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Information on EC 2.8.2.2 - alcohol sulfotransferase and Organism(s) Mus musculus and UniProt Accession O35400
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EC Tree
2.8.2.2 alcohol sulfotransferaseIUBMB Comments
Primary and secondary alcohols, including aliphatic alcohols, ascorbic acid, chloramphenicol, ephedrine and hydroxysteroids, but not phenolic steroids, can act as acceptors (cf. EC 2.8.2.15 steroid sulfotransferase).
Specify your search results
Word Map
- 2.8.2.2
- dehydrogenases
- testosterone
- estradiol
- androgen
-
sulfotransferases
- progesterone
- glucocorticoid
- adrenal
- estrone
-
steroidogenic
- cortisol
- phenol
- testis
- testicular
- aromatase
-
steroidogenesis
- sult1e1
-
sulfatase
- xenobiotics
- pregnenolone
-
sults
-
mineralocorticoid
- gonad
-
11-beta
- androstenedione
-
aldo-keto
-
leydig
- 3'-phosphoadenosine
- 5'-phosphosulfate
- aldosterone
-
sulfoconjugation
-
beta-hsd
-
estrogen-dependent
- beta-estradiol
- 3'-phosphoadenosine-5'-phosphosulfate
-
sulfurylation
- 17beta-hsds
- 5alpha-dihydrotestosterone
- cyp17a1
- sulphotransferase
-
intracrine
-
pnpla3
- 2,6-dichloro-4-nitrophenol
-
pre-receptor
- 3-ketosteroids
-
3alpha
- 3alpha-hsds
- hsd17b2
- synthesis
- diagnostics
- medicine
- analysis
The taxonomic range for the selected organisms is: Mus musculus
The expected taxonomic range for this enzyme is: Eukaryota, Bacteria
The expected taxonomic range for this enzyme is: Eukaryota, Bacteria
Synonyms
hydroxysteroid, estrogen sulfotransferase, dhea st, sult2b1a, sult6b1, iodothyronine sulfotransferase, ast-rb2, pz-sult, hydroxysteroid sulfotransferase sult2a1, hydroxysteroid sulfotransferase 2b1b, 
more
topSYNONYM 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
3-hydroxysteroid sulfotransferase
-
-
-
-
3beta-hydroxy steroid sulfotransferase
-
-
-
-
3beta-hydroxysteroid sulfotransferase
-
-
-
-
5alpha-androstenol sulfotransferase
-
-
-
-
alcohol/hydroxysteroid sulfotransferase
-
-
-
-
cholesterol sulfotransferase
-
-
-
-
dehydroepiandrosterone sulfotransferase
DELTA5-3beta-hydroxysteroid sulfokinase
-
-
-
-
estrogen sulfokinase
-
-
-
-
estrogen sulfotransferase
HST
-
-
-
-
hydroxysteroid sulfotransferase
steroid alcohol sulfotransferase
-
-
-
-
steroid sulfokinase
-
-
-
-
steroid sulfotransferase
-
-
-
-
sterol sulfokinase
-
-
-
-
sterol sulfotransferase
-
-
-
-
additional information
dehydroepiandrosterone sulfotransferase
-
-
-
-
estrogen sulfotransferase
-
-
-
-
hydroxysteroid sulfotransferase
-
-
-
-
REACTION TYPE
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
sulfate group transfer
-
-
-
-
PATHWAY SOURCE
PATHWAYS
SYSTEMATIC NAME
IUBMB Comments
3'-phosphoadenylyl-sulfate:alcohol sulfotransferase
Primary and secondary alcohols, including aliphatic alcohols, ascorbic acid, chloramphenicol, ephedrine and hydroxysteroids, but not phenolic steroids, can act as acceptors (cf. EC 2.8.2.15 steroid sulfotransferase).
CAS REGISTRY NUMBER
COMMENTARY
9032-76-2
-
SUBSTRATE
PRODUCT
REACTION DIAGRAM
ORGANISM
UNIPROT
COMMENTARY
(Substrate)
(Substrate)
LITERATURE
(Substrate)
(Substrate)
COMMENTARY
(Product)
(Product)
LITERATURE
(Product)
(Product)
Reversibility
r=reversible
ir=irreversible
?=not specified
r=reversible
ir=irreversible
?=not specified
3'-phosphoadenylyl sulfate + (S)-cholest-5-ene-3beta,24S-diol
adenosine 3',5'-bisphosphate + (S)-cholest-5-ene-3beta,24S-diol 3-sulfate
-
-
-
?
