000 Novel characteristics of glutamate-induced cell death in primary septohippocampal cultures: relationship to calpain and caspase-3 protease activation. Glutamic Acid 25-34 caspase 3 Homo sapiens 120-129 10724120-1 2000 Studies examined the phenotypic characteristics of glutamate-induced cell death and their relationship to calpain and caspase-3 activation. Glutamic Acid 51-60 caspase 3 Homo sapiens 118-127 10724120-9 2000 Incubation with varying doses of glutamate produced calpain and caspase-3 activation. Glutamic Acid 33-42 caspase 3 Homo sapiens 64-73 10521575-4 1999 The temporal profile of p53, c-Myc, Bcl-2, Bax expression and caspases activation after glutamate treatment suggest that Bcl-2, c-Myc and caspase-3 play important roles in the excitotoxic neuronal cell death. Glutamic Acid 88-97 caspase 3 Homo sapiens 138-147 32477148-8 2020 In addition, our experimental results demonstrated that resveratrol markedly enhanced the decreased levels of Bcl-2 and significantly reduced the increased expression of Bax and Caspase-3 in hippocampal neurons induced by glutamate exposure. Glutamic Acid 222-231 caspase 3 Homo sapiens 178-187 34423383-11 2021 The contents of caspase-9 and caspase-3 were elevated following exposure to GLU more than IFO. Glutamic Acid 76-79 caspase 3 Homo sapiens 30-39 35187882-11 2022 Glutamate increased caspase-3 expression, and quercetin attenuated this increase in both parvalbumin siRNA transfected and non-transfected cells. Glutamic Acid 0-9 caspase 3 Homo sapiens 20-29 9326666-0 1997 Activation of a caspase 3-related cysteine protease is required for glutamate-mediated apoptosis of cultured cerebellar granule neurons. Glutamic Acid 68-77 caspase 3 Homo sapiens 16-25 9326666-3 1997 Glutamate-induced apoptosis of CGNs is, however, associated with a concentration- and time-dependent activation of the interleukin 1beta-converting enzyme (ICE)/CED-3-related protease, CPP32/Yama/apopain (now designated caspase 3). Glutamic Acid 0-9 caspase 3 Homo sapiens 185-190 9326666-3 1997 Glutamate-induced apoptosis of CGNs is, however, associated with a concentration- and time-dependent activation of the interleukin 1beta-converting enzyme (ICE)/CED-3-related protease, CPP32/Yama/apopain (now designated caspase 3). Glutamic Acid 0-9 caspase 3 Homo sapiens 191-195 9326666-3 1997 Glutamate-induced apoptosis of CGNs is, however, associated with a concentration- and time-dependent activation of the interleukin 1beta-converting enzyme (ICE)/CED-3-related protease, CPP32/Yama/apopain (now designated caspase 3). Glutamic Acid 0-9 caspase 3 Homo sapiens 196-203 9326666-3 1997 Glutamate-induced apoptosis of CGNs is, however, associated with a concentration- and time-dependent activation of the interleukin 1beta-converting enzyme (ICE)/CED-3-related protease, CPP32/Yama/apopain (now designated caspase 3). Glutamic Acid 0-9 caspase 3 Homo sapiens 220-229 9326666-4 1997 Further, the time course of caspase 3 activation after glutamate exposure of CGNs parallels the development of apoptosis. Glutamic Acid 55-64 caspase 3 Homo sapiens 28-37 9326666-5 1997 Moreover, glutamate-induced apoptosis of CGNs is almost completely blocked by the selective cell permeable tetrapeptide inhibitor of caspase 3, Ac-DEVD-CHO but not by the ICE (caspase 1) inhibitor, Ac-YVAD-CHO. Glutamic Acid 10-19 caspase 3 Homo sapiens 133-142 9326666-6 1997 Western blots of cytosolic extracts from glutamate-exposed CGNs reveal both cleavage of the caspase 3 substrate, poly(ADP-ribose) polymerase, as well as proteolytic processing of pro-caspase 3 to active subunits. Glutamic Acid 41-50 caspase 3 Homo sapiens 92-101 9326666-6 1997 Western blots of cytosolic extracts from glutamate-exposed CGNs reveal both cleavage of the caspase 3 substrate, poly(ADP-ribose) polymerase, as well as proteolytic processing of pro-caspase 3 to active subunits. Glutamic Acid 41-50 caspase 3 Homo sapiens 