Date published: 2026-7-5

1-800-457-3801

SCBT Portrait Logo
Seach Input

CEP55 CRISPR Activation Plasmid (h): sc-417522-ACT

0.0(0)
Write a reviewAsk a question

Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • CEP55 CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
  • CEP55 CRISPR Activation Plasmid (h) consists of three plasmids at a 1:1:1 mass ratio: a plasmid encoding the deactivated Cas9 (dCas9) nuclease (D10A and N863A) fused to the transactivation domain VP64, and a blasticidin resistance gene; a plasmid encoding the MS2-p65-HSF1 fusion protein, and a hygromycin resistance gene; a plasmid encoding a target-specific 20 nt guide RNA fused to two MS2 RNA aptamers, and a puromycin resistance gene
  • The resulting SAM complex binds to a site-specific region approximately 200-250 nt upstream of the transcriptional start site and provides robust recruitment of transcription factors for highly efficient gene activation
  • gRNAs encoded by CEP55 CRISPR Activation Plasmid (h) and CEP55 CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the CEP55 transcriptional start site. One or both designs may be available
  • Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: CEP55 Antibody (B-8): sc-374051
    Gene Editing Promo Banner

    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    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.