
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Cdk9 Double Nickase Plasmid (m) | sc-430774-NIC | 20 µg | $410.00 |
Cyclin-dependent kinase 9 (Cdk9) is the catalytic component of P-TEFb that phosphorylates the C-terminal domain of RNA polymerase II and negative elongation factors to promote transcriptional pause release and productive elongation. In mouse cells, Cdk9 coordinates stimulus-responsive gene expression programs, integrating signaling inputs that control cell-cycle progression, DNA damage responses, and differentiation. Through regulation of transcriptional elongation, Cdk9 influences chromatin-associated processes and can modulate apoptosis and stress-adaptive pathways. Dysregulated CDK9 activity or P-TEFb recruitment is associated with altered transcriptional control in proliferative and inflammatory contexts, supporting its study in disease-relevant gene expression networks.
Cdk9 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Cdk9 locus in mouse 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.