SNAT1 Double Nickase Plasmid (m): sc-430613-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SNAT1 Double Nickase Plasmid (m) 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
- SNAT1 Double Nickase Plasmid (m) and SNAT1 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Slc38a1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: SNAT1 Antibody (H-9): sc-137032
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SNAT1 Double Nickase Plasmid (m) | sc-430613-NIC | 20 µg | $410.00 |
Slc38a1 encodes the sodium-coupled neutral amino acid transporter SNAT1 (system A), a major route for cellular uptake of glutamine, alanine, serine, and related substrates in mouse tissues. By regulating intracellular amino acid pools, SNAT1 influences nutrient sensing and metabolic homeostasis, including pathways linked to mTORC1 signaling, redox balance, and neurotransmitter precursor availability. In the nervous system, SNAT1 contributes to glutamine handling that supports glutamatergic and GABAergic neurotransmission and overall synaptic metabolism. Altered amino acid transport and glutamine dependency are implicated in neurodevelopmental and neurodegenerative processes as well as metabolic remodeling, making Slc38a1 a useful node for mechanistic studies of nutrient-driven cellular phenotypes.
SNAT1 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Slc38a1 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Slc38a1. 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 Slc38a1 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 Slc38a1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.