ChREBP Double Nickase Plasmid (m): sc-425525-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ChREBP 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
- ChREBP Double Nickase Plasmid (m) and ChREBP Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Mlxipl. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ChREBP Double Nickase Plasmid (m) | sc-425525-NIC | 20 µg | $410.00 | |||
ChREBP Double Nickase Plasmid (m2) | sc-425525-NIC-2 | 20 µg | $410.00 |
Mlxipl encodes carbohydrate response element–binding protein (ChREBP), a glucose-responsive transcription factor that coordinates conversion of excess carbohydrate into lipids by inducing glycolytic and de novo lipogenic genes. In mouse tissues such as liver and adipose, ChREBP integrates carbohydrate flux with metabolic gene programs downstream of glucose metabolism and insulin signaling, shaping triglyceride synthesis, hepatocyte metabolic zonation, and adipocyte function. Dysregulated ChREBP activity is linked to metabolic phenotypes including hepatic steatosis, insulin resistance, and altered lipid handling, making Mlxipl a key node for studying nutrient-driven transcriptional control. As a transcriptional regulator, ChREBP also provides a tractable entry point for investigating cross-talk between carbohydrate metabolism, lipogenesis, and oxidative stress responses.
ChREBP Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Mlxipl locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Mlxipl. 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 Mlxipl 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 Mlxipl-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.