PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
18669898-11	2008	CONCLUSIONS: In good grade elderly SAH patients with small anterior circulation aneurysms, EVT should probably be the favored treatment for ruptured internal carotid and posterior communicating artery aneurysms, whereas elderly patients with ruptured middle cerebral artery aneurysms appear to benefit from NST.	EVT	91-94	sulfotransferase family 4A member 1	Homo sapiens	307-310
21521020-8	2011	CONCLUSION: If validated, determination of SULT4A1-1 haplotype status might be useful for identifying patients who show an enhanced response to long-term olanzapine treatment.	Olanzapine	154-164	sulfotransferase family 4A member 1	Homo sapiens	43-50
20920535-5	2011	In this study, we show that the Thr(11) residue of SULT4A1, which is involved in Pin1 binding is phosphorylated.	Threonine	32-35	sulfotransferase family 4A member 1	Homo sapiens	51-58
20920535-6	2011	MEK inhibition was shown to abolish Pin1 mediated degradation of SULT4A1 while in vitro phosphorylation assays using alanine substitution mutants of SULT4A1 demonstrated phosphorylation of Thr(11) by ERK1.	Alanine	117-124	sulfotransferase family 4A member 1	Homo sapiens	149-156
20920535-6	2011	MEK inhibition was shown to abolish Pin1 mediated degradation of SULT4A1 while in vitro phosphorylation assays using alanine substitution mutants of SULT4A1 demonstrated phosphorylation of Thr(11) by ERK1.	Threonine	189-192	sulfotransferase family 4A member 1	Homo sapiens	149-156
23106027-11	2012	When data for all phases were evaluated, SULT4A1-1(-) status was associated with increased hospitalization risk for subjects treated with olanzapine, with a hazard ratio of 8.26 (P = .041), and possibly for subjects treated with quetiapine, with a hazard ratio of 6.80 (P = .070).	Olanzapine	138-148	sulfotransferase family 4A member 1	Homo sapiens	41-48
23106027-11	2012	When data for all phases were evaluated, SULT4A1-1(-) status was associated with increased hospitalization risk for subjects treated with olanzapine, with a hazard ratio of 8.26 (P = .041), and possibly for subjects treated with quetiapine, with a hazard ratio of 6.80 (P = .070).	Quetiapine Fumarate	229-239	sulfotransferase family 4A member 1	Homo sapiens	41-48
23106027-13	2012	SULT4A1-1(+) status was significantly associated with decreased risk of hospitalization when the subjects were treated with olanzapine.	Olanzapine	124-134	sulfotransferase family 4A member 1	Homo sapiens	0-7
21521020-5	2011	RESULTS: For the CATIE sample, patients carrying a haplotype designated SULT4A1-1(+) displayed higher baseline PANSS (p = 0.03) and, when treated with olanzapine, demonstrated a significant interaction with time (p = 0.009) in the MMRM.	Olanzapine	151-161	sulfotransferase family 4A member 1	Homo sapiens	72-79
21521020-6	2011	SULT4A1-1(+) patients treated with olanzapine displayed improved response compared with SULT4A1-1(-) patients treated with olanzapine (p = 0.008) or to SULT4A1-1(+) patients treated with risperidone (p = 0.006).	Olanzapine	35-45	sulfotransferase family 4A member 1	Homo sapiens	0-7
21521020-6	2011	SULT4A1-1(+) patients treated with olanzapine displayed improved response compared with SULT4A1-1(-) patients treated with olanzapine (p = 0.008) or to SULT4A1-1(+) patients treated with risperidone (p = 0.006).	Risperidone	187-198	sulfotransferase family 4A member 1	Homo sapiens	0-7
21521020-7	2011	In the replication sample, SULT4A1-1(+) patients treated with olanzapine demonstrated greater improvement than SULT4A1-1(-) patients treated with olanzapine (p = 0.05) or than SULT4A1-1(+) patients treated with risperidone (p = 0.05).	Olanzapine	62-72	sulfotransferase family 4A member 1	Homo sapiens	27-34
21521020-7	2011	In the replication sample, SULT4A1-1(+) patients treated with olanzapine demonstrated greater improvement than SULT4A1-1(-) patients treated with olanzapine (p = 0.05) or than SULT4A1-1(+) patients treated with risperidone (p = 0.05).	Risperidone	211-222	sulfotransferase family 4A member 1	Homo sapiens	27-34
19439498-9	2009	Pin1 destabilized SULT4A1, decreasing its half-life from more than 8 h to approximately 4.5 h. This effect was dependent on the isomerase activity of Pin1 and was inhibited by okadaic acid, suggesting a role for the phosphatase PP2A.	Okadaic Acid	176-188	sulfotransferase family 4A member 1	Homo sapiens	18-25
