
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CEP55 CRISPR Activation Plasmid (h) | sc-417522-ACT | 20 µg | $397.00 |
Human CEP55 (centrosomal protein 55) is a cytokinesis regulator that localizes to the midbody and coordinates abscission during late mitosis by engaging ESCRT-dependent membrane fission machinery. Through its roles in centrosome function, spindle organization, and cell-cycle progression, CEP55 helps maintain proliferative fidelity and proper daughter-cell separation. Altered CEP55 expression has been associated with chromosomal instability and dysregulated proliferation programs observed across multiple cancer contexts. Consequently, CEP55 is frequently studied in pathways linking mitotic control, genome maintenance, and tumor cell fitness.
CEP55 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CEP55 expression without altering the underlying DNA sequence.
CEP55 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CEP55 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 CEP55 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous CEP55 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CEP55 locus and enabling the study of CEP55-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of CEP55 pathway restoration in tumor cells with silenced or reduced CEP55 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.