Cdk4 Double Nickase Plasmid (h): sc-400148-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Cdk4 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
- Cdk4 Double Nickase Plasmid (h) and Cdk4 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CDK4. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Cdk4 Antibody (DCS-35): sc-23896
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Cdk4 Double Nickase Plasmid (h) | sc-400148-NIC | 20 µg | $410.00 | |||
Cdk4 Double Nickase Plasmid (h2) | sc-400148-NIC-2 | 20 µg | $410.00 |
CDK4 encodes cyclin-dependent kinase 4 (Cdk4), a core G1-phase regulator that partners with D-type cyclins to phosphorylate RB family proteins and promote E2F-dependent transcription required for S-phase entry. Through integration of mitogenic signaling and cell-cycle checkpoints, Cdk4 helps coordinate proliferation, cellular senescence, and responses to growth-inhibitory cues. Dysregulated CDK4 activity is frequently linked to aberrant cell-cycle control in cancer biology, including contexts involving CCND amplification, RB pathway disruption, and altered CDKN2A/p16 regulation. As a result, CDK4 is widely studied in pathways governing proliferation, differentiation, and stress-induced growth arrest.
Cdk4 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CDK4 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CDK4. 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 CDK4 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 CDK4-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.