
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
KIF2C CRISPR Activation Plasmid (h) | sc-404645-ACT | 20 µg | $397.00 |
KIF2C (also known as MCAK) encodes a kinesin-13 family microtubule depolymerase that regulates spindle microtubule dynamics and kinetochore–microtubule attachments during mitosis. By promoting microtubule turnover, KIF2C supports accurate chromosome congression and segregation within the cell cycle and mitotic checkpoint–associated processes. Dysregulated KIF2C expression or activity is linked to chromosomal instability and aneuploidy, molecular phenotypes frequently observed in proliferative disease biology. Accordingly, KIF2C is widely studied in pathways governing mitotic fidelity, centrosome/spindle organization, and genome maintenance.
KIF2C CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous KIF2C expression without altering the underlying DNA sequence.
KIF2C CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the KIF2C 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 KIF2C transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous KIF2C expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native KIF2C locus and enabling the study of KIF2C-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of KIF2C pathway restoration in tumor cells with silenced or reduced KIF2C expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.