3'-phosphoadenylyl sulfate + 24(R/S),25-epoxycholesterol
adenosine 3',5'-bisphosphate + ?
-
-
-
?
3'-phosphoadenylyl sulfate + 4beta-hydroxycholesterol
adenosine 3',5'-bisphosphate + 4beta-hydroxycholesterol 3-sulfate
-
-
-
?
3'-phosphoadenylyl sulfate + 7-oxocholesterol
adenosine 3',5'-bisphosphate + 7-oxocholesterol 3-sulfate
-
-
-
?
3'-phosphoadenylyl sulfate + 7alpha-hydroxycholesterol
adenosine 3',5'-bisphosphate + 7alpha-hydroxycholesterol 3-sulfate
-
-
-
?
3'-phosphoadenylyl sulfate + 7beta-hydroxycholesterol
adenosine 3',5'-bisphosphate + 7beta-hydroxycholesterol 3-sulfate
-
-
-
?
3'-phosphoadenylyl sulfate + cholest-5-ene-3beta,25-diol
adenosine 3',5'-bisphosphate + cholest-5-ene-3beta,25-diol 3-sulfate
-
-
-
?
3'-phosphoadenylyl sulfate + cholest-5-ene-3beta,27-diol
adenosine 3',5'-bisphosphate + cholest-5-ene-3beta,27-diol 3-sulfate
-
-
-
?
3'-phosphoadenylyl sulfate + cholesterol
adenosine 3',5'-bisphosphate + cholesterol 3-sulfate
3'-phosphoadenylyl sulfate + dehydroepiandrosterone
adenosine 3',5'-bisphosphate + dehydroepiandrosterone 3-sulfate
-
-
-
?
3'-phosphoadenylylsulfate + 22-hydroxycholesterol
adenosine 3',5'-bisphosphate + 22-hydroxycholesterol sulfate
-
-
-
?
3'-phosphoadenylylsulfate + 24,25-epoxycholesterol
adenosine 3',5'-bisphosphate + 24,25-epoxycholesterol sulfate
-
-
-
?
3'-phosphoadenylylsulfate + 25-hydroxycholesterol
adenosine 3',5'-bisphosphate + 25-hydroxycholesterol sulfate
-
-
-
?
3'-phosphoadenylylsulfate + 4-methylumbelliferone
adenosine 3',5'-bisphosphate + 4-methylumbelliferone sulfate
-
-
-
r
3'-phosphoadenylylsulfate + cholesterol
adenosine 3',5'-bisphosphate + cholesterol sulfate
-
-
-
?
3'-phosphoadenylylsulfate + estriol
adenosine 3',5'-bisphosphate + estriol sulfate
-
-
-
r
3'-phosphoadenylylsulfate + estrone
adenosine 3',5'-bisphosphate + estrone sulfate
-
-
-
r
3'-phosphoadenylylsulfate + ethynylestradiol
adenosine 3',5'-bisphosphate + ethynylestradiol sulfate
-
-
-
r
3'-phosphoadenylylsulfate + methyl 4-hydroxybenzoate
adenosine 3',5'-bisphosphate + methyl 4-(sulfooxy)benzoate
-
-
-
r
3'-phosphoadenylylsulfate + p-nitrocatechol
adenosine 3',5'-bisphosphate + p-nitrocatechol sulfate
-
-
-
r
3'-phosphoadenylylsulfate + p-nitrophenol
adenosine 3',5'-bisphosphate + p-nitrophenyl sulfate
-
-
-
r
3'-phosphoadenylyl sulfate + estradiol
adenosine 3',5'-bisphosphate + estradiol 3-sulfate
-
-
-
-
?
3'-phosphoadenylyl sulfate + cholesterol
adenosine 3',5'-bisphosphate + cholesterol 3-sulfate
-
-
-
?
3'-phosphoadenylyl sulfate + cholesterol
adenosine 3',5'-bisphosphate + cholesterol 3-sulfate
-
-
-
-
?
3'-phosphoadenylyl sulfate + cholesterol
adenosine 3',5'-bisphosphate + cholesterol 3-sulfate
-
-
-
?
