PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
33964050-2	2021	We investigated the effects of CAV1-T29107A and endothelial nitric oxide synthase (eNOS) G894T polymorphisms on the serum levels of testosterone, NO and prostate-specific antigen (PSA) in patients with PC.	Testosterone	132-144	nitric oxide synthase 3	Homo sapiens	48-81	
34543641-4	2021	Recent evidence demonstrates testosterone activates androgen receptors (AR) and generates nitric oxide (NO) through the Akt-endothelial NO synthase (eNOS) pathway; however, it remains unknown how castration impacts this signaling pathway.	Testosterone	29-41	nitric oxide synthase 3	Homo sapiens	120-147	
34543641-4	2021	Recent evidence demonstrates testosterone activates androgen receptors (AR) and generates nitric oxide (NO) through the Akt-endothelial NO synthase (eNOS) pathway; however, it remains unknown how castration impacts this signaling pathway.	Testosterone	29-41	nitric oxide synthase 3	Homo sapiens	149-153	
34496169-0	2021	The serum levels of testosterone in coronary artery disease patients; relation to NO, eNOS, endothelin-1, and disease severity.	Testosterone	20-32	nitric oxide synthase 3	Homo sapiens	86-90	
22771325-1	2012	Our previous study has demonstrated that testosterone rapidly activates endothelial nitric oxide synthase (eNOS), enhancing nitric oxide (NO) release from endothelial cells (ECs) via the phosphatidylinositol 3-kinase/Akt (PI3-kinase/Akt) pathway.	Testosterone	41-53	nitric oxide synthase 3	Homo sapiens	72-105	
26746999-7	2016	Consistently, testosterone enhanced the phosphorylation of AKT and nitric oxide synthase 3.	Testosterone	14-26	nitric oxide synthase 3	Homo sapiens	67-90	
26746999-10	2016	CONCLUSIONS: Testosterone protects cardiomyocytes against senescence caused by doxorubicin at least in part by modulating telomere binding factor 2 via a pathway involving the androgen receptor, phosphatidylinositol 3 kinase, AKT, and nitric oxide synthase 3.	Testosterone	13-25	nitric oxide synthase 3	Homo sapiens	235-258	
32550542-7	2019	Conclusion: T786C polymorphism at eNOS locus appeared to be a major contributor in the variable erectile function iPDE5/testosterone response in Spaniards.	Testosterone	120-132	nitric oxide synthase 3	Homo sapiens	34-38	
23471592-6	2014	In agreement, our in vitro studies show that testosterone inhibits the gene expression of endothelial NO synthase (eNOS) after 48 hours.	Testosterone	45-57	nitric oxide synthase 3	Homo sapiens	115-119	
23471592-9	2014	CONCLUSION: These results show that a supraphysiological dose of testosterone decreases the expression of eNOS and consequently the formation of NO, which could partly be explained by oxidative stress.	Testosterone	65-77	nitric oxide synthase 3	Homo sapiens	106-110	
19650200-9	2009	The plasma testosterone and osteocalcin concentrations in the subjects of eNOS G894T G/T genotype were evidently higher than those in the subjects of other genotypes (P<0.05); the plasma estradiol concentration in the subjects of eNOS 27 bp-VNTR a/a genotype was obviously higher than that in the subjects of b/b genotype (P<0.01).	Testosterone	11-23	nitric oxide synthase 3	Homo sapiens	74-78	
19650200-16	2009	CONCLUSION: eNOS G894T G/T genotype influenced the plasma testosterone and osteocalcin concentrations, and T/T genotype influenced BMD.	Testosterone	58-70	nitric oxide synthase 3	Homo sapiens	12-16	
16157773-7	2005	A nitric oxide (NO) scavenger and an inhibitor of NO synthase 3 (NOS3) reversed the effects of testosterone on APD, which suggests that NO released from NOS3 is responsible for the electrophysiological effects of testosterone.	Testosterone	95-107	nitric oxide synthase 3	Homo sapiens	50-63	
16157773-7	2005	A nitric oxide (NO) scavenger and an inhibitor of NO synthase 3 (NOS3) reversed the effects of testosterone on APD, which suggests that NO released from NOS3 is responsible for the electrophysiological effects of testosterone.	Testosterone	95-107	nitric oxide synthase 3	Homo sapiens	65-69	
16157773-7	2005	A nitric oxide (NO) scavenger and an inhibitor of NO synthase 3 (NOS3) reversed the effects of testosterone on APD, which suggests that NO released from NOS3 is responsible for the electrophysiological effects of testosterone.	Testosterone	95-107	nitric oxide synthase 3	Homo sapiens	153-157	
16157773-7	2005	A nitric oxide (NO) scavenger and an inhibitor of NO synthase 3 (NOS3) reversed the effects of testosterone on APD, which suggests that NO released from NOS3 is responsible for the electrophysiological effects of testosterone.	Testosterone	213-225	nitric oxide synthase 3	Homo sapiens	50-63	
16157773-7	2005	A nitric oxide (NO) scavenger and an inhibitor of NO synthase 3 (NOS3) reversed the effects of testosterone on APD, which suggests that NO released from NOS3 is responsible for the electrophysiological effects of testosterone.	Testosterone	213-225	nitric oxide synthase 3	Homo sapiens	65-69	
16157773-7	2005	A nitric oxide (NO) scavenger and an inhibitor of NO synthase 3 (NOS3) reversed the effects of testosterone on APD, which suggests that NO released from NOS3 is responsible for the electrophysiological effects of testosterone.	Testosterone	213-225	nitric oxide synthase 3	Homo sapiens	153-157	
16157773-9	2005	Immunoblot analysis revealed that testosterone induced phosphorylation of Akt and NOS3.	Testosterone	34-46	nitric oxide synthase 3	Homo sapiens	82-86