Disease relevance of Sult2a1

• Protective role of hydroxysteroid sulfotransferase in lithocholic acid-induced liver toxicity [1].
• Hybridizations were done on bovine enterotoxigenic Escherichia coli with 2 heat-stable (ST) enterotoxin gene probes from porcine and human origin (STp and STh) [2].
• Androgenic repression of the Std gene in rat liver can be recapitulated in androgen receptor (AR)-negative HepG2 hepatoma cells after cotransfection with an AR expression plasmid [3].
• We previously showed that murine polyomavirus mutants that lack both middle T (MT) and small T (ST) functions have a severe pleiotropic defect in early and late viral gene expression as well as genome amplification [4].
• Heat-stable enterotoxin (ST) of Yersinia enterocolitica was produced under defined conditions [5].

Psychiatry related information on Sult2a1

• Optimal conjugation conditions were identified as a carbodiimide-to-toxin ratio of 10:1 by weight, an initial molar ratio of ST to LT of 100:1, and a conjugation reaction time of 96 h [6].

High impact information on Sult2a1

• An anomalous suppression of Std transcription was observed in db/db females, but not in normal females [7].
• From the nucleotide sequence, we deduced a probable amino acid sequence for ST I [8].
• By subcloning restriction fragments and by insertion mutagenesis, we located precisely the gene for ST I within the transposon [8].
• ST promoted cell cycle progression in a manner dependent on its binding of protein phosphatase 2A (PP2A) [9].
• In addition, CAR agonists upregulated bile acid-sulfating Sult2a1 and bilirubin-glucuronidating Ugt1a1 [10].

Chemical compound and disease context of Sult2a1

• Escherichia coli heat-stable enterotoxin (ST) appears to cause intestinal fluid secretion by activating intestinal particulate guanylate cyclase [11].
• We studied the effect of chlorpromazine on fluid accumulation caused by purified heat-stable enterotoxin (ST) from enterotoxigenic Escherichia coli in suckling mice [12].
• These data indicate that indomethacin markedly decreases the net intestinal fluid accumulation induced by E. coli ST enterotoxin [13].
• We examined the effects of disulfide and thiol compounds on Escherichia coli heat-stable enterotoxin (ST) and cyclic GMP-induced secretion [14].
• The effect of lodoxamide tromethamine, a calcium antagonist, on intestinal fluid accumulation induced by Escherichia coli heat-stable (ST) and Vibrio cholerae (CT) enterotoxins in infant mice was investigated [15].

Biological context of Sult2a1

• Alignment of mSTa1 and mSTa2 cDNAs' nucleotide sequences with those of other sulfotransferase cDNAs revealed the greatest sequence identity with the rat STsmp cDNA [16].
• The present data support our previous view that the liver is involved in the combat against malarial blood stages and that down-regulation of the genes DUSP1 and Sult2a1/2 signals dysregulation of protective liver responses, thus possibly contributing to male susceptibility of LTbetaR(-/-) mice [17].
• Our recent unpublished results have focused on elucidating the patterns of ST gene expression in cultured keratinocytes and fibroblasts derived from human skin using RT-PCR, to understand which of the 5 different ST genes in involved in the regulation of keratinocyte differentiation and minoxidil-induced hair growth [18].
• The deduced amino acid sequence of the protein shares 65/79, 65/80, and 62/76% identity/similarity with rat, mouse, and human HST, respectively [19].
• The full-length gp3 alpha-HST cDNA consisted of 1182 base pairs and coded for a protein containing 287 amino acids [19].

Anatomical context of Sult2a1

• CAR activators increased Mrp4 and Sult2a1 expression in primary human hepatocytes and HepG2, a human liver cell line [20].
• Hepatic ST from normal adult females sulfurylated dehydroepiandrosterone (DHEA), whereas this activity disappeared in cytosols of normal adult males by 8 weeks of age [21].
• Cytosolic sulfotransferases (ST) catalyze the sulfation of various phenolic agents, catecholamines, thyroid hormones, steroids, drugs, and procarcinogens, usually resulting in the inactivation and subsequent excretion of the compound [18].
• Evidence for 3 alpha-HST mRNA was not detected in kidney, heart, lung, muscle, spleen, or uterus [19].
• Transformed NIH/3T3 cells obtained by transfection of total or subgenomic ST-FeSV DNA expressed normal levels of the ST-FeSV gene product ST P85 and of its associated protein kinase activity [22].

Associations of Sult2a1 with chemical compounds

• Based on the hydrophilic nature of sulfated bile acids and the Mrp4 capability to transport sulfated steroids, our findings suggest that Mrp4 and Sult2a1 participate in an integrated pathway mediating elimination of sulfated steroid and bile acid metabolites from the liver [20].
• We determined that the nuclear receptor CAR is required to coordinately up-regulate hepatic expression of Mrp4 and an enzyme known to sulfate hydroxy-bile acids and steroids, Sult2a1 [20].
• Among food constituents tested, tannic acid and epigallocatechin gallate strongly inhibited the P-ST activity in vitro [23].
• Importantly, in contrast to the prototypical mouse hydroxysteroid sulfotransferase SULT2A1, the SULT2B1 isoforms have a predilection for cholesterol [24].
• Kinetic analysis of semipurified hepatic ST from BKs-db/db females showed a 10-fold decrease in Km for E1 (apparent Km = 0.9 microM in mutants vs. 9.0 microM in normals) [21].

Physical interactions of Sult2a1

• Gonadectomized mutants were analyzed to correlate how strain- and gender-dependent variation in ST activities interacted with db to achieve diabetogenesis [21].

Other interactions of Sult2a1

• Two of the clones, mSTa1 and mSTa2, were highly homologous to each other [16].
• Marked increases in hepatic sulfating activity for LCA (5.5-fold) and hydroxysteroid sulfotransferase (St) 2a (5.8-fold) were detected in liver of FXR-null mice [1].
• The abnormally elevated frequencies of CD69(+)CD4(+) T cells and decreased frequencies of CD62L(+) naive and/or NTA260(+) memory CD4(+) T cells were under the common genetic control, in which the interaction between MHC and a hitherto unknown locus, designated Sta-1 (spontaneous T-cell activation) on chromosome 12, plays a major role [25].

Analytical, diagnostic and therapeutic context of Sult2a1

• RT-PCR analyses showed abundant expression of the P-ST mRNA in the intestine as well as in the liver in the mouse tissues examined (brain, heart, intestine, kidney, liver and lung) of both sexes [23].
• Molecular cloning of the alcohol/hydroxysteroid form (mSTa1) of sulfotransferase from mouse liver [26].
• Northern blot analysis of guinea pig tissues revealed no apparent gender differences in either mRNA species or distribution; a single 1.4-kilobase HST mRNA species was present in adrenal and liver tissue [19].
• The Y-1 adrenal cell and an enzyme-linked immunosorbent assay (ELISA) detected LT in 85 and 93%, respectively, of stool specimens obtained from adults with acute diarrhea from whom an LT- and ST-producing organism had been isolated [27].
• The first fraction recovered after gel chromatography contained ST with a negligible amount of cAMP [28].

References