SULT1A2 Double Nickase Plasmid (h): sc-405799-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SULT1A2 Double Nickase Plasmid (h) consists of a pair of plasmids each encoding a D10A mutated Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed to knockout gene expression with greater specificity than its CRISPR/Cas9 KO counterpart
- Paired gRNA sequences are offset by approximately 20 bp to allow for specific Cas9-mediated double nicking of the genomic DNA, which mimics a DSB
- One plasmid in the pair contains a puromycin-resistance gene for selection; the other plasmid in the pair contains a GFP marker to visually confirm transfection
- SULT1A2 Double Nickase Plasmid (h) and SULT1A2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting SULT1A2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SULT1A2 Double Nickase Plasmid (h) | sc-405799-NIC | 20 µg | $410.00 | |||
SULT1A2 Double Nickase Plasmid (h2) | sc-405799-NIC-2 | 20 µg | $410.00 |
Human SULT1A2 encodes a cytosolic sulfotransferase that catalyzes the sulfate conjugation of phenolic compounds using 3′-phosphoadenosine-5′-phosphosulfate (PAPS) as the sulfate donor, increasing substrate solubility and modulating bioactivity. This phase II metabolism activity contributes to xenobiotic clearance and the biotransformation of endogenous small molecules, intersecting with cellular detoxification networks that shape exposure to reactive intermediates. Variation in sulfation capacity can influence the balance between detoxification and bioactivation for certain chemicals, linking SULT1A2 activity to inter-individual differences in susceptibility in toxicology and chemical carcinogenesis research. SULT1A2 is therefore relevant to studies of metabolic enzyme regulation, substrate specificity, and systems-level responses to environmental and pharmacologic stressors.
SULT1A2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the SULT1A2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within SULT1A2. When directed to adjacent sites on opposite DNA strands, the two nickases generate offset single-strand nicks that together produce a staggered double-strand break, requiring coordinated on-target activity from both guides. The resulting DNA break is resolved by endogenous cellular repair pathways, most commonly through non-homologous end joining (NHEJ), leading to insertions or deletions that disrupt SULT1A2 function. By requiring dual sgRNA engagement at the target locus, the double nicking approach enhances editing specificity and provides a complementary CRISPR strategy for applications where additional control over targeting precision is desired.
To support efficient identification of edited cells, one plasmid encodes GFP for fluorescent visualization of transfected populations, while the companion plasmid carries a puromycin resistance gene for antibiotic selection. Together, these features support efficient enrichment of co-transfected populations and simplify the validation of SULT1A2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.