
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MKLP-1 CRISPR Activation Plasmid (h) | sc-400696-ACT | 20 µg | $397.00 |
KIF23 encodes the kinesin family motor protein MKLP-1, a central component of the centralspindlin complex that coordinates central spindle assembly and midbody formation during cytokinesis. MKLP-1 integrates microtubule-based transport with RhoA signaling to position the cleavage furrow and regulate contractile ring dynamics, supporting accurate chromosome segregation and cell-cycle progression. Dysregulated KIF23/MKLP-1 activity is linked to aberrant mitosis, aneuploidy, and altered proliferative states, making it relevant to studies of tumor cell division, genomic instability, and cell-cycle checkpoint control. Because MKLP-1 functions at the interface of spindle mechanics and cortical remodeling, it is frequently used to interrogate pathways governing mitotic exit and cytokinetic abscission.
MKLP-1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous KIF23 expression without altering the underlying DNA sequence.
MKLP-1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the KIF23 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 KIF23 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous MKLP-1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native KIF23 locus and enabling the study of MKLP-1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of MKLP-1 pathway restoration in tumor cells with silenced or reduced KIF23 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.