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