
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Centriolin CRISPR Activation Plasmid (h) | sc-404195-ACT | 20 µg | $397.00 |
Human CNTRL encodes centriolin, a centrosome- and midbody-associated scaffold protein required for centrosome maturation, mitotic spindle organization, and the final abscission step of cytokinesis. Centriolin helps coordinate microtubule anchoring and recruitment of regulatory complexes that govern cell-cycle progression and faithful chromosome segregation. Disruption of centrosome integrity and cytokinetic completion can promote aneuploidy and genomic instability, linking CNTRL-dependent pathways to mechanisms frequently investigated in cancer biology. CNTRL has also been studied in the context of centrosome-related developmental defects and ciliopathy-adjacent phenotypes due to shared centrosomal architecture.
Centriolin CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CNTRL expression without altering the underlying DNA sequence.
Centriolin CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CNTRL 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 CNTRL transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Centriolin expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CNTRL locus and enabling the study of Centriolin-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Centriolin pathway restoration in tumor cells with silenced or reduced CNTRL expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.