183-192 9326666-7 1997 Our data demonstrate that glutamate-induced apoptosis of CGNs is mediated by a posttranslational activation of the ICE/CED-3-related cysteine protease caspase 3. Glutamic Acid 26-35 caspase 3 Homo sapiens 151-160 28400209-3 2017 AST pretreatment attenuated glutamate-induced activation of caspase-3, reduction of anti-apoptotic protein Bcl-2, and increase of pro-apoptotic protein Bak. Glutamic Acid 28-37 caspase 3 Homo sapiens 60-69 31129157-7 2019 In addition, KHG21834 effectively attenuated glutamate-induced levels of Bax, Bcl-2, cleaved caspase-3, p-p38, p-JNK proteins, and TUNEL positive cells. Glutamic Acid 45-54 caspase 3 Homo sapiens 93-102 30872014-4 2019 Pretreatment with neurosteroids significantly reduced acute L-glutamic acid or NMDA excitotoxicity mediated by Ca2+ entry and consequent ROS (reactive oxygen species) release and caspase-3 activation. Glutamic Acid 60-75 caspase 3 Homo sapiens 179-188 31050222-4 2019 Furthermore, we also show that the collective secretome rescues cortical neurons from glutamate toxicity as evidenced by increased neurite outgrowth, reduced LDH release, and reduced caspase 3/7 activity. Glutamic Acid 86-95 caspase 3 Homo sapiens 183-192 29909197-3 2018 Caspase-3 as an apoptosis indicator could specifically cleave the N-terminus of biotinylated DEVD-peptide (biotin-Gly-Asp-Gly-Asp-Glu-Val-Asp-Gly-Cys) immobilized on the Au nanoparticle-decorated TiO2 nanotube arrays (TiO2/Au NTAs) substrate. Glutamic Acid 130-133 caspase 3 Homo sapiens 0-9 29859204-6 2018 Zolpidem prevented death of P19 neurons exposed to glutamate, and abolished the glutamate-induced increase in ROS production, p53 and Bax expression, and caspase-3/7 activity. Glutamic Acid 80-89 caspase 3 Homo sapiens 154-163 30872014-7 2019 This drop in Ca2+ level resulted in corresponding ROS suppression and prevented glutamate-induced caspase-3 activation. Glutamic Acid 80-89 caspase 3 Homo sapiens 98-107 30606992-5 2019 ALA pretreatment dose-dependently suppressed glutamate-induced apoptotic events including altered nuclear morphology and activation of caspase-3. Glutamic Acid 45-54 caspase 3 Homo sapiens 135-144 28653316-7 2017 Altogether, we found that AFP interacts with caspase-3 through precise amino acids, namely loop-4 residues Glu-248, Asp-253 and His-257. Glutamic Acid 107-110 caspase 3 Homo sapiens 45-54 25298748-7 2014 The tissue was then processed for histology, measurement of intracellular caspase-3 activity (using the caspase-3 substrate N-acetyl-asp-glu-val-asp-7-amino-4-methylcoumarin), and immunohistochemical detection of the apoptotic biomarkers caspase-3, cytochrome C, and annexin A2. Glutamic Acid 137-140 caspase 3 Homo sapiens 74-83 27168077-3 2016 A variety of modifications of the classical caspase-3 and caspase-7 substrate sequence Asp-Glu-Val-Asp were carried out in order to increase caspase-3 affinity and eliminate caspase-7 cross-reactivity. Glutamic Acid 91-94 caspase 3 Homo sapiens 141-150 26876755-4 2016 Metformin significantly attenuated neuronal apoptosis in glutamate-treated CGN by reducing cytochrome c releasing, caspase-3 activation and phosphorylation of MAP kinases. Glutamic Acid 57-66 caspase 3 Homo sapiens 115-124 26788243-6 2016 Furthermore, our results demonstrated that green tea polyphenols restored the dysfunction of mitochondrial pro- or antiapoptotic proteins Bax, Bcl-2, and caspase-3 caused by glutamate. Glutamic Acid 174-183 caspase 3 Homo sapiens 154-163 21320517-3 2011 We found that glutamate-induced apoptosis in cultured hippocampal neurons was significantly attenuated by the ensuing PQQ treatment, which also inhibited the glutamate-induced increase in Ca2+ influx, caspase-3 activity, and ROS production, and reversed the glutamate-induced decrease in Bcl-2/Bax ratio. Glutamic Acid 14-23 caspase 3 Homo sapiens 201-210 24587873-4 2014 RESULTS: In semiquantitative analysis of the Glu-treated