SULT is a class of proteins that are highly conserved in plants, animals, and microorganisms. It catalyzes the transfer of the sulfonic acid group (SO3-) of the universal donor 3′-phosphoadenosine-5′-phosphosulfate to a hydroxyl- or amino-containing substrate, and generating adenosine 3′,5′-diphosphate. SULT catalyzes the sulfonation of a range of compounds to produce sulfate esters, amino acid esters, and sulfate binders. According to the different forms of SULT in cells, SULT can be classified into cytosolic SULT and membrane-associated SULT. Cytosolic SULT mainly catalyzes the sulfonation of small endogenous and exogenous compounds, such as steroids, flavonoids, thioglucosides, hormones, biogenic amines, drugs, etc. Membrane-associated SULT primarily sulfonates macromolecular compounds such as complex carbohydrates, peptides, and proteins.
At CD BioGlyco, our expertise lies in the sophisticated engineering of SULT and their corresponding genetic sequences. This capability serves as a robust resource for researchers and developers, enabling them to precisely regulate sulfation patterns, boost the effectiveness of pharmaceutical agents, and uncover previously unrecognized therapeutic targets.
We employ highly accurate tools to introduce directed modifications into SULT genes. This methodology facilitates the knockout of specific SULT genes to eliminate undesirable sulfation, the insertion of gain-of-function genetic variations to modify substrate preferences, or the expression of newly designed, engineered SULT molecules.
CD BioGlyco has ultra-efficient technologies for gene editing. We also perform downstream functional validation, phenotyping, and other experiments upon request. Several SULTs have been identified and characterized in bacteria, algae, higher plants, animals, and humans. Our SULT gene editing service focuses on SULTs of human origin and plant SULTs.
Fig.1 Gene editing process. (CD BioGlyco)
Paper Title: Suppression of indoxyl sulfate accumulation reduces renal fibrosis in sulfotransferase 1a1-deficient mice
Technology: Gene Knockout
Journal: International Journal of Molecular Sciences
IF: 5.6
Published: 2023
Results: A Sult1a1-deficient (Sult1a1-KO) mouse unilateral ureteral obstruction (UUO) model was constructed to investigate the pathological effects of IS on renal fibrosis and its potential mechanisms. The results showed that renal fibrosis markers, fibronectin, and col1a1, were suppressed in the Sult1a1-KO UUO group. TNF-α and IL-1β gene expression was also reduced. Meanwhile, serum and renal IS concentrations were also relatively low. The study shows that UUO-induced inflammatory response and renal fibrosis were alleviated with the reduction of serum and renal IS accumulation.
Fig.2 Effect of Sult1a1-KO on inflammation, renal fibrosis. (Hou, et al., 2023)
CD BioGlyco integrates R&D, services, and products, and is committed to providing better and more comprehensive Gene Editing Services to our global partners. contact us to learn more about the full range of solutions offered by CD BioGlyco.
Confirm the sulfation patterns and other glycan structures on your engineered products with our state-of-the-art analytical services.
Develop high-affinity antibodies against your newly engineered sulfated glycans for use in diagnostics or therapeutic applications.
Glycoengineering Expression Systems
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