Cdk9 Double Nickase Plasmid (h): sc-400242-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Cdk9 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
- Cdk9 Double Nickase Plasmid (h) and Cdk9 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CDK9. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Cdk9 Antibody (D-7): sc-13130
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Cdk9 Double Nickase Plasmid (h) | sc-400242-NIC | 20 µg | $410.00 | |||
Cdk9 Double Nickase Plasmid (h2) | sc-400242-NIC-2 | 20 µg | $410.00 |
CDK9 encodes the catalytic subunit of positive transcription elongation factor b (P-TEFb), a kinase complex that phosphorylates the RNA polymerase II C-terminal domain and pausing factors to promote productive transcriptional elongation. Through control of promoter-proximal pause release, Cdk9 regulates rapid-response gene programs, cell cycle progression, and stress-adaptive transcription, and it integrates with cyclin T-dependent signaling and chromatin-associated regulatory networks. Dysregulated CDK9 activity or dependency has been linked to altered transcriptional homeostasis in cancer and to perturbations in inflammatory and viral transcriptional circuits, making it a central node for studying transcriptional control mechanisms.
Cdk9 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CDK9 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CDK9. 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 CDK9 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 CDK9-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.