SGC, FasL, and caspase 3 expression intensity were increased with concentration- and time-dependent manner. Glutamic Acid 45-48 caspase 3 Homo sapiens 72-81 22143383-1 2012 A new label-free method for the detection of apoptosis was proposed based on colorimetric assay of caspase-3 activity using an unlabeled Asp-Glu-Val-Asp (DEVD)-containing peptide substrate and unmodified gold nanoparticles (AuNPs). Glutamic Acid 141-144 caspase 3 Homo sapiens 99-108 22294086-11 2012 We used a bi-functional caspase-3 substrate containing a DEVD (Asp-Glu-Val-Asp) caspase-3 recognition subunit and a DNA-binding dye. Glutamic Acid 67-70 caspase 3 Homo sapiens 24-33 21671003-9 2011 The increase caspase-3 of and decrease of procaspase-3 expression levels after administration of 0.2 mmol/l Glu suggested the apoptotic effects of Glu. Glutamic Acid 147-150 caspase 3 Homo sapiens 13-22 21671003-9 2011 The increase caspase-3 of and decrease of procaspase-3 expression levels after administration of 0.2 mmol/l Glu suggested the apoptotic effects of Glu. Glutamic Acid 147-150 caspase 3 Homo sapiens 42-54 21320517-3 2011 We found that glutamate-induced apoptosis in cultured hippocampal neurons was significantly attenuated by the ensuing PQQ treatment, which also inhibited the glutamate-induced increase in Ca2+ influx, caspase-3 activity, and ROS production, and reversed the glutamate-induced decrease in Bcl-2/Bax ratio. Glutamic Acid 158-167 caspase 3 Homo sapiens 201-210 21320517-3 2011 We found that glutamate-induced apoptosis in cultured hippocampal neurons was significantly attenuated by the ensuing PQQ treatment, which also inhibited the glutamate-induced increase in Ca2+ influx, caspase-3 activity, and ROS production, and reversed the glutamate-induced decrease in Bcl-2/Bax ratio. Glutamic Acid 158-167 caspase 3 Homo sapiens 201-210 20673301-4 2010 Removal of B27 supplement from the culture medium for 24 h or the addition of glutamate (3-10mum) decreased neuronal viability (P<0.05) and increased Tdt-mediated dUTP nick-end labelling (TUNEL) staining and caspase-3 activity (P<0.05), which is consistent with apoptotic cell death. Glutamic Acid 78-87 caspase 3 Homo sapiens 211-220 20416364-6 2010 Meanwhile, the activation of c-Jun N-terminal kinase and caspase-3 induced by l-glutamate was suppressed by l-theanine. Glutamic Acid 78-89 caspase 3 Homo sapiens 57-66 20528251-9 2010 The ratio of Bcl-2/Bax protein decreased, and the percentage of activated caspase-3 increased in myeloma cells treated by matrine for 48 h, but this matrine-induced activity of caspase-3 was completely canceled by the addition of Z-Asp(O-Me)-Glu(O-Me)-Val-Asp(O-Me) fluoromethyl ketone (Z-DEVD-FMK), a caspase-3 inhibitor. Glutamic Acid 242-245 caspase 3 Homo sapiens 177-186 20528251-9 2010 The ratio of Bcl-2/Bax protein decreased, and the percentage of activated caspase-3 increased in myeloma cells treated by matrine for 48 h, but this matrine-induced activity of caspase-3 was completely canceled by the addition of Z-Asp(O-Me)-Glu(O-Me)-Val-Asp(O-Me) fluoromethyl ketone (Z-DEVD-FMK), a caspase-3 inhibitor. Glutamic Acid 242-245 caspase 3 Homo sapiens 177-186 20642015-17 2004 Asp-Glu-Val-Asp (DEVD) is the peptide sequence optimal for caspase-3 and -7, while the Val-Glu-His-Asp (VEHD) sequence is preferred by caspase-6 (5). Glutamic Acid 4-7 caspase 3 Homo sapiens 59-75 19235896-4 2009 Preincubation with the caspase-9 inhibitor z-LEHD-fmk, the caspase-3 inhibitor z-DEVD-fmk, or the specific pan-caspase inhibitor Q-VD-oph decreased the percentage of propidium iodide-positive neurons (52.5% +/- 3.1%, 39.4% +/- 3.5%, 44.6% +/- 3%, respectively, vs. 65% +/- 3% in glutamate + vehicle). Glutamic Acid 279-288 caspase 3 Homo sapiens 59-68 20187571-8 2010 The decrease of procaspase-3 expression levels after application of 0.2 mmol/L Glu suggested the apoptotic effects of Glu. Glutamic Acid 79-82 caspase 3 