PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
21825026-5	2011	In rats, the nNOS inhibitor SMTC did not significantly affect MR (67 +- 4 vs. 57 +- 4 units).	smtc	28-32	nitric oxide synthase 1	Rattus norvegicus	13-17
21825026-7	2011	The same was found when SMTC was combined with angiotensin II to reproduce the hypertension and vasoconstriction seen with l-NAME (58 +- 3 vs. 54 +- 7 units, l-NAME 81 +- 2 units), or when SMTC was replaced by the nNOS inhibitor NPA (57 +- 5 vs. 56 +- 7 units, l-NAME 79 +- 4 units) or by the iNOS inhibitor 1400W (50 +- 1 vs. 55 +- 4 units, l-NAME 81 +- 3 units).	smtc	24-28	nitric oxide synthase 1, neuronal	Mus musculus	214-218
21825026-7	2011	The same was found when SMTC was combined with angiotensin II to reproduce the hypertension and vasoconstriction seen with l-NAME (58 +- 3 vs. 54 +- 7 units, l-NAME 81 +- 2 units), or when SMTC was replaced by the nNOS inhibitor NPA (57 +- 5 vs. 56 +- 7 units, l-NAME 79 +- 4 units) or by the iNOS inhibitor 1400W (50 +- 1 vs. 55 +- 4 units, l-NAME 81 +- 3 units).	smtc	24-28	nitric oxide synthase 2, inducible	Mus musculus	293-297
18505586-5	2008	S-methionyl-L-thiocitrulline (SMTC), and tin protoporphyrin (SnPP) were used to inhibit neuronal/constitutive NOS-1 and heme-oxygenase, respectively, and alter NO and CO production, respectively, as assessed by paired t-tests.	smtc	30-34	nitric oxide synthase 1, neuronal	Mus musculus	110-115
20521125-4	2010	The presence of the polymorphic change L769L in the RET gene predisposes to the development of sMTC and also lowers the age of onset of MTC in carriers of the homozygous polymorphic variant L769L.	smtc	95-99	ret proto-oncogene	Homo sapiens	52-55
18284634-10	2008	CONCLUSIONS: RET genotypes including two intronic RET variants were associated with the risk of developing sMTC and to more aggressive behaviour.	smtc	107-111	ret proto-oncogene	Homo sapiens	13-16
18284634-10	2008	CONCLUSIONS: RET genotypes including two intronic RET variants were associated with the risk of developing sMTC and to more aggressive behaviour.	smtc	107-111	ret proto-oncogene	Homo sapiens	50-53
18331611-9	2008	CONCLUSIONS: Our data demonstrate that the RET G691S variant could modulate the age of onset of sMTC as demonstrated previously for familial tumours.	smtc	96-100	ret proto-oncogene	Homo sapiens	43-46
18440890-7	2008	Mechanical strain still increased NO production in the absence of eNOS, and was abolished by SMTC, a specific nNOS inhibitor.	smtc	93-97	nitric oxide synthase 1, neuronal	Mus musculus	110-114
18440890-9	2008	When NO synthesis was blocked with either SMTC or siRNA targeting nNOS in eNOS(-/-) cells however, strain still was able to suppress RANKL expression by 34%.	smtc	42-46	tumor necrosis factor (ligand) superfamily, member 11	Mus musculus	133-138
16973184-2	2006	We predicted that injection of L-NAME (non-selective NO synthase (NOS) inhibitor) and SMTC (neuronal NOS (nNOS) inhibitor) would restore the huddling behavior and eliminate the reduction of Tb caused by hypoxia.	smtc	86-90	nitric oxide synthase 1	Rattus norvegicus	92-104
16973184-2	2006	We predicted that injection of L-NAME (non-selective NO synthase (NOS) inhibitor) and SMTC (neuronal NOS (nNOS) inhibitor) would restore the huddling behavior and eliminate the reduction of Tb caused by hypoxia.	smtc	86-90	nitric oxide synthase 1	Rattus norvegicus	106-110
16091499-9	2005	We not only confirmed the previously described association with G691S and S904S (for heterozygotes: odds ratio, 1.85; range, 1.22-2.82; P = 0.004), but we found a novel protective effect associated with a specific haplotype (odds ratio, 0.39; range, 0.21-0.72; P = 0.005) revealing the existence of different genetic variants in the RET oncogene that either increase or decrease risk of sMTC.	smtc	387-391	ret proto-oncogene	Homo sapiens	333-336
34822305-4	2022	Multiple linear regression was used to analyze the correlation of risk factors (PCT or ATF4 expression, RET mutation, tumor differentiation, SMTC stage, lymphatic metastasis) for 5-year recurrence and survival of SMTC.	smtc	213-217	activating transcription factor 4	Homo sapiens	87-91
12490080-3	2002	So far, S836S of RET, is the only variant whose association with sMTC has been found in several European cohorts.	smtc	65-69	ret proto-oncogene	Homo sapiens	17-20
