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HGNC Approved Gene Symbol: SULT1E1
Cytogenetic location: 4q13.3 Genomic coordinates (GRCh38): 4:69,821,122-69,860,145 (from NCBI)
SULT1E1 (EC 2.8.2.4) catalyzes sulfation of estrogens, leading to their inactivation due to the inability of estrogen sulfates to bind estrogen receptor (see ESR1, 133430) (Ihunnah et al., 2014).
By PCR of human liver cDNA using oligonucleotide primers based on highly conserved estrogen sulfotransferase sequences from nonhuman mammalian species, Aksoy et al. (1994) cloned a cDNA corresponding to human liver estrogen sulfotransferase.
Her et al. (1995) found that the liver STE gene spans approximately 20 kb and consists of 8 exons, ranging in length from 95 to 181 bp. The locations of most exon-intron splice junctions within STE were identical to those found in a human phenol ST gene (STM; 600641). In addition, the locations of 5 STE introns were conserved in the human DHEA-sulfotransferase gene, which is located on chromosome 19.
Her et al. (1995) mapped liver estrogen sulfotransferase cDNA (SULT1E1) to chromosome 4q13.1 by fluorescence in situ hybridization.
Weinshilboum et al. (1997) reviewed the genes in the mouse corresponding to the sulfotransferase genes in the human. The Ste gene is located on mouse chromosome 5.
Ihunnah et al. (2014) had previously identified mouse Est as a negative regulator of adipogenesis. However, in humans, Ihunnah et al. (2014) found that EST expression was induced during adipogenesis in preadipocytes. Furthermore, forced expression of EST in human preadipocytes promoted adipogenesis, and knockdown of EST expression inhibited adipogenesis. The proadipogenic effect of EST in human preadipocytes was recapitulated by knockdown of ER-alpha (ESR1) or pharmacologic ER inhibition. Linear regression analysis revealed a positive correlation between expression of EST and body mass index (BMI) and a negative correlation between ER-alpha expression and BMI.
Tong et al. (2005) generated Ste -/- mice and observed placental thrombosis and spontaneous fetal loss. This phenotype was associated with elevated free estrogen levels systemically and in the amniotic fluid, increased tissue factor expression in the placenta, and heightened platelet sensitivity to agonist-induced activation ex vivo. Treatment of pregnant Ste-null mice with either an anticoagulant or antiestrogen prevented fetal loss. Tong et al. (2005) concluded that STE is a critical estrogen modulator in the placenta and suggested that there is a link between estrogen excess and thrombotic fetal loss.
Aksoy, I. A., Wood, T. C., Weinshilboum, R. Human liver estrogen sulfotransferase: identification by cDNA cloning and expression. Biochem. Biophys. Res. Commun. 200: 1621-1629, 1994. [PubMed: 8185618] [Full Text: https://doi.org/10.1006/bbrc.1994.1637]
Her, C., Aksoy, I. A., Kimura, S., Brandriff, B. F., Wasmuth, J. J., Weinshilboum, R. M. Human estrogen sulfotransferase gene (STE): cloning, structure, and chromosomal localization. Genomics 29: 16-23, 1995. [PubMed: 8530066] [Full Text: https://doi.org/10.1006/geno.1995.1210]
Ihunnah, C. A., Wada, T., Philips, B. J., Ravuri, S. K., Gibbs, R. B., Kirisci, L., Rubin, J. P., Marra, K. G., Xie, W. Estrogen sulfotransferase/SULT1E1 promotes human adipogenesis. Molec. Cell. Biol. 34: 1682-1694, 2014. [PubMed: 24567372] [Full Text: https://doi.org/10.1128/MCB.01147-13]
Tong, M. H., Jiang, H., Liu, P., Lawson, J. A., Brass, L. F., Song, W.-C. Spontaneous fetal loss caused by placental thrombosis in estrogen sulfotransferase-deficient mice. Nature Med. 11: 153-159, 2005. [PubMed: 15685171] [Full Text: https://doi.org/10.1038/nm1184]
Weinshilboum, R. M., Otterness, D. M., Aksoy, I. A., Wood, T. C., Her, C., Raftogianis, R. B. Sulfotransferase molecular biology: cDNAs and genes. FASEB J. 11: 3-14, 1997. [PubMed: 9034160]