SLC43A2 Double Nickase Plasmid (m): sc-431993-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SLC43A2 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
- SLC43A2 Double Nickase Plasmid (m) and SLC43A2 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Slc43a2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SLC43A2 Double Nickase Plasmid (m) | sc-431993-NIC | 20 µg | $410.00 |
Slc43a2 encodes the mouse SLC43A2 large neutral amino acid transporter (LAT4), a membrane protein that facilitates sodium-independent uptake and efflux of essential and branched-chain amino acids such as leucine, isoleucine, and valine. By regulating intracellular amino acid availability, SLC43A2 influences nutrient-sensing programs including mTORC1 signaling, translational control, and broader metabolic homeostasis. Altered amino acid transport is frequently linked to changes in cell growth, stress adaptation, and immune cell function, making Slc43a2 relevant to studies of metabolic reprogramming and microenvironmental nutrient competition. Dysregulated transporter activity has been associated with proliferative phenotypes in experimental cancer and immunometabolism models, supporting its use as a mechanistic node connecting transport to signaling.
SLC43A2 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Slc43a2 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Slc43a2. 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 Slc43a2 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 Slc43a2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.