3'-phosphoadenylyl sulfate + estradiol
adenosine 3',5'-bisphosphate + estradiol sulfate
-
-
-
-
?
3'-phosphoadenylyl sulfate + estradiol
adenosine 3',5'-bisphosphate + estradiol sulfate
-
estrogen sulfotransferase expression in adipose tissue is regulated by testosterone, overview
-
-
?
additional information
?
-
exhibits sulfotransferase activity with phenolic hydroxy groups of steroids and artificial substrates, best acceptor substrate is estrogen
-
-
?
additional information
?
-
-
exhibits sulfotransferase activity with phenolic hydroxy groups of steroids and artificial substrates, best acceptor substrate is estrogen
-
-
?
additional information
?
-
hydroxysteroid sulfotransferase 2B1b (SULT2B1b) is highly selective for the sulfation of 3beta-hydroxysteroids such as cholesterol, oxysterols, DHEA, D5-adiol, 5alpha-androstane-3beta, 17beta-diol (anstane-diol), and pregnenolone
-
-
-
additional information
?
-
-
hydroxysteroid sulfotransferase 2B1b (SULT2B1b) is highly selective for the sulfation of 3beta-hydroxysteroids such as cholesterol, oxysterols, DHEA, D5-adiol, 5alpha-androstane-3beta, 17beta-diol (anstane-diol), and pregnenolone
-
-
-
additional information
?
-
-
is a target for transcriptional induction by the vitamin D receptor
-
-
?
additional information
?
-
-
hydroxysteroid sulfotransferase SULT2A enzymes play important roles in hepatic steroid and xenobiotic metabolism
-
-
?
NATURAL SUBSTRATE
NATURAL PRODUCT
REACTION DIAGRAM
ORGANISM
UNIPROT
COMMENTARY
(Substrate)
(Substrate)
LITERATURE
(Substrate)
(Substrate)
COMMENTARY
(Product)
(Product)
LITERATURE
(Product)
(Product)
REVERSIBILITY
r=reversible
ir=irreversible
?=not specified
r=reversible
ir=irreversible
?=not specified
3'-phosphoadenylyl sulfate + (S)-cholest-5-ene-3beta,24S-diol
adenosine 3',5'-bisphosphate + (S)-cholest-5-ene-3beta,24S-diol 3-sulfate
-
-
-
?
3'-phosphoadenylyl sulfate + 24(R/S),25-epoxycholesterol
adenosine 3',5'-bisphosphate + ?
-
-
-
?
3'-phosphoadenylyl sulfate + 4beta-hydroxycholesterol
adenosine 3',5'-bisphosphate + 4beta-hydroxycholesterol 3-sulfate
-
-
-
?
3'-phosphoadenylyl sulfate + 7-oxocholesterol
adenosine 3',5'-bisphosphate + 7-oxocholesterol 3-sulfate
-
-
-
?
3'-phosphoadenylyl sulfate + 7alpha-hydroxycholesterol
adenosine 3',5'-bisphosphate + 7alpha-hydroxycholesterol 3-sulfate
-
-
-
?
3'-phosphoadenylyl sulfate + 7beta-hydroxycholesterol
adenosine 3',5'-bisphosphate + 7beta-hydroxycholesterol 3-sulfate
-
-
-
?
3'-phosphoadenylyl sulfate + cholest-5-ene-3beta,25-diol
adenosine 3',5'-bisphosphate + cholest-5-ene-3beta,25-diol 3-sulfate
-
-
-
?
3'-phosphoadenylyl sulfate + cholest-5-ene-3beta,27-diol
adenosine 3',5'-bisphosphate + cholest-5-ene-3beta,27-diol 3-sulfate
-
-
-
?
3'-phosphoadenylyl sulfate + cholesterol
adenosine 3',5'-bisphosphate + cholesterol 3-sulfate
3'-phosphoadenylyl sulfate + dehydroepiandrosterone
adenosine 3',5'-bisphosphate + dehydroepiandrosterone 3-sulfate
-
-
-
?
3'-phosphoadenylyl sulfate + estradiol
adenosine 3',5'-bisphosphate + estradiol 3-sulfate
-
-
-
-
?
