
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Ki67 CRISPR Activation Plasmid (h) | sc-400081-ACT | 20 µg | $397.00 | |||
Ki67 CRISPR Activation Plasmid (h2) | sc-400081-ACT-2 | 20 µg | $397.00 |
MKI67 encodes the human Ki67 protein, a nuclear proliferation marker that is expressed throughout active phases of the cell cycle and is largely absent in quiescent cells. Ki67 contributes to higher-order chromatin organization and is required for proper mitotic chromosome architecture, supporting processes such as cell-cycle progression, DNA replication-associated chromatin dynamics, and mitosis. As a readout of proliferative index, Ki67 is widely used in studies of tissue homeostasis and cell population kinetics, and altered MKI67 expression is frequently associated with dysregulated proliferation in cancer biology and other hyperproliferative states. Experimental modulation of MKI67 supports investigations into proliferation-coupled transcriptional programs and cell-cycle control pathways.
Ki67 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous MKI67 expression without altering the underlying DNA sequence.
Ki67 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the MKI67 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 MKI67 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Ki67 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native MKI67 locus and enabling the study of Ki67-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Ki67 pathway restoration in tumor cells with silenced or reduced MKI67 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.