19439498-10	2009	Pin1-mediated SULT4A1 degradation did not involve the proteosomes or macroautophagy, but it was inhibited by the calpain antagonists N-acetyl-Leu-Leu-Nle-CHO and Z-Val-Phe-CHO.	n-acetyl-leu-leu-nle-cho	133-157	sulfotransferase family 4A member 1	Homo sapiens	14-21
19439498-10	2009	Pin1-mediated SULT4A1 degradation did not involve the proteosomes or macroautophagy, but it was inhibited by the calpain antagonists N-acetyl-Leu-Leu-Nle-CHO and Z-Val-Phe-CHO.	Calpain Inhibitor III	162-175	sulfotransferase family 4A member 1	Homo sapiens	14-21
11906176-6	2002	With the exception of SULT1B1, SULT1C1, and SULT4A1, all of the human SULTs studied catalyzed the sulfate conjugation of CEs.	Estrogens, Catechol	121-124	sulfotransferase family 4A member 1	Homo sapiens	44-51
17469359-6	2006	This PEG system is one of the functions of "Community NST".	Polyethylene Glycols	5-8	sulfotransferase family 4A member 1	Homo sapiens	54-58
2437403-4	1987	Of eight patients studied, a single dose of 90 mg diltiazem administered 3 h before dipyridamole infusion inhibited dipyridamole-induced ST-segment depression completely in seven (nST = 0) and incompletely in one (nST = from 24 to 5).	Diltiazem	50-59	sulfotransferase family 4A member 1	Homo sapiens	180-183
8951131-5	1996	RESULTS: Significantly more NSTs were nonreactive after methadone (P < .001), and it took more time for the NST to become reactive (P < .01).	Methadone	56-65	sulfotransferase family 4A member 1	Homo sapiens	28-31
1540485-2	1992	The activity of N-sulphotransferase (N-ST) with desipramine (DMI) as substrate was measured in 118 human liver specimens, in platelets obtained from 105 subjects, in 12 specimens of human ileum and colon mucosa and in five specimens of human kidney and lung.	Desipramine	48-59	sulfotransferase family 4A member 1	Homo sapiens	16-35
1540485-2	1992	The activity of N-sulphotransferase (N-ST) with desipramine (DMI) as substrate was measured in 118 human liver specimens, in platelets obtained from 105 subjects, in 12 specimens of human ileum and colon mucosa and in five specimens of human kidney and lung.	Desipramine	48-59	sulfotransferase family 4A member 1	Homo sapiens	37-41
1540485-2	1992	The activity of N-sulphotransferase (N-ST) with desipramine (DMI) as substrate was measured in 118 human liver specimens, in platelets obtained from 105 subjects, in 12 specimens of human ileum and colon mucosa and in five specimens of human kidney and lung.	Desipramine	61-64	sulfotransferase family 4A member 1	Homo sapiens	16-35
1540485-2	1992	The activity of N-sulphotransferase (N-ST) with desipramine (DMI) as substrate was measured in 118 human liver specimens, in platelets obtained from 105 subjects, in 12 specimens of human ileum and colon mucosa and in five specimens of human kidney and lung.	Desipramine	61-64	sulfotransferase family 4A member 1	Homo sapiens	37-41
18823757-3	2008	Sult4A1 is related to metabolism of monoamines, particularly dopamine and norepinephrine, both of which have been implicated in the pathophysiology of the psychopathology and cognitive dysfunction components of schizophrenia.	monoamines	36-46	sulfotransferase family 4A member 1	Homo sapiens	0-7
18823757-3	2008	Sult4A1 is related to metabolism of monoamines, particularly dopamine and norepinephrine, both of which have been implicated in the pathophysiology of the psychopathology and cognitive dysfunction components of schizophrenia.	Dopamine	61-69	sulfotransferase family 4A member 1	Homo sapiens	0-7
18823757-3	2008	Sult4A1 is related to metabolism of monoamines, particularly dopamine and norepinephrine, both of which have been implicated in the pathophysiology of the psychopathology and cognitive dysfunction components of schizophrenia.	Norepinephrine	74-88	sulfotransferase family 4A member 1	Homo sapiens	0-7
34113937-1	2021	A blue light activated anti-cancer prodrug, NST, was designed based on a photoactive 4-aminonaphthalimide derivative and an anticancer drug, 10-hydroxycamptothecin.	4-amino-1,8-naphthalimide	85-105	sulfotransferase family 4A member 1	Homo sapiens	44-47
