CEP192 CRISPR Activation Plasmid (h): sc-406971-ACT

CEP192 (centrosomal protein 192) is a conserved pericentriolar material scaffold that organizes centrosome maturation by recruiting key regulators of microtubule nucleation, including components of the γ-tubulin ring complex and kinases such as PLK1 and AURKA. By coordinating centriole duplication, spindle assembly, and accurate chromosome segregation, CEP192 supports orderly cell cycle progression through mitosis. Disruption or misregulation of centrosome architecture and amplification linked to CEP192-dependent pathways is frequently associated with chromosomal instability, aneuploidy, and altered proliferative capacity in cancer biology. Human CEP192 therefore serves as a useful node for studying centrosome-driven signaling, mitotic checkpoint dynamics, and microtubule organization in proliferating cells.

CEP192 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CEP192 expression without altering the underlying DNA sequence.

CEP192 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CEP192 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 CEP192 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous CEP192 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CEP192 locus and enabling the study of CEP192-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of CEP192 pathway restoration in tumor cells with silenced or reduced CEP192 expression.

For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.