ADSL Double Nickase Plasmid (h): sc-404936-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ADSL 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
- ADSL Double Nickase Plasmid (h) and ADSL Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ADSL. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: ADSL Antibody (C-11): sc-365623
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ADSL Double Nickase Plasmid (h) | sc-404936-NIC | 20 µg | $410.00 | |||
ADSL Double Nickase Plasmid (h2) | sc-404936-NIC-2 | 20 µg | $410.00 |
Adenylosuccinate lyase (ADSL) is a bifunctional enzyme in de novo purine biosynthesis that catalyzes the conversion of adenylosuccinate to AMP and SAICAR to AICAR, linking nucleotide metabolism to cellular energy balance and proliferative capacity. By regulating pools of purine nucleotides and pathway intermediates, ADSL activity influences DNA/RNA synthesis, replication stress responses, and metabolic signaling in rapidly dividing cells. Loss-of-function variants in human ADSL disrupt purine homeostasis and are associated with adenylosuccinate lyase deficiency, a neurometabolic disorder characterized by accumulation of succinylpurines and impaired neurodevelopment. In research settings, ADSL is studied to dissect purinosome dynamics, metabolic control of gene expression, and the contribution of purine pathway perturbations to cellular stress phenotypes.
ADSL Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ADSL locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ADSL. 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 ADSL 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 ADSL-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.