PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 26741264-7 2016 Results of Western blot analysis indicated that ASP attenuated Caspase-3-dependent apoptosis by Caspase-8 and JNK-mediated pathway and inhibited the activation of IL-6/STAT3 and NF-kappaB signaling pathways in ConA-induced liver damage in mice. Aspartic Acid 48-51 caspase 3 Mus musculus 63-72 28342750-4 2017 Here, we report that mutating the caspase-3 consensus site in the EAAT2 sequence with an aspartate to asparagine mutation (D504N), thereby inhibiting caspase-3 cleavage of EAAT2, confers protection to the SOD1-G93A mouse. Aspartic Acid 89-98 caspase 3 Mus musculus 34-43 28342750-4 2017 Here, we report that mutating the caspase-3 consensus site in the EAAT2 sequence with an aspartate to asparagine mutation (D504N), thereby inhibiting caspase-3 cleavage of EAAT2, confers protection to the SOD1-G93A mouse. Aspartic Acid 89-98 caspase 3 Mus musculus 150-159 21098975-7 2011 As expected, induction of caspase-3 activation and cleavage of tau protein at its specific site (aspartic acid 421) was observed by Western blot and immunofluorescence analyses in mice neuronal primary cultures infected with HSV-1. Aspartic Acid 97-110 caspase 3 Mus musculus 26-35 17045926-7 2006 Since caspase-3 cleaves PKCdelta between proline and aspartate residues at the cleavage site 324DIPD327 to activate the kinase, we developed an irreversible and competitive peptide inhibitor, Z-Asp(OMe)-Ile-Pro-Asp(OMe)-FMK (z-DIPD-fmk), to mimic the caspase-3 cleavage site of PKCdelta and tested its efficacy against oxidative stress-induced cell death in PD models. Aspartic Acid 53-62 caspase 3 Mus musculus 6-15 16386699-1 2006 A probe consisting of Discosoma red fluorescent protein (DsRed) and enhanced yellow fluorescent protein (EYFP) linked by a 19-amino-acid chain containing the caspase-3 cleavage site Asp-Glu-Val-Asp was developed to monitor caspase-3 activation in living cells. Aspartic Acid 182-185 caspase 3 Mus musculus 158-167 12598529-1 2003 Bid is instrumental in death receptor-mediated apoptosis where it is cleaved by caspase 8 at aspartate 60 and aspartate 75 to generate truncated Bid (tBID) forms that facilitate release of mitochondrial cytochrome c. Bid is also cleaved at these sites by caspase 3 that is activated downstream of cytochrome c release after diverse apoptotic stimuli. Aspartic Acid 93-102 caspase 3 Mus musculus 255-264 15332996-3 2004 A 21-kDa fragment of LyGDI, resulting from activated caspase 3-induced cleavage at an N-terminal consensus site following the Asp(18) residue, accumulated at peak quantities between 5 and 12 h after irradiation. Aspartic Acid 126-129 caspase 3 Mus musculus 53-62 12598529-1 2003 Bid is instrumental in death receptor-mediated apoptosis where it is cleaved by caspase 8 at aspartate 60 and aspartate 75 to generate truncated Bid (tBID) forms that facilitate release of mitochondrial cytochrome c. Bid is also cleaved at these sites by caspase 3 that is activated downstream of cytochrome c release after diverse apoptotic stimuli. Aspartic Acid 110-119 caspase 3 Mus musculus 255-264 12011074-5 2002 In bid-deficient mice, caspase-3 activation was arrested after the initial cleavage at Asp(175). Aspartic Acid 87-90 caspase 3 Mus musculus 23-32 31253191-8 2019 To therapeutically target the tau-PSR, we bilaterally injected caspase 3-cleaved tau truncated at aspartate 421 (AAV9 Tau DeltaD421) into the hippocampus and cortex of spermidine/spermine-N1-acetyltransferase (SSAT), a key regulator of the tau-PSR, knock out (SSAT-/-), and wild type littermates, and the effects on tau neuropathology, polyamine dysregulation, and behavior were measured. Aspartic Acid 98-107 caspase 3 Mus musculus 63-72 10764048-5 2000 Caspase-3 is a group II member (2, 3, 7) categorized by an absolute substrate requirement for aspartic acid in the P4 position of the scissile bond. Aspartic Acid 94-107 caspase 3 Mus musculus 0-9 9570797-1 1998 We examined the expression, activation, and cellular localization of caspase-3 (CPP32) using immunohistochemistry, immunoblots, and cleavage of the fluorogenic substrate N-benzyloxycarbonyl-Asp-Glu-Val-Asp-7-amino-4-trifluoromethyl coumarin (zDEVD-afc) in adult mouse brain after temporary (2 hr) middle cerebral artery occlusion produced by filament insertion into the carotid artery. Aspartic Acid 202-205 caspase 3 Mus musculus 69-78 9570797-1 1998 We examined the expression, activation, and cellular localization of caspase-3 (CPP32) using immunohistochemistry, immunoblots, and cleavage of the fluorogenic substrate N-benzyloxycarbonyl-Asp-Glu-Val-Asp-7-amino-4-trifluoromethyl coumarin (zDEVD-afc) in adult mouse brain after temporary (2 hr) middle cerebral artery occlusion produced by filament insertion into the carotid artery. Aspartic Acid 202-205 caspase 3 Mus musculus 80-85 32571324-8 2020 The data showed that ASP decreased damage to the mitochondrial outer membrane, improved the stabilization of the mitochondrial membrane, and corrected the abnormal levels of ROS and mitochondrial-associated apoptosis proteins, including the Bcl-2/Bax ratio and caspase-3 and caspase-9 expression, in BMNCs which were sorted from the bone marrow cells of AA mice. Aspartic Acid 21-24 caspase 3 Mus musculus 261-270 30902848-7 2019 By engineering a novel Gsdmd D88A knock-in mouse, we further demonstrate that this proinflammatory function of caspase-8 is counteracted by caspase-3-dependent cleavage and inactivation of GSDMD at aspartate 88, and is essential to suppress GSDMD-dependent cell lysis during caspase-8-dependent apoptosis. Aspartic Acid 198-207 caspase 3 Mus musculus 140-149