3'-phosphoadenylyl sulfate + estradiol
adenosine 3',5'-bisphosphate + estradiol sulfate
-
estrogen sulfotransferase expression in adipose tissue is regulated by testosterone, overview
-
-
?
3'-phosphoadenylyl sulfate + cholesterol
adenosine 3',5'-bisphosphate + cholesterol 3-sulfate
-
-
-
?
3'-phosphoadenylyl sulfate + cholesterol
adenosine 3',5'-bisphosphate + cholesterol 3-sulfate
-
-
-
-
?
3'-phosphoadenylyl sulfate + cholesterol
adenosine 3',5'-bisphosphate + cholesterol 3-sulfate
-
-
-
?
additional information
?
-
-
is a target for transcriptional induction by the vitamin D receptor
-
-
?
additional information
?
-
-
hydroxysteroid sulfotransferase SULT2A enzymes play important roles in hepatic steroid and xenobiotic metabolism
-
-
?
ACTIVATING COMPOUND
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
IMAGE
additional information
-
liver X receptor antagonist TO-901317 induces estrogen sulfotransferase expression in female liver, but not in the adipose tissue
-
SPECIFIC ACTIVITY [µmol/min/mg]
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
pH OPTIMUM
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
pH RANGE
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
TEMPERATURE OPTIMUM
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
ORGANISM
COMMENTARY
LITERATURE
UNIPROT
SEQUENCE DB
SOURCE
SOURCE TISSUE
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
SOURCE
abundant SULT2B1 expression in normal gastric epithelium
SULT2B1b mRNA levels in clinical hepatocarcinoma tumor samples are higher than in the non-tumorous tissue adjacent to the tumors
-
of male, but not of female mice. Testosterone-dependent, gender-specific expression of estrogen sulfotransferase in adipose tissue
additional information
-
expression of three of the SULT2A isoforms is abundant in pre-pubertal male and female mouse liver but is essentially silenced in the livers of adult male mice, overview
additional information
no expression of SULT2B1b in placental, prostate and breast tissues in rodents
additional information
-
no estrogen sulfotransferase expression in brown adipose tissue, differential expression of estrogen sulfotransferase in fat and liver, overview
LOCALIZATION
ORGANISM
UNIPROT
COMMENTARY
GeneOntology No.
LITERATURE
SOURCE
GENERAL INFORMATION
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
malfunction
metabolism
physiological function
malfunction
downregulation or ablation of Sult2B1b enhances the gluconeogenic activity of HNF4alpha, which may cause increased acetylation of HNF4alpha as a result of decreased expression of the HNF4alpha deacetylase sirtuin 1 (Sirt1). Sult2B1b-/- mice exhibit elevated fasting blood glucose levels. Thiocholesterol is a hydrolysis-resistant derivative of cholesterol, which shows superior activity to that of the native cholesterol in inhibiting gluconeogenesis and improving insulin sensitivity in high-fat-diet-induced diabetic mice
malfunction
gastric tumor incidence is higher in the SULT2B1-/- mice than in the wild-type mice. In gastric epithelial cells, adenovirus-mediated SULT2B1b overexpression reduces the levels of oxysterols, such as 24(R/S),25-epoxycholesterol (24(R/S),25-EC) and 27-hydroxycholesterol. This condition also increases PI3K/AKT signaling to promote gastric epithelial cell proliferation, epithelization, and epithelial development. SULT2B1 deletion or SULT2B1 knockdown suppresses PI3K/AKT signaling, epithelial cell epithelization, and wound healing and induced gastric epithelial cell malignant transition upon 3-MCA induction. SULT2B1 deletion inhibited PI3K/AKT signaling in response to growth factors, but SULT2B1 overexpression promotes this pathway
malfunction
upregulation of hydroxysteroid sulfotransferase 2B1b promotes hepatic oval cell (HOC) proliferation by modulating oxysterol-induced LXR activation in a mouse model of liver injury. HOCs derived from SULT2B1-/- mice show lower proliferative capability than those from wild-type mice. SULT2B1b overexpression promotes growth of the WB-F344 hepatic oval cell line, whereas SULT2B1b knockdown inhibits growth of these cells. The levels of 22-hydroxycholesterol, 25-hydroxycholesterol, and 24,25-epoxycholesterol(all physiological ligands of liver X receptors) are higher in the DDC-injured livers of SULT2B1-/- mice than in livers of wild-type mice. Knockdown of SULT2B1b expression inhibited proliferation of mouse and human hepatocellular carcinoma cells (Hepa1-6, Huh-7, SMMC-7721, and BEL-7402), whereas overexpression of SULT2B1b promoted such proliferation in vitro and in vivo
metabolism
isoform SULT2B1b and its enzymatic by-product cholesterol sulfate are important metabolic regulators that control glucose metabolism. Mechanistically, cholesterol sulfate and SULT2B1b inhibit gluconeogenesis by suppressing the expression of acetyl coenzyme A synthetase, leading to decreased acetylation and nuclear exclusion of hepatocyte nuclear factor 4alpha.
