
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SULT1A3/1A4 Lentiviral Activation Particles (h) | sc-417824-LAC | 200 µl | $455.00 |
SULT1A3 encodes a cytosolic sulfotransferase that catalyzes the sulfate conjugation of catecholamines and related monoamines, contributing to phase II xenobiotic metabolism and neurotransmitter homeostasis. The SULT1A3/1A4 protein activity regulates the biotransformation and clearance of dopamine, norepinephrine, and serotonin metabolites, influencing cellular redox balance and metabolite flux through sulfation pathways. This enzyme family is highly expressed in select tissues and can shape local signaling by controlling bioactive amine availability. Altered sulfotransferase expression or activity has been investigated in the context of neuropsychiatric traits, pharmacologic response variability, and cancer-associated metabolic reprogramming where sulfation capacity can modulate tumor microenvironment chemistry.
SULT1A3/1A4 Lentiviral Activation Particles (h) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient SULT1A3 upregulation across a broader range of human cell types.
SULT1A3/1A4 Lentiviral Activation Particles (h) deliver all functional components of the synergistic activation mediator (SAM) system via lentiviral transduction. The system comprises three particle preparations co-transduced into target cells: one encoding catalytically inactive dCas9 (D10A and N863A mutations) fused to the VP64 transactivation domain with a blasticidin resistance gene; one encoding the MS2-p65-HSF1 fusion protein with a hygromycin resistance gene; and one encoding a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers with a puromycin resistance gene. Following lentiviral transduction and genomic integration of the expression cassettes, the SAM components are stably expressed and assemble at the target locus within the proximal promoter region upstream of the SULT1A3 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous SULT1A3/1A4 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native SULT1A3 genomic locus and regulatory architecture.
The lentiviral format offers several practical advantages: stable genomic integration supports heritable activation across cell divisions; high-titer particle preparations eliminate the need for in-house viral production; and compatibility with primary, non-dividing, and transfection-resistant cell types expands experimental accessibility. Successful transduction can be confirmed and enriched through triple antibiotic selection using puromycin, hygromycin, and blasticidin.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.