34113937-1	2021	A blue light activated anti-cancer prodrug, NST, was designed based on a photoactive 4-aminonaphthalimide derivative and an anticancer drug, 10-hydroxycamptothecin.	10-hydroxycamptothecin	141-163	sulfotransferase family 4A member 1	Homo sapiens	44-47
2437403-4	1987	Of eight patients studied, a single dose of 90 mg diltiazem administered 3 h before dipyridamole infusion inhibited dipyridamole-induced ST-segment depression completely in seven (nST = 0) and incompletely in one (nST = from 24 to 5).	Diltiazem	50-59	sulfotransferase family 4A member 1	Homo sapiens	214-217
2437403-4	1987	Of eight patients studied, a single dose of 90 mg diltiazem administered 3 h before dipyridamole infusion inhibited dipyridamole-induced ST-segment depression completely in seven (nST = 0) and incompletely in one (nST = from 24 to 5).	Dipyridamole	116-128	sulfotransferase family 4A member 1	Homo sapiens	180-183
24988429-10	2014	Mutation of the dimerization motif resulted in a monomeric form of SULT4A1 that was rapidly degraded by polyubiquitination on the lysine located within the dimerization motif.	Lysine	130-136	sulfotransferase family 4A member 1	Homo sapiens	67-74
32152050-8	2020	Inhibition of SULT4A1 using siRNA abrogated the loss in SULT1A1/3 and reversed dopamine toxicity.	Dopamine	79-87	sulfotransferase family 4A member 1	Homo sapiens	14-21
32152050-11	2020	In neuron-like cells, SULT4A1 is able to modulate dopamine toxicity by interacting with SULT1A3, potentially decreasing the metabolism of dopamine.	Dopamine	50-58	sulfotransferase family 4A member 1	Homo sapiens	22-29
32152050-11	2020	In neuron-like cells, SULT4A1 is able to modulate dopamine toxicity by interacting with SULT1A3, potentially decreasing the metabolism of dopamine.	Dopamine	138-146	sulfotransferase family 4A member 1	Homo sapiens	22-29
33171978-6	2020	Using this approach, SULT4A1-dependent sulfation of 1-naphthol was observed.	1-naphthol	52-62	sulfotransferase family 4A member 1	Homo sapiens	21-28
33171978-8	2020	It is based on the sulfation of a proluciferin compound, which was catalyzed by SULT1E1, SULT2A1, SULT4A1, and SULT6B1.	proluciferin	34-46	sulfotransferase family 4A member 1	Homo sapiens	98-105
31266751-7	2019	SULT4A1 expressing cells display significant protection against H2O2-mediated defects in mitochondrial function and loss of mitochondrial membrane potential.	Hydrogen Peroxide	64-68	sulfotransferase family 4A member 1	Homo sapiens	0-7
31266751-8	2019	Expression of SULT4A1 in SH-SY5Y cells also protects against H2O2-induced cell death.	Hydrogen Peroxide	61-65	sulfotransferase family 4A member 1	Homo sapiens	14-21
25340730-5	2014	SULT4A1-1(-) patients had better treatment response to risperidone in one schizophrenia trial, but not in another schizophrenia trial or bipolar mania trial.	Risperidone	55-66	sulfotransferase family 4A member 1	Homo sapiens	0-7
24956247-0	2014	Replication of SULT4A1-1 as a pharmacogenetic marker of olanzapine response and evidence of lower weight gain in the high response group.	Olanzapine	56-66	sulfotransferase family 4A member 1	Homo sapiens	15-22
24956247-2	2014	This study examined the effect of SULT4A1-1 haplotype status (rs2285162 [A]-rs2285167 [G]) on olanzapine response.	Olanzapine	94-104	sulfotransferase family 4A member 1	Homo sapiens	34-41
24956247-5	2014	RESULTS: SULT4A1-1-positive status correlated with superior olanzapine response in Phase 1 (p = 0.004 for model 1 and p = 0.001 for model 2) and Phases 1B/2 (p = 0.05 for model 1 and p = 0.007 for model 2).	Olanzapine	60-70	sulfotransferase family 4A member 1	Homo sapiens	9-16
24956247-6	2014	SULT4A1-1-positive subjects gained significantly less weight per month on olanzapine, 0.15 lbs, than did SULT4A1-1-negative subjects, 2.27 lbs (p = 0.04).	Olanzapine	74-84	sulfotransferase family 4A member 1	Homo sapiens	0-7
24956247-7	2014	CONCLUSION: This study provides a second replication of superior olanzapine response in SULT4A1-1-positive subjects compared with SULT4A1-1-negative subjects.	Olanzapine	65-75	sulfotransferase family 4A member 1	Homo sapiens	88-95
24956247-8	2014	SULT4A1-1-positive subjects treated with olanzapine also gained less weight than SULT4A1-1-negative subjects.	Olanzapine	41-51	sulfotransferase family 4A member 1	Homo sapiens	0-7