metabolism
regulation of cholesterol sulfotransferase SULT2B1b by hepatocyte nuclear factor 4alpha constitutes a negative feedback control of hepatic gluconeogenesis. The SULT2B1b gene is a transcriptional target of HNF4alpha. Recruitment of HNF4alpha to the mouse Sult2B1b gene promoter is confirmed by chromatin immunoprecipitation assay on mouse primary hepatocytes
metabolism
SULT2B1b overexpression reduces the levels of oxysterols, such as 24(R/S),25-epoxycholesterol (24(R/S),25-EC) and 27-hydroxycholesterol. This condition also increases PI3K/AKT signaling to promote gastric epithelial cell proliferation, epithelization, and epithelial development. The PI3K/AKT signaling pathway plays essential roles in normal cellular functions, such as protein synthesis, growth control, and nutrition/energy balance. PI3K/AKT activation by growth factors can stimulate protein synthesis and cell growth
physiological function
upregulation of SULT2B1b promotes hepatic oval cell proliferation and aggravate liver injury via the suppression of oxysterol-induced LXR activation in chemically induced mouse liver injury
physiological function
hydroxysteroid sulfotransferase 2B1 (SULT2B1) affects gastric epithelial function and carcinogenesis induced by a carcinogenic agent. The abundant SULT2B1 expression in normal gastric epithelium might maintain epithelial function via the PI3K/AKT signaling pathway and suppress gastric carcinogenesis induced by a carcinogenic agent. Enzyme SULT2B1 is involved in epithelial development
physiological function
hydroxysteroid sulfotransferase 2B1b (SULT2B1b) sulfates cholesterol and oxysterols. Hepatic oval cells (HOCs), thought to be progenitor cells, can be triggered in chemically injured livers. Role of SULT2B1b in HOC proliferation after liver injury, overview. The IL-6/STAT3 signaling pathway is promoted by SULT2B1b. Liver X receptors (LXRs) activation inhibits HOC proliferation and the IL-6/STAT3 signaling pathway, and these effects can be reversed by SULT2B1b activity. SULT2B1b promotes IL-6/STAT3 signaling and HOC proliferation by suppressing oxysterol-induced LXR activation
physiological function
sulfotransferases (SULTs) catalyze the transfer of a sulfate group from 3'-phosphoadenosine 5'-phosphosulfate (PAPS) to an acceptor molecule. Sulfation plays an essential role in regulating the chemical and functional homeostasis of endogenous and exogenous molecules. The cholesterol sulfotransferase SULT2B1b preferentially catalyzes the sulfoconjugation of cholesterol to synthesize cholesterol sulfate. SULT2B1b inhibits hepatic gluconeogenesis by antagonizing the gluconeogenic activity of hepatocyte nuclear factor 4alpha (HNF4alpha). Regulation of cholesterol sulfotransferase SULT2B1b by hepatocyte nuclear factor 4alpha constitutes a negative feedback control of hepatic gluconeogenesis. SULT2B1b also plays a restrictive role in HNF4alpha-mediated fasting-responsive gluconeogenesis
UNIPROT
ENTRY NAME
ORGANISM
NO. OF AA
NO. OF TRANSM. HELICES
MOLECULAR WEIGHT[Da]
SOURCE
SEQUENCE
LOCALIZATION PREDICTION
The reliability class of the localization prediction ranges from 1 (very reliable) to 5 (not reliable).
