
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Cdk3 CRISPR Activation Plasmid (h) | sc-400846-ACT | 20 µg | $397.00 |
CDK3 encodes cyclin-dependent kinase 3 (Cdk3), a serine/threonine kinase that contributes to cell-cycle control by partnering with cyclins to regulate transitions through G1 and entry into S phase. Cdk3 has been linked to phosphorylation events that modulate transcriptional programs, including regulation of cell-cycle–responsive gene expression through pathways such as RB/E2F signaling. Altered CDK3 activity or expression can impact proliferation and checkpoint control, processes frequently perturbed in cancer and other hyperproliferative states. As a result, CDK3 is commonly studied in the context of cell-cycle dynamics, oncogenic signaling networks, and transcriptional regulation.
Cdk3 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CDK3 expression without altering the underlying DNA sequence.
Cdk3 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CDK3 locus in human cell lines. The system is built around a catalytically inactive Cas9 (dCas9) carrying two inactivating mutations (D10A and N863A) that eliminate nuclease activity while preserving DNA binding. This dCas9 is fused to VP64, a potent transcriptional activator, and is co-expressed with a blasticidin resistance gene for selection. The second plasmid encodes the MS2-p65-HSF1 fusion protein, a secondary activator complex that works in concert with dCas9-VP64, alongside a hygromycin resistance gene. The third plasmid encodes a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers that recruit the MS2-p65-HSF1 complex to the activation site, accompanied by a puromycin resistance gene. The three plasmids are delivered at a 1:1:1 mass ratio for balanced expression of all system components.
Once assembled at the target locus, the SAM complex binds within approximately 200 bp upstream of the CDK3 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Cdk3 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CDK3 locus and enabling the study of Cdk3-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Cdk3 pathway restoration in tumor cells with silenced or reduced CDK3 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.