cyclin M1 Double Nickase Plasmid (m): sc-429932-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- cyclin M1 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
- cyclin M1 Double Nickase Plasmid (m) and cyclin M1 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Cnnm1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
cyclin M1 Double Nickase Plasmid (m) | sc-429932-NIC | 20 µg | $410.00 |
Cnnm1 encodes cyclin M1, a conserved membrane-associated regulator of divalent cation transport that contributes to cellular magnesium homeostasis and ion-dependent signaling. Through control of intracellular Mg²⁺ levels, cyclin M1 can influence ATP-dependent enzymatic activity, kinase signaling, and metabolic processes that are sensitive to magnesium availability. In mouse systems, Cnnm1 function is relevant to studies of electrolyte handling and cell stress responses, and altered cation balance has been associated with phenotypes impacting excitable tissues and renal physiology. These features make Cnnm1 a useful target for dissecting ion-transport pathways and downstream signaling networks in biomedical research models.
cyclin M1 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Cnnm1 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Cnnm1. 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 Cnnm1 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 Cnnm1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.