CEP55 Double Nickase Plasmid (h): sc-417522-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CEP55 Double Nickase Plasmid (h) consists of a pair of plasmids each encoding a D10A mutated Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed to knockout gene expression with greater specificity than its CRISPR/Cas9 KO counterpart
- Paired gRNA sequences are offset by approximately 20 bp to allow for specific Cas9-mediated double nicking of the genomic DNA, which mimics a DSB
- One plasmid in the pair contains a puromycin-resistance gene for selection; the other plasmid in the pair contains a GFP marker to visually confirm transfection
- CEP55 Double Nickase Plasmid (h) and CEP55 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CEP55. 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
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CEP55 Double Nickase Plasmid (h) | sc-417522-NIC | 20 µg | $410.00 | |||
CEP55 Double Nickase Plasmid (h2) | sc-417522-NIC-2 | 20 µg | $410.00 |
CEP55 (centrosomal protein 55) encodes a mitotic regulator that localizes to the centrosome and midbody, where it helps coordinate abscission during the terminal stages of cytokinesis. The protein engages the ESCRT machinery and associated midbody components to ensure proper cleavage furrow resolution and completion of cell division. Disruption of CEP55 perturbs centrosome dynamics, spindle organization, and chromosomal stability, linking its dysregulation to proliferative phenotypes and genome instability observed in multiple cancer contexts. As a result, CEP55 is frequently used to study cell-cycle control, mitotic exit, and mechanisms of aneuploidy in human cellular models.
CEP55 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CEP55 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CEP55. When directed to adjacent sites on opposite DNA strands, the two nickases generate offset single-strand nicks that together produce a staggered double-strand break, requiring coordinated on-target activity from both guides. The resulting DNA break is resolved by endogenous cellular repair pathways, most commonly through non-homologous end joining (NHