Ignet

Gene Information

Gene symbol: SULT2A1

Gene name: sulfotransferase family, cytosolic, 2A, dehydroepiandrosterone (DHEA)-preferring, member 1

HGNC ID: 11458

Synonyms: DHEA-ST

Related Genes

#	Gene Symbol	Number of hits
1	ACOT2	1 hits
2	ARPC1A	1 hits
3	BCL2L11	1 hits
4	BRD2	1 hits
5	CYP2C9	1 hits
6	ENPEP	1 hits
7	FSHB	1 hits
8	IGF1	1 hits
9	IGFBP1	1 hits
10	IL18	1 hits
11	INS	1 hits
12	MIOX	1 hits
13	POMC	1 hits
14	PRL	1 hits
15	PTDSS1	1 hits
16	REN	1 hits
17	SHBG	1 hits
18	SST	1 hits
19	SULT1A1	1 hits
20	SULT1A3	1 hits
21	SULT1E1	1 hits
22	ZKSCAN5	1 hits

Related Sentences

#	PMID	Sentence
1	1653039	One-month-old Syrian hamsters of the APA and Std: golden strains were inoculated intraperitoneally with 10(5) PFU/head of the D variant of encephalomyocarditis (EMC) virus and examined virologically and pathologically up to 7 days after inoculation.
2	7600911	The effects of streptozotocin (STZ)-induced diabetes on rat hepatic hydroxysteroid sulfotransferase-a (HST-a) and aryl sulfotransferase IV (ASTIV) gene expression were characterized.
3	8182132	The Std locus encoding dehydroepiandrosterone sulfotransferase was mapped to proximal Chromosome 7, and the Ste locus encoding estrogen sulfotransferase was mapped to Chromosome 5.
4	8182132	These reciprocal changes in mRNA concentrations in mutant females were reflected by an induction of a high affinity estrogen sulfotransferase activity and a concomitant loss of dehydroepiandrosterone sulfotransferase activity.
5	8182132	The Std locus encoding dehydroepiandrosterone sulfotransferase was mapped to proximal Chromosome 7, and the Ste locus encoding estrogen sulfotransferase was mapped to Chromosome 5.
6	8182132	These reciprocal changes in mRNA concentrations in mutant females were reflected by an induction of a high affinity estrogen sulfotransferase activity and a concomitant loss of dehydroepiandrosterone sulfotransferase activity.
7	9633024	At baseline, all groups had similar basal and OGTT-induced glucose, insulin and glucose insulin ratio (GIR) levels as well as IGF-I and DHEA-S levels.
8	9633024	SBP and DBP decreased HOB-NIFE (p < 0.02) but also during diet alone in both HOB and OB, though to a lesser extent (p < 0.05).
9	9633024	Both basal and OGTT-stimulated glucose and insulin levels as well as IGF-I and DHEA-S levels were not modified in HOB-NIFE as well as in HOB and OB.
10	9633024	In conclusion, our data indicate that nifedipine treatment does not modify glucose tolerance as well as insulin secretion and sensitivity, IGF-I and DHEA-S levels in hypertensive abdominal obese patients.
11	9633024	At baseline, all groups had similar basal and OGTT-induced glucose, insulin and glucose insulin ratio (GIR) levels as well as IGF-I and DHEA-S levels.
12	9633024	SBP and DBP decreased HOB-NIFE (p < 0.02) but also during diet alone in both HOB and OB, though to a lesser extent (p < 0.05).
13	9633024	Both basal and OGTT-stimulated glucose and insulin levels as well as IGF-I and DHEA-S levels were not modified in HOB-NIFE as well as in HOB and OB.
14	9633024	In conclusion, our data indicate that nifedipine treatment does not modify glucose tolerance as well as insulin secretion and sensitivity, IGF-I and DHEA-S levels in hypertensive abdominal obese patients.
15	9633024	At baseline, all groups had similar basal and OGTT-induced glucose, insulin and glucose insulin ratio (GIR) levels as well as IGF-I and DHEA-S levels.
16	9633024	SBP and DBP decreased HOB-NIFE (p < 0.02) but also during diet alone in both HOB and OB, though to a lesser extent (p < 0.05).
17	9633024	Both basal and OGTT-stimulated glucose and insulin levels as well as IGF-I and DHEA-S levels were not modified in HOB-NIFE as well as in HOB and OB.
18	9633024	In conclusion, our data indicate that nifedipine treatment does not modify glucose tolerance as well as insulin secretion and sensitivity, IGF-I and DHEA-S levels in hypertensive abdominal obese patients.
19	9831304	A total of 12 women (24.2 +/- 1.6 years old, BMI 36.7 +/- 1.5 Kg/m2) with hyperandrogenism (HA) and with normal glucose tolerance test were studied to evaluate the involvement of endogenous opioids in the pathophysiology of insulin secretion and insulin sensitivity in HA by administering naltrexone, an oral opioid receptor antagonist.
20	9831304	SHBG, DHEAS, testosterone, free androgen index (FAI) and plasma concentrations of IGF-I and IGFBP-1 were determined in 3 basal samples, before and after therapy.
21	10902292	Each serum sample was analyzed by duplicate for luteinizing hormone (LH), follicle-stimulating hormone (FSH), estradiol (E2), free-testosterone (T), 17 alpha-hydroxyprogesterone (17OHP), androstenedione (A), dehydroepiandrosterone-sulphate (DHEA-S), prolactin (PRL), insulin, glucose, total cholesterol and triclylcerides.
22	10908163	DHEA-S, SHBG, DHT and 3alpha diol G concentrations in patients with diabetes were not significantly different from those in controls.
23	10908163	These data suggest that adolescents with diabetes have similar serum levels of DHEA-S, SHBG, DHT and 3alpha diol G as healthy subjects at all stages of puberty.
24	10908163	DHEA-S, SHBG, DHT and 3alpha diol G concentrations in patients with diabetes were not significantly different from those in controls.
25	10908163	These data suggest that adolescents with diabetes have similar serum levels of DHEA-S, SHBG, DHT and 3alpha diol G as healthy subjects at all stages of puberty.
26	11241888	A unifying hypothesis explaining the relationship between aging and insulin resistance might encompass four main pathways, namely: (a) anthropometric changes (relative and absolute increase in body fat combined with a decline in fat free mass) which could be the anatomic substrate for explaining the reduction in active metabolic tissue; (b) environmental causes, mainly diet style and physical activity; (c) neuro-hormonal variations [decline in plasma dehydroepandrosterone sulphate (DHEAS) and IGF-1]; and finally (d) the rise in oxidative stress.
27	14599113	Basal ACTH and DHEA-S levels were significantly lower (p < 0.05 and p < 0.01, respectively), and midnight cortisol and 24-hour urinary free cortisol levels were significantly higher in patients with SCS (p < 0.001 and p < 0.05, respectively).
28	14599113	Suppressed ACTH and DHEA-S levels, and high midnight cortisol levels may be some clues for SCS in patients with adrenal incidentaloma.
29	14599113	Basal ACTH and DHEA-S levels were significantly lower (p < 0.05 and p < 0.01, respectively), and midnight cortisol and 24-hour urinary free cortisol levels were significantly higher in patients with SCS (p < 0.001 and p < 0.05, respectively).
30	14599113	Suppressed ACTH and DHEA-S levels, and high midnight cortisol levels may be some clues for SCS in patients with adrenal incidentaloma.
31	15031776	Twelve women with polycystic ovary syndrome (PCOS), 10 women with idiopathic hirsutism (IH), and 10 women with late onset adrenal hyperplasia due to 21-hydroxylase deficiency (LOCAH) were studied.
32	15031776	The decrease in aMT6s excretion together with reduced serum LH, FSH, DHEAS and testosterone values during treatment with cyproterone acetate-ethinyl estradiol, suggest that sex steroids either directly or through the suppression of gonadotropins, modulate melatonin secretion in these patients.
33	15808380	DHEA-S and PRL levels were found to be lower in subjects with RH (P < 0.05 and P > 0.05, respectively).
34	16943580	Elevated serum levels of interleukin-18 are associated with insulin resistance in women with polycystic ovary syndrome.
35	16943580	Interleukin (IL)-18 as a member of IL-1 cytokine family is increased in obese, in diabetic, and even in polycystic ovary syndrome (PCOS) patients.
36	16943580	In the present study we evaluated the association of serum IL-18 levels with insulin resistance in PCOS women.
37	16943580	IL-18 levels were positively correlated with homeostasis model assessment index (HOMA) beta index, which assesses beta cell function (p = 0.035), but were inversely correlated with clamp indices, which best represent insulin resistance status: M, Clamp ISI*100, and MCRg values (p = 0.006, 0.010, and 0.009 respectively).
38	16943580	No correlation was found between IL-18 and age, BMI, waist-to-hip ratio (WHR), lipid profile, dehydroepiandrosterone-sulfate (DHEAS), sex hormone- binding globulin (SHBG), or fasting insulin levels.
39	16943580	In conclusion, in the present study, serum IL-18 levels were significantly increased in PCOS women and firmly associated with insulin resistance displayed by euglycemic hyperinsulinemic clamp test.
40	16943580	It indicates that IL-18 may be a contributing factor linking inflammation and insulin resistance in PCOS women.
41	19882253	Hormonal evaluation included 8.00 a.m. cortisol, DHEA-S, ACTH and in hypertensive subjects, plasma renin activity, and serum aldosterone.
42	21533175	Genes at or near the identified loci include ZKSCAN5 (rs11761528; p = 3.15 × 10(-36)), SULT2A1 (rs2637125; p = 2.61 × 10(-19)), ARPC1A (rs740160; p = 1.56 × 10(-16)), TRIM4 (rs17277546; p = 4.50 × 10(-11)), BMF (rs7181230; p = 5.44 × 10(-11)), HHEX (rs2497306; p = 4.64 × 10(-9)), BCL2L11 (rs6738028; p = 1.72 × 10(-8)), and CYP2C9 (rs2185570; p = 2.29 × 10(-8)).
43	22707198	Microarray data demonstrated for the first time that overexpression of the genes encoding IL-1 receptor, lipid metabolic enzymes (e.g.
44	22707198	Mte1, Ptdss1, and Sult2a1), myo-inositol oxygenase, glucagon, and somatostatin as well as down-regulation of olfactory receptor 984 and mitochondrial ribosomal protein, which are highly linked to T1DM etiology.
45	22707198	The results of the microarray analysis revealed that up-regulation of IL-2, IL12a, and leptin receptor and down-regulation of PIK3 played important physiological roles in the onset of T2DM.
46	23775849	In the present study of normal subjects with nonfatty livers and patients with steatosis, diabetic cirrhosis, and alcoholic cirrhosis, we sought to determine SULT1A1, SULT2A1, SULT1E1, and SULT1A3 activity and mRNA and protein expression in human liver tissue.
47	23775849	Specifically, SULT1A1 and SULT1A3 activities were lower in disease states relative to nonfatty tissues.