The reliability class of the localization prediction ranges from 1 (very reliable) to 5 (not reliable). ST2B1_MOUSE
338
0
38347
Swiss-Prot
other Location (Reliability: 1)
PROTEIN VARIANTS
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
additional information
additional information
SULT2B1b overexpression promotes gastric epithelial cell proliferation via the PI3K/AKT signaling pathway
additional information
-
SULT2B1b overexpression promotes gastric epithelial cell proliferation via the PI3K/AKT signaling pathway
additional information
the male and female homozygous SULT2B1 knockout mice, SULT2B1 knockout mouse line, B6;129-Sult2b1tm1Rus/J, are used in which exons 4-8 of the SULT2B1 gene are removed abolishing the gene expression, but the mutant mice are viable and fertile. They lack cholesterol sulfate in the dermis but otherwise appear to have normal lipid metabolism. The mouse liver injury model is established utilizing the SULT2B1-/- mice and their wild-type littermates. To induce liver injury, male C57BL/6 mice (age, 6-8 weeks) are fed a diet containing 0.1% DDC or 0.025% alpha-naphthylisothiocyanate (ANIT) for 4 weeks, or intraperitoneally injected with carbon tetrachloride (0.4 ml/kg body weight) or thioacetamide (200 mg/kg) twice a week for 4 weeks. SULT2B1-deficient HOCs display decreased proliferative capability, and IL-6/STAT3 signaling is involved in the effect of SULT2B1b on HOC proliferation. Oxysterol-induced LXR activation is enhanced in SULT2B1-deficient liver
additional information
-
the male and female homozygous SULT2B1 knockout mice, SULT2B1 knockout mouse line, B6;129-Sult2b1tm1Rus/J, are used in which exons 4-8 of the SULT2B1 gene are removed abolishing the gene expression, but the mutant mice are viable and fertile. They lack cholesterol sulfate in the dermis but otherwise appear to have normal lipid metabolism. The mouse liver injury model is established utilizing the SULT2B1-/- mice and their wild-type littermates. To induce liver injury, male C57BL/6 mice (age, 6-8 weeks) are fed a diet containing 0.1% DDC or 0.025% alpha-naphthylisothiocyanate (ANIT) for 4 weeks, or intraperitoneally injected with carbon tetrachloride (0.4 ml/kg body weight) or thioacetamide (200 mg/kg) twice a week for 4 weeks. SULT2B1-deficient HOCs display decreased proliferative capability, and IL-6/STAT3 signaling is involved in the effect of SULT2B1b on HOC proliferation. Oxysterol-induced LXR activation is enhanced in SULT2B1-deficient liver
additional information
-
male estrogen sulfotransferase-knockout mice develop increased epididymal fat accumulation with enlarged adipocyte size, phenotype, overview
CLONED (Commentary)
ORGANISM
UNIPROT
LITERATURE
gene Sult2b1, recombinant overexpression of Ad-CMV-SULT2B1b via adenovirus vector in human wild-type and SULT2B1b-knockout GES-1 cells, quantitative RT-PCR enzyme expression analysis
SULT2B1a and SULT2B1b, DNA and amino acid sequence determination and analysis, genetic structure
presence of seven SULT2A genes, including SULT2A1, within a cluster on chromosome 7, DNA and amino acid sequence determination and analysis, age- and sex-dependent expressions of the seven genes, overview
-
EXPRESSION
ORGANISM
UNIPROT
LITERATURE
HNF4alpha positively regulates the expression of Sult2B1b in mouse primary hepatocytes and in mouse liver, expression of Sult2B1b is induced by HNF4alpha upon fasting
the expression of SULT2B1b in the liver is induced in obese mice and during the transition from the fasted to the fed state
the expression of SULT2B1b is increased dramatically in a chemical-induced liver injury model (using a hepatotoxic diet containing 0.1% 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC)), mainly in hepatic oval cells (HOCs)
the expression of SULT2B1b is increased dramatically in a chemical-induced liver injury model, mainly in hepatic oval cells
REF.
AUTHORS
TITLE
JOURNAL
VOL.
PAGES
YEAR
ORGANISM (UNIPROT)
PUBMED ID
SOURCE
Kakuta, Y.; Pedersen, L.C.; Chae, K.; Song, W.C.; Leblanc, D.; London, R.; Carter, C.W.; Negishi, M.
Mouse steroid sulfotransferases. Substrate specificity and preliminary X-ray crystallographic analysis
Biochem. Pharmacol.
