
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CENP-F CRISPR Activation Plasmid (h) | sc-402178-ACT | 20 µg | $397.00 |
CENPF encodes CENP-F, a large kinetochore-associated coiled-coil protein that accumulates through S/G2 and peaks in mitosis, coordinating chromosome alignment, spindle checkpoint signaling, and faithful segregation. CENP-F participates in kinetochore–microtubule attachment, centrosome function, and progression through the G2/M transition, linking cell-cycle control to nuclear architecture. Dysregulation of CENPF expression has been associated with chromosomal instability and proliferative phenotypes reported across multiple cancer types, consistent with its role in mitotic fidelity. As a cell-cycle–regulated structural effector, CENP-F is frequently studied in pathways governing mitosis, genome maintenance, and aneuploidy.
CENP-F CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CENPF expression without altering the underlying DNA sequence.
CENP-F CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CENPF 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 CENPF transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous CENP-F expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CENPF locus and enabling the study of CENP-F-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of CENP-F pathway restoration in tumor cells with silenced or reduced CENPF expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.