CDKN2A/p16 Double Nickase Plasmid (m): sc-419610-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CDKN2A/p16 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
- CDKN2A/p16 Double Nickase Plasmid (m) and CDKN2A/p16 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Cdkn2a. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: CDKN2A/p19ARF Antibody (5-C3-1): sc-32748
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CDKN2A/p16 Double Nickase Plasmid (m) | sc-419610-NIC | 20 µg | $410.00 | |||
CDKN2A/p16 Double Nickase Plasmid (m2) | sc-419610-NIC-2 | 20 µg | $410.00 |
Mouse Cdkn2a encodes CDKN2A/p16, a cyclin-dependent kinase inhibitor that restrains CDK4/6 activity and helps maintain RB-dependent control of the G1/S cell-cycle checkpoint. By limiting phosphorylation of RB family proteins, p16 coordinates proliferative arrest programs and interfaces with senescence-associated signaling in response to oncogenic stress and tissue damage. Cdkn2a regulation is closely linked to pathways governing cellular aging, stem and progenitor cell proliferation, and checkpoint integrity. Altered Cdkn2a/p16 expression or function is widely used as a molecular readout for senescence, tumor suppressor pathway engagement, and cell-cycle dysregulation in mouse models.
CDKN2A/p16 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Cdkn2a locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Cdkn2a. 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 Cdkn2a 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 Cdkn2a-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.