Homo sapiens 16-28 20187571-8 2010 The decrease of procaspase-3 expression levels after application of 0.2 mmol/L Glu suggested the apoptotic effects of Glu. Glutamic Acid 118-121 caspase 3 Homo sapiens 16-28 19235896-3 2009 Glutamate treatment induced early cytochrome c release, followed by activation of caspase-9 and caspase-3. Glutamic Acid 0-9 caspase 3 Homo sapiens 96-105 19389388-8 2009 Glutamate treatment significantly increased both intracellular free Ca(2+) and the activities of downstream proteases such as calpain and caspase-3. Glutamic Acid 0-9 caspase 3 Homo sapiens 138-147 19428819-7 2009 Glu+AA applied together had a synergistic effect on the levels of Caspase-3 gene expression, and Bcl-2 and Hsp70 protein. Glutamic Acid 0-3 caspase 3 Homo sapiens 66-75 19389388-12 2009 From these observations, we conclude that estrogen limits glutamate-induced cell death in VSC 4.1 cells through effects on L-type Ca(2+) channels, inhibiting Ca(2+) influx as well as activation of the pro-apoptotic proteases calpain and caspase-3. Glutamic Acid 58-67 caspase 3 Homo sapiens 237-246 18854175-0 2008 Human caspase-3 inhibition by Z-tLeu-Asp-H: tLeu(P2) counterbalances Asp(P4) and Glu(P3) specific inhibitor truncation. Glutamic Acid 81-84 caspase 3 Homo sapiens 6-15 19054278-5 2009 Both OA and glutamate induced cell death via increased reactive oxygen species, protein carbonylation, lipid peroxidation, caspase-3 activity, and mitochondrial dysfunction. Glutamic Acid 12-21 caspase 3 Homo sapiens 123-132 17418815-8 2007 For the first time it was shown that glutamate induces apoptosis of spiral ganglion neurons, which could be blocked selectively by a caspase-3 inhibitor. Glutamic Acid 37-46 caspase 3 Homo sapiens 133-142 18930139-8 2008 Immunoblot analysis shows that apoptosis is mediated by the cleavage of caspase-3 and caspase-7 in glutamate treated neurons. Glutamic Acid 99-108 caspase 3 Homo sapiens 72-81 18316066-5 2008 Vulnerability of the differentiated cells towards the oxidizer, arsenite, and the excitotoxic glutamate/glycine is demonstrated by the dose-dependent cytotoxic effects of these agents on cell viability and activation of caspase 3/7. Glutamic Acid 94-103 caspase 3 Homo sapiens 220-229 19099901-16 2008 And the relative Caspase-3 activity which was enhanced by the treatment with glutamate (0.1428 +/- 0.0495 and 0.8616 +/- 0.1051, P < 0.01), was suppressed by Par-4-SiRNA-1 and Par-4-SiRNA-2 (0.8616 +/- 0.1051 and 0.6581 +/- 0.0555, respectively, P < 0.01). Glutamic Acid 77-86 caspase 3 Homo sapiens 17-26 18755243-6 2008 The enzymatic assay indicated that COSs antagonized glutamate-evoked activation of caspase-3. Glutamic Acid 52-61 caspase 3 Homo sapiens 83-92 18755243-7 2008 These results collectively suggest that COSs prevent cultured hippocampal neurons from glutamate-induced cell damage by interfering with an increase in [Ca(2+)](c) and inhibiting caspase-3 activity. Glutamic Acid 87-96 caspase 3 Homo sapiens 179-188 18265412-3 2008 This glutamate-mediated excitotoxicity is caused by intracellular Ca2+ overload via the N-methyl-D-aspartate receptor NMDAR), reactive oxygen species (ROS) generation, and caspase-3 activation. Glutamic Acid 5-14 caspase 3 Homo sapiens 172-181 18265412-7 2008 Finally, glutamate-induced activation of caspase-3 was reduced by myricetin treatment. Glutamic Acid 9-18 caspase 3 Homo sapiens 41-50 18041091-0 2008 alpha-Amino-3-hydroxy-5-methyl-4-isoxazole propionate attenuates glutamate-induced caspase-3 cleavage via regulation of glycogen synthase kinase 3beta. Glutamic Acid 65-74 caspase 3 Homo sapiens 83-92 18041091-9 2008 Glutamate (100 microM) increased cleaved caspase-3, an apoptosis-related cysteine protease, and caspase-3 inhibitor (Ac-DEVD-CHO; 1 microM) blocked glutamate-induced excitotoxicity in our culture. Glutamic Acid 0-9 caspase 3 Homo sapiens 41-50 18041091-9 2008 Glutamate (100 microM) increased