55
313-317
1998
Mus musculus
Strott, C.A.
Steroid sulfotransferases
Endocr. Rev.
17
670-697
1996
Cavia porcellus, Homo sapiens, Mus musculus, Rattus norvegicus
Takehara, K.; Kubushiro, K.; Iwamori, Y.; Tsukazaki, K.; Nozawa, S.; Iwamori, M.
Expression of an isoform of testis-specific estrogen sulfotransferase in murine placenta during late gestational period
Arch. Biochem. Biophys.
394
201-208
2001
Mus musculus (O35400), Mus musculus
Echchgadda, I.; Song, C.S.; Roy, A.K.; Chatterjee, B.
Dehydroepiandrosterone sulfotransferase is a target for transcriptional induction by the vitamin D receptor
Mol. Pharmacol.
65
720-729
2004
Mus musculus
Falany, C.N.; He, D.; Dumas, N.; Frost, A.R.; Falany, J.L.
Human cytosolic sulfotransferase 2B1: isoform expression, tissue specificity and subcellular localization
J. Steroid Biochem. Mol. Biol.
102
214-221
2006
Homo sapiens (O00204), Homo sapiens, Mus musculus (O35400), Rattus norvegicus (Q29YR5)
Kocarek, T.A.; Duanmu, Z.; Fang, H.L.; Runge-Morris, M.
Age- and sex-dependent expression of multiple murine hepatic hydroxysteroid sulfotransferase (SULT2A) genes
Biochem. Pharmacol.
76
1036-1046
2008
Mus musculus
Khor, V.K.; Tong, M.H.; Qian, Y.; Song, W.C.
Gender-specific expression and mechanism of regulation of estrogen sulfotransferase in adipose tissues of the mouse
Endocrinology
149
5440-5448
2008
Mus musculus
Wang, Z.; Yang, X.; Chen, L.; Zhi, X.; Lu, H.; Ning, Y.; Yeong, J.; Chen, S.; Yin, L.; Wang, X.; Li, X.
Upregulation of hydroxysteroid sulfotransferase 2B1b promotes hepatic oval cell proliferation by modulating oxysterol-induced LXR activation in a mouse model of liver injury
Arch. Toxicol.
91
271-287
2016
Mus musculus (O35400), Mus musculus
Shi, X.; Cheng, Q.; Xu, L.; Yan, J.; Jiang, M.; He, J.; Xu, M.; Stefanovic-Racic, M.; Sipula, I.; ODoherty, R.M.; Ren, S.; Xie, W.
Cholesterol sulfate and cholesterol sulfotransferase inhibit gluconeogenesis by targeting hepatocyte nuclear factor 4?
Mol. Cell. Biol.
34
485-497
2014
Mus musculus (O35400)
Wang, Z.; Yang, X.; Chen, L.; Zhi, X.; Lu, H.; Ning, Y.; Yeong, J.; Chen, S.; Yin, L.; Wang, X.; Li, X.
Upregulation of hydroxysteroid sulfotransferase 2B1b promotes hepatic oval cell proliferation by modulating oxysterol-induced LXR activation in a mouse model of liver injury
Arch. Toxicol.
91
271-287
2017
Mus musculus (O35400), Mus musculus, Mus musculus C57BL/6 (O35400)
Hong, W.; Guo, F.; Yang, M.; Xu, D.; Zhuang, Z.; Niu, B.; Bai, Q.; Li, X.
Hydroxysteroid sulfotransferase 2B1 affects gastric epithelial function and carcinogenesis induced by a carcinogenic agent
Lipids Health Dis.
18
203
2019
Mus musculus (O35400), Mus musculus
Bi, Y.; Shi, X.; Zhu, J.; Guan, X.; Garbacz, W.G.; Huang, Y.; Gao, L.; Yan, J.; Xu, M.; Ren, S.; Ren, S.; Liu, Y.; Ma, X.; Li, S.; Xie, W.
Regulation of cholesterol sulfotransferase SULT2B1b by hepatocyte nuclear factor 4alpha constitutes a negative feedback control of hepatic gluconeogenesis
Mol. Cell. Biol.
38
e00654-17
2018
Homo sapiens (O00204), Mus musculus (O35400)
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Release 2023.1 (January 2023)
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