Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
p19 INK4D/CDKN2D Double Nickase Plasmid (h): sc-401761-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- p19 INK4D/CDKN2D 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
- p19 INK4D/CDKN2D Double Nickase Plasmid (h) and p19 INK4D/CDKN2D Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CDKN2D. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: p19 INK4D/CDKN2D Antibody (DCS-100): sc-56334
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
p19 INK4D/CDKN2D Double Nickase Plasmid (h) | sc-401761-NIC | 20 µg | $410.00 | |||
p19 INK4D/CDKN2D Double Nickase Plasmid (h2) | sc-401761-NIC-2 | 20 µg | $410.00 |
CDKN2D encodes p19 INK4D, a cyclin-dependent kinase inhibitor that preferentially binds CDK4 and CDK6 to restrain cyclin D–dependent phosphorylation of RB1 and enforce the G1/S checkpoint. By limiting E2F-driven transcription, p19 INK4D integrates antiproliferative signals with cell-cycle exit and differentiation programs, including in hematopoietic and neural lineages. CDKN2D function intersects with mitogenic RAS–MAPK signaling and stress-responsive pathways that converge on CDK activity and checkpoint control. Altered regulation of the INK4 family and RB pathway components is frequently implicated in dysregulated proliferation across disease-relevant cellular models, making CDKN2D a useful node for studying cell-cycle control and growth suppression mechanisms.
p19 INK4D/CDKN2D Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CDKN2D locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CDKN2D. 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 CDKN2D 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 CDKN2D-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.