PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 16987501-0 2006 Involvement of nitric oxide synthase and ROS-mediated activation of L-type voltage-gated Ca2+ channels in NMDA-induced DPYSL3 degradation. ros 41-44 dihydropyrimidinase like 3 Homo sapiens 119-125 16987501-0 2006 Involvement of nitric oxide synthase and ROS-mediated activation of L-type voltage-gated Ca2+ channels in NMDA-induced DPYSL3 degradation. N-Methylaspartate 106-110 dihydropyrimidinase like 3 Homo sapiens 119-125 16987501-2 2006 Recently, we have shown that in primary cortical neurons (PCN) NMDA and oxidative stress (H(2)O(2)) caused a calpain-dependent cleavage of DPYSL3 (62 kDa) resulting in the appearance of a lower molecular weight form (60 kDa) of DPYSL3. N-Methylaspartate 63-67 dihydropyrimidinase like 3 Homo sapiens 139-145 16987501-2 2006 Recently, we have shown that in primary cortical neurons (PCN) NMDA and oxidative stress (H(2)O(2)) caused a calpain-dependent cleavage of DPYSL3 (62 kDa) resulting in the appearance of a lower molecular weight form (60 kDa) of DPYSL3. N-Methylaspartate 63-67 dihydropyrimidinase like 3 Homo sapiens 228-234 16987501-3 2006 Our preliminary results had shown that antioxidants significantly reduced NMDA-induced DPYSL3 degradation, indicating involvement of ROS in calpain activation. N-Methylaspartate 74-78 dihydropyrimidinase like 3 Homo sapiens 87-93 16987501-3 2006 Our preliminary results had shown that antioxidants significantly reduced NMDA-induced DPYSL3 degradation, indicating involvement of ROS in calpain activation. ros 133-136 dihydropyrimidinase like 3 Homo sapiens 87-93 16987501-4 2006 The aim of this study was to investigate the possible involvement of NOS in NMDA-induced DPYSL3 degradation. N-Methylaspartate 76-80 dihydropyrimidinase like 3 Homo sapiens 89-95 16987501-5 2006 We found that NOS inhibitor (L-NAME) significantly prevented NMDA-induced ROS formation, as well as intracellular Ca(2+) increase [Ca(2+)](i), DPYSL3 degradation and cell death. NG-Nitroarginine Methyl Ester 29-35 dihydropyrimidinase like 3 Homo sapiens 143-149 16987501-6 2006 Further, exposure of PCN to NO donor (SNP) resulted in significant [Ca(2+)](i) increase, ROS generation and probable calpain-mediated DPYSL3 truncation. PREGNENOLONE CARBONITRILE 21-24 dihydropyrimidinase like 3 Homo sapiens 134-140 16987501-7 2006 The NMDA- and oxidative stress (ROS)-induced DPYSL3 truncation was totally dependent on extracellular [Ca(2+)](i). N-Methylaspartate 4-8 dihydropyrimidinase like 3 Homo sapiens 45-51 16987501-7 2006 The NMDA- and oxidative stress (ROS)-induced DPYSL3 truncation was totally dependent on extracellular [Ca(2+)](i). ros 32-35 dihydropyrimidinase like 3 Homo sapiens 45-51 16987501-8 2006 While NMDA-induced DPYSL3 truncation was blocked by both NMDA receptor antagonist (MK801) [Kowara, R., Chen, Q., Milliken, M., Chakravarthy, B., 2005. N-Methylaspartate 6-10 dihydropyrimidinase like 3 Homo sapiens 19-25 16987501-8 2006 While NMDA-induced DPYSL3 truncation was blocked by both NMDA receptor antagonist (MK801) [Kowara, R., Chen, Q., Milliken, M., Chakravarthy, B., 2005. Dizocilpine Maleate 83-88 dihydropyrimidinase like 3 Homo sapiens 19-25 16987501-9 2006 Calpain-mediated degradation of dihydropyrimidinase-like 3 protein (DPYSL3) in response to NMDA and H(2)O(2) toxicity. N-Methylaspartate 91-95 dihydropyrimidinase like 3 Homo sapiens 32-66 16987501-9 2006 Calpain-mediated degradation of dihydropyrimidinase-like 3 protein (DPYSL3) in response to NMDA and H(2)O(2) toxicity. N-Methylaspartate 91-95 dihydropyrimidinase like 3 Homo sapiens 68-74 16987501-11 2006 95 (2), 466-474] and L-VGCC (nimodipine) inhibitors, H(2)O(2)-induced increase in [Ca(2+)](i), ROS generation and DPYSL3 truncation was blocked only by nimodipine. Hydrogen Peroxide 53-61 dihydropyrimidinase like 3 Homo sapiens 114-120 16987501-12 2006 These results indicate that changes in Ca(2+) homeostasis resulting from ROS-dependent activation of L-VGCC are sufficient to induce probable calpain-mediated DPYSL3 truncation and demonstrate for the first time the role of ROS in the mechanism leading to glutamate-induced calpain activation and DPYSL3 protein degradation. ros 73-76 dihydropyrimidinase like 3 Homo sapiens 159-165 16987501-12 2006 These results indicate that changes in Ca(2+) homeostasis resulting from ROS-dependent activation of L-VGCC are sufficient to induce probable calpain-mediated DPYSL3 truncation and demonstrate for the first time the role of ROS in the mechanism leading to glutamate-induced calpain activation and DPYSL3 protein degradation. ros 73-76 dihydropyrimidinase like 3 Homo sapiens 297-303 16987501-12 2006 These results indicate that changes in Ca(2+) homeostasis resulting from ROS-dependent activation of L-VGCC are sufficient to induce probable calpain-mediated DPYSL3 truncation and demonstrate for the first time the role of ROS in the mechanism leading to glutamate-induced calpain activation and DPYSL3 protein degradation. Glutamic Acid 256-265 dihydropyrimidinase like 3 Homo sapiens 159-165