Target intelligence / Profile preview

Sulfotransferase family 1A member 1 (SULT1A1)

Target
SULT1A1
Molecular classification
Enzyme, Transferase
01

Overview

Sulfotransferase family 1A member 1 (SULT1A1) is a cytosolic enzyme in the sulfotransferase family that catalyzes the transfer of a sulfate group from the donor molecule 3'-phosphoadenosine-5'-phosphosulfate (PAPS) to a wide range of acceptor molecules, including phenolic drugs, hormones, and environmental chemicals. SULT1A1 is highly expressed in the human liver and is a major enzyme responsible for the phase II metabolism (specifically, sulfation) of xenobiotics and endogenous compounds. It plays a critical role in chemical detoxification and in the regulation of hormone bioactivity. SULT1A1 exhibits substrate flexibility due to the plasticity of its active site and is subject to genetic polymorphisms, which alter enzyme activity and impact individual variation in drug metabolism, efficacy, and toxicity, particularly in the metabolism of anti-cancer drugs such as tamoxifen. Variations in SULT1A1 are associated with different responses to therapy and susceptibility to disease, making it both a therapeutic target and a biomarker in pharmacogenetics and cancer treatment.

Other names
Sulfotransferase 1A1STPSTP1OK/SW-cl.88ST1A1P-PST 1Ts-PSTP-PSTAryl sulfotransferase 1HAST1/HAST2Phenol sulfotransferase 1Phenol-sulfating phenol sulfotransferase 1ST1A3Thermostable phenol sulfotransferaseTSPST1ts-PSTthermostable phenol sulfotransferase 1aryl sulfotransferase 1
02

Mechanism of action

Sulfation (conjugation) of substrates to increase solubility, facilitate elimination, and modulate biological activity. Inactivation of drugs and transformation of prodrugs via phase II metabolism

03

Biological functions

Xenobiotic detoxificationPhase II drug metabolismSulfonation of phenols, hormones, and drugsRegulation of hormone activity
04

Disease associations

Cancer (notably breast cancer)Pharmacogenetics (variation impacts drug response)Other (potential roles in susceptibility to other diseases due to xenobiotic and hormone metabolism)
05

Safety considerations

Genetic polymorphisms may lead to variability in drug efficacy and toxicityOveractivity may cause reduced bioavailability of some drugs (e.g., rapid clearance of ABT-751)Underactivity may lead to inadequate detoxification or altered hormone regulation
06

Interacting drugs

Tamoxifen

5 more in the full profile.

07

Biomarkers

SULT1A1 genotype and copy number variation (for drug metabolism rate; e.g., tamoxifen and ABT-751 response in cancer patients)SULT1A1 enzymatic activity levels

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