3′-Phosphoadenosine-5′-phosphosulfate (PAPS) is a derivative of adenosine monophosphate (AMP) that is phosphorylated at the 3′ position and has a sulfate group attached to the 5′ phosphate. It is the most common coenzyme in sulfotransferase reactions and hence part of sulfation pathways. It is endogenously synthesized by organisms via the phosphorylation of adenosine 5′-phosphosulfate (APS), an intermediary metabolite. In humans such reaction is performed by bifunctional 3′-phosphoadenosine 5′-phosphosulfate synthases using ATP as the phosphate donor.
An aryl sulfotransferase is an enzyme that transfers a sulfate group from phenolic sulfate esters to a phenolic acceptor substrate.
Estrone sulfotransferase (EST), also known as estrogen sulfotransferase, is an enzyme that catalyzes the transformation of an unconjugated estrogen like estrone into a sulfated estrogen like estrone sulfate. It is a steroid sulfotransferase and belongs to the family of transferases, to be specific, the sulfotransferases, which transfer sulfur-containing groups. This enzyme participates in androgen and estrogen metabolism and sulfur metabolism.
In enzymology, a steroid sulfotransferase is an enzyme that catalyzes the chemical reaction
Sulfotransferase 1A3/1A4 is an enzyme that in humans is encoded by the SULT1A3 gene.
UDP-glucuronosyltransferase 1-6 is an enzyme that in humans is encoded by the UGT1A6 gene.
Estrogen sulfotransferase is an enzyme that in humans is encoded by the SULT1E1 gene.
Carbohydrate sulfotransferase 6 is an enzyme that in humans is encoded by the CHST6 gene.
Sulfotransferase family cytosolic 2B member 1 is an enzyme that in humans is encoded by the SULT2B1 gene.
Sulfotransferase 1A2 is an enzyme that in humans is encoded by the SULT1A2 gene.
Sulfotransferase 1C2 is an enzyme that in humans is encoded by the SULT1C2 gene.
Sulfotransferase 4A1 is an enzyme that in humans is encoded by the SULT4A1 gene.
Carbohydrate sulfotransferase 1 is an enzyme that in humans is encoded by the CHST1 gene.
Sulfotransferase family cytosolic 1B member 1 is an enzyme that in humans is encoded by the SULT1B1 gene.
Carbohydrate sulfotransferase 5 is an enzyme that in humans is encoded by the CHST5 gene.
Heparan sulfate glucosamine 3-O-sulfotransferase 1 is an enzyme that in humans is encoded by the HS3ST1 gene.
Sulfotransferase 1C4 is an enzyme that in humans is encoded by the SULT1C4 gene.
Bile salt sulfotransferase also known as hydroxysteroid sulfotransferase (HST) or sulfotransferase 2A1 (ST2A1) is an enzyme that in humans is encoded by the SULT2A1 gene.
Phenol sulfur transferase deficiency, in short PST deficiency, is the lack or the reduced activity of the functional enzyme phenol sulfur transferase, which is crucial in the detoxification of mainly phenolic compounds by catalysing the sulfate conjugation of the hydroxyl groups in the toxic phenolic compounds to result in more hydrophilic forms for more efficient excretion. This metabolic disorder was first discovered in the late 1990s by Dr. Rosemary Waring during her researches with autistic children, which also made this deficiency commonly associated to the topics of autism. Mutations in the PST genes account for the genetic causes of the deficiency, of which single nucleotide polymorphism and methylation of promoters are two examples of mutations that respectively cause conformational abnormalities and diminished expressions to the enzyme, resulting in the reduced detoxification of phenolic compounds and regulation of phenolic neurotransmitter. The deficiency may cause symptoms like flushing, tachycardia, and depression, and be a risk factor for disorders like autism, migraine, and cancer, while it also limits the use of phenolic drugs in PST deficient patients. There is currently no drug available for treating PST deficiency. However, some people suffering from PST deficiency have found taking a digestive enzyme supplement containing Xylanase 10 minutes before eating to greatly reduce symptoms.
Minoxidil sulfate, also known as minoxidil sulfate ester or minoxidil N-O-sulfate, is an active metabolite of minoxidil and is the active form of this agent. Minoxidil acts as a prodrug of minoxidil sulfate. Minoxidil sulfate is formed from minoxidil via sulfotransferase enzymes, with the predominant enzyme responsible, at least in hair follicles, being SULT1A1. Minoxidil sulfate acts as a potassium channel opener, among other actions, and has vasodilating, hypotensive, and trichogenic or hypertrichotic effects. Its mechanism of action in terms of hair growth is still unknown, although multiple potential mechanisms have been implicated.
