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Mutation in SULT2B1 leads to an autosomal-recessive congenital ichthyosis (zeige LBR Proteine) phenotype via increased proliferation of human keratinocytes, thickening of epithelial layers, and altered epidermal cholesterol metabolism.
Since 1'-hydroxyestragole exposure readily produced DNA injury in B-13/H cells, these data suggest that cholangiocarcinomas generated in rats fed estragole may be dependent, in part, on SULT2B1 activation of the 1'-hydroxyestragole metabolite.
Overexpression of SULT2B1b is an independent prognostic indicator and promotes cell growth and invasion in colorectal carcinoma.
This study identified specific germline variations in estradiol metabolism-related pathways, namely CYP1B1, SULT2B1, and HSD17B2, as novel prognostic markers that are cumulatively associated with increased risk of prostate cancer progression
The SULT2B1 isoforms have a unique 50 amino acid carboxy-terminal sequence that is not present in the other human SULT isoforms (review).
Data indicate that cholesterol sulfate (CS) and SULT2B1b inhibited gluconeogenesis by targeting the gluconeogenic factor hepatocyte nuclear factor 4alpha (HNF4alpha (zeige HNF4A Proteine)) in both cell cultures and human SULT2B1b transgenic mice.
SULT2B1 is induced by calcitriol activated vitamin D receptor (zeige VDR Proteine) in human prostate cancer cells.
SULT2B1b expression promotes proliferation of hepatocellular carcinoma cells in vitro and in vivo, which may contribute to the progression of HCC (zeige FAM126A Proteine).
In HT29 cells expression of SULT2B1 was enhanced by probiotic fermentation supernatants without aleurone.
Sulfation of 25-hydroxycholesterol by SULT2B1b plays an important role in the maintenance of intracellular lipid homeostasis via the LXR (zeige NR1H3 Proteine)/SREBP-1c (zeige SREBF1 Proteine) signaling pathway in endothelial cells.
SULT2B1b may promote hepatocyte proliferation by inactivating oxysterol/LXR signaling.
increases in SULT2B1b expression were accompanied by reduction in key regulators and enzymes involved in lipid metabolism, including liver X receptor alpha (zeige NR1H3 Proteine), SREBP-1 (zeige SREBF1 Proteine), SREBP-2 (zeige SREBF2 Proteine), acetyl-CoA carboxylase-1, and fatty acid synthase (zeige FASN Proteine).
results suggested that the unique, extended proline/serine-rich C-terminus of SULT2B1b is important for its interaction with cytoskeletal proteins
Elevation of hepatic sulphotransferase activities in mice with resistance to cystic fibrosis (zeige S100A8 Proteine)
during embryonic development, SULT2B1b is required for production of cholesterol sulfate essential for normal skin development
Sulfotransferase enzymes catalyze the sulfate conjugation of many hormones, neurotransmitters, drugs, and xenobiotic compounds. These cytosolic enzymes are different in their tissue distributions and substrate specificities. The gene structure (number and length of exons) is similar among family members. This gene sulfates dehydroepiandrosterone but not 4-nitrophenol, a typical substrate for the phenol and estrogen sulfotransferase subfamilies. Two alternatively spliced variants that encode different isoforms have been described.
sulfotransferase family, cytosolic, 2B, member 1
, cytosolic hydroxysteroid sulfotransferase 2b member 1
, alcohol sulfotransferase
, hydroxysteroid sulfotransferase
, hydroxysteroid sulfotransferase 2
, sulfotransferase 2B1
, sulfotransferase family cytosolic 2B member 1
, sulfotransferase 2B