34822305-4	2022	Multiple linear regression was used to analyze the correlation of risk factors (PCT or ATF4 expression, RET mutation, tumor differentiation, SMTC stage, lymphatic metastasis) for 5-year recurrence and survival of SMTC.	smtc	213-217	ret proto-oncogene	Homo sapiens	104-107
34822305-8	2022	ATF4 and PCT expressions combined with RET mutation are related to the clinical prognosis of SMTC and can predict SMTC staging.	smtc	93-97	activating transcription factor 4	Homo sapiens	0-4
34822305-8	2022	ATF4 and PCT expressions combined with RET mutation are related to the clinical prognosis of SMTC and can predict SMTC staging.	smtc	93-97	ret proto-oncogene	Homo sapiens	39-42
34822305-8	2022	ATF4 and PCT expressions combined with RET mutation are related to the clinical prognosis of SMTC and can predict SMTC staging.	smtc	114-118	activating transcription factor 4	Homo sapiens	0-4
34822305-8	2022	ATF4 and PCT expressions combined with RET mutation are related to the clinical prognosis of SMTC and can predict SMTC staging.	smtc	114-118	ret proto-oncogene	Homo sapiens	39-42
31077271-13	2019	Also, SMTC had greater (P < 0.05) abundance of VEGFA mRNA than LGTC.	smtc	6-10	vascular endothelial growth factor A	Bos taurus	50-55
32228166-2	2020	Previous studies evaluated whether single nucleotide polymorphisms (SNPs) within RET (a pivotal proto-oncogene for this disease) are associated with the risk for developing sMTC, but the results are inconclusive.	smtc	173-177	ret proto-oncogene	Homo sapiens	81-84
32228166-3	2020	METHODS: In this work we evaluated the association of RET-SNPs c.74-126G>T (rs2565206), p.Gly691Ser (rs1799939, G>A), p.Leu769= (rs1800861, G>T), p.Ser836= (rs1800862, C>T), and p.Ser904= (rs1800863, C>G) (listed in the order of their chromosomal location) with sMTC.	smtc	262-266	ret proto-oncogene	Homo sapiens	54-57
29288804-3	2018	Consequently, we tested the hypothesis that selective nNOS inhibition (S-methyl-l-thiocitrulline; SMTC, 2.1 mumol/kg) would produce attenuated reductions in muscle blood flow during moderate/heavy submaximal exercise in sedentary HF rats compared to their healthy counterparts.	smtc	98-102	nitric oxide synthase 1	Rattus norvegicus	54-58
27158388-4	2016	The mechanical threshold in rats was significantly enhanced by the sGC inhibitor ODQ and neuronal NO synthase (nNOS) inhibitor SMTC, indicating the role of sGC and nNOS in the process of neuropathic pain.	smtc	127-131	nitric oxide synthase 1	Rattus norvegicus	111-115
27158388-4	2016	The mechanical threshold in rats was significantly enhanced by the sGC inhibitor ODQ and neuronal NO synthase (nNOS) inhibitor SMTC, indicating the role of sGC and nNOS in the process of neuropathic pain.	smtc	127-131	guanylate cyclase 1 soluble subunit beta 2	Rattus norvegicus	156-159
27158388-4	2016	The mechanical threshold in rats was significantly enhanced by the sGC inhibitor ODQ and neuronal NO synthase (nNOS) inhibitor SMTC, indicating the role of sGC and nNOS in the process of neuropathic pain.	smtc	127-131	nitric oxide synthase 1	Rattus norvegicus	164-168
27158388-6	2016	Finally, the protein levels of sGC was greatly increased by SNP and Zaprinast but decreased by WAY100635 and SMTC, showing the regulation of NO/cGMP pathway and 5-HT1ARs on the protein expression of sGC.	smtc	109-113	guanylate cyclase 1 soluble subunit beta 2	Rattus norvegicus	31-34
27158388-6	2016	Finally, the protein levels of sGC was greatly increased by SNP and Zaprinast but decreased by WAY100635 and SMTC, showing the regulation of NO/cGMP pathway and 5-HT1ARs on the protein expression of sGC.	smtc	109-113	guanylate cyclase 1 soluble subunit beta 2	Rattus norvegicus	199-202
25694125-5	2015	Gain-of-function mutations in the REarranged during transfection (RET) proto-oncogene have been identified in 98 % of hMTC and 50 % of sMTC.	smtc	135-139	ret proto-oncogene	Homo sapiens	34-64
25694125-5	2015	Gain-of-function mutations in the REarranged during transfection (RET) proto-oncogene have been identified in 98 % of hMTC and 50 % of sMTC.	smtc	135-139	ret proto-oncogene	Homo sapiens	66-69
25694125-11	2015	In the present study, six different mutations were identified in exon10 of RET in 14 patients with sMTC and FMTC that were restricted to codons 611, 618, and 620, but not in codon 609.	smtc	99-103	ret proto-oncogene	Homo sapiens	75-78