|Other Names||Sulfotransferase 1A1, ST1A1, Aryl sulfotransferase 1, HAST1/HAST2, Phenol sulfotransferase 1, Phenol-sulfating phenol sulfotransferase 1, P-PST 1, ST1A3, Thermostable phenol sulfotransferase, Ts-PST, SULT1A1, STP, STP1|
|Target/Specificity||The synthetic peptide sequence used to generate the antibody AP2606b was selected from the Center region of human SULT1A1. A 10 to 100 fold molar excess to antibody is recommended. Precise conditions should be optimized for a particular assay.|
|Format||Peptides are lyophilized in a solid powder format. Peptides can be reconstituted in solution using the appropriate buffer as needed.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.|
|Precautions||This product is for research use only. Not for use in diagnostic or therapeutic procedures.|
|Function||Sulfotransferase that utilizes 3'-phospho-5'-adenylyl sulfate (PAPS) as sulfonate donor to catalyze the sulfate conjugation of catecholamines, phenolic drugs and neurotransmitters. Has also estrogen sulfotransferase activity. responsible for the sulfonation and activation of minoxidil. Is Mediates the metabolic activation of carcinogenic N-hydroxyarylamines to DNA binding products and could so participate as modulating factor of cancer risk.|
|Tissue Location||Liver, lung, adrenal, brain, platelets and skin.|
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Provided below are standard protocols that you may find useful for product applications.
Sulphation is a significant detoxification pathway for diverse xenobiotics, yet this modification also plays an important role in the metabolism and bioactivation of many dietary and environmental mutagens, including heterocyclic amines implicated in the pathogenesis of several cancers. A major human sulfotransferase, SULT1A1, metabolizes and/or bioactivates many endogenous compounds and is implicated in a range of cancers because of its ability to transform xenobiotics to cellular mutagens and carcinogens. Genetic polymorphisms in human sulfotransferase 1A1 SULT1A1 have a major impact on SULT1A1 enzyme activity and affect the risk for cancer development in humans. A G--->A transition at codon 213 (CGC/Arg to CAC/His) of the SULT1A1 gene has been identified (SULT1A1*2), and individuals homozygous for the His allele have a markedly lower activity and stability of this enzyme than those with the high activity SULT1A1*1 allozyme, which has been associated with protection against dietary toxins and reduced susceptibility to colorectal and breast cancers.There is an increasing incidence of SULT1A1*1 homozygosity and decreasing incidence of SULT1A1*2 homozygosity with increasing age, indicating a potential association of SULT1A1*1 allozyme(s) with protection against cell and/or tissue damage during aging. CLN3, the locus for Batten disease, maps to the same region 16p12.1-p11.2 as SULT12A1, making SULT1A1 a candidate gene for this disorder.
Carcinogenesis 25 (5), 773-778 (2004)J. Biol. Chem. 279 (18), 18799-18805 (2004)Cancer Lett. 202 (1), 61-69 (2003)J. Biol. Chem. 278 (9), 7655-7662 (2003)Int. J. Cancer 103 (1), 101-104 (2003)Chem. Biol. Interact. 129 (1-2), 141-170 (2000)
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