Mig12 Double Nickase Plasmid (h): sc-412921-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Mig12 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
- Mig12 Double Nickase Plasmid (h) and Mig12 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting MID1IP1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Mig12 Double Nickase Plasmid (h) | sc-412921-NIC | 20 µg | $410.00 | |||
Mig12 Double Nickase Plasmid (h2) | sc-412921-NIC-2 | 20 µg | $410.00 |
MID1IP1 encodes Mig12, a cytosolic regulator of lipid metabolism that interfaces with acetyl‑CoA carboxylase (ACC) to modulate malonyl‑CoA production and de novo fatty acid synthesis. By influencing ACC activity, Mig12 participates in metabolic programs that impact membrane biogenesis, energy storage, and nutrient-responsive signaling linked to lipogenesis. Altered MID1IP1 expression has been associated with metabolic rewiring observed in obesity, insulin resistance, and lipid-driven cellular stress states, making it relevant for studies of metabolic disease biology. This target is also of interest in systems where lipogenic flux supports proliferation and survival, enabling mechanistic interrogation of metabolic vulnerabilities.
Mig12 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the MID1IP1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within MID1IP1. 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 MID1IP1 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 MID1IP1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.