cleaved caspase-3, an apoptosis-related cysteine protease, and caspase-3 inhibitor (Ac-DEVD-CHO; 1 microM) blocked glutamate-induced excitotoxicity in our culture. Glutamic Acid 0-9 caspase 3 Homo sapiens 96-105 18041091-9 2008 Glutamate (100 microM) increased cleaved caspase-3, an apoptosis-related cysteine protease, and caspase-3 inhibitor (Ac-DEVD-CHO; 1 microM) blocked glutamate-induced excitotoxicity in our culture. Glutamic Acid 148-157 caspase 3 Homo sapiens 96-105 18041091-10 2008 AMPA (10 microM, 24 hr) and SB216763 (10 microM) prominently decreased glutamate-induced caspase-3 cleavage. Glutamic Acid 71-80 caspase 3 Homo sapiens 89-98 18041091-11 2008 These findings suggest that AMPA activates PI3K-Akt and subsequently inhibits GSK3beta and that inactivated GSK3beta attenuates glutamate-induced caspase-3 cleavage and neurotoxicity. Glutamic Acid 128-137 caspase 3 Homo sapiens 146-155 17616814-5 2008 This action of glutamate was accompanied by cytochrome c release, caspase-3 activation and DNA fragmentation. Glutamic Acid 15-24 caspase 3 Homo sapiens 66-75 17616814-6 2008 Glutamate at low concentration (10 microM) induced caspase-3 activation and DNA fragmentation, but it did not cause cytochrome c release and, it did not alter the viability of slices. Glutamic Acid 0-9 caspase 3 Homo sapiens 51-60 17762198-2 2007 Here, we demonstrate that IGF-1 prevents caspase 3 activation in late OPs when administered up to 16 h following exposure to glutamate. Glutamic Acid 125-134 caspase 3 Homo sapiens 41-50 17118359-6 2006 Both curcumin and TA inhibited glutamate-induced caspase-3 activation. Glutamic Acid 31-40 caspase 3 Homo sapiens 49-58 17118359-1 2006 Glutamate excitotoxicity is mediated by intracellular Ca(2+) overload, caspase-3 activation, and ROS generation. Glutamic Acid 0-9 caspase 3 Homo sapiens 71-80 15193297-5 2004 Glutamate, which is elevated in the cerebrospinal fluid of ALS patients, induced DNA fragmentation and caspase-3 cleavage in the spinal cord motor neurons. Glutamic Acid 0-9 caspase 3 Homo sapiens 103-112 16420423-8 2006 In electrophysiological experiments with identified snail neurons, selective blockade of the caspase-3 with the irreversible and cell-permeable inhibitor of caspase-3 N-benzyloxycarbonyl-Asp(OMe)-Glu(OMe)-Val-Asp-(OMe)-fluoro-methylketone prevented development of the long-term stage of synaptic input sensitization, suggesting that caspase is necessary for normal synaptic plasticity in snails. Glutamic Acid 196-199 caspase 3 Homo sapiens 93-102 16420423-8 2006 In electrophysiological experiments with identified snail neurons, selective blockade of the caspase-3 with the irreversible and cell-permeable inhibitor of caspase-3 N-benzyloxycarbonyl-Asp(OMe)-Glu(OMe)-Val-Asp-(OMe)-fluoro-methylketone prevented development of the long-term stage of synaptic input sensitization, suggesting that caspase is necessary for normal synaptic plasticity in snails. Glutamic Acid 196-199 caspase 3 Homo sapiens 157-166 15986728-4 2005 Cell stimulation by glutamate, correlated with expression of the pro-apoptotic genes Caspase-3, Caspase-2L and Bax. Glutamic Acid 20-29 caspase 3 Homo sapiens 85-94 16806165-4 2006 Glutamate exposure also induced a transient increase in caspase-3 activity. Glutamic Acid 0-9 caspase 3 Homo sapiens 56-65 16806165-5 2006 A membrane-permeable inhibitor of caspase-3 (DEVD-CHO) prevented the glutamate neurotoxicity. Glutamic Acid 69-78 caspase 3 Homo sapiens 34-43 16806165-12 2006 Moreover, serofendic acid reduced the activation of caspase-3 induced by glutamate. Glutamic Acid 73-82 caspase 3 Homo sapiens 52-61 16806165-14 2006 These results indicate that serofendic acid prevents glutamate-induced apoptosis in cultured cortical neurons by the prevention of loss of mitochondrial membrane potential and the reduction of the process of caspase-3 activation. Glutamic Acid 53-62 caspase 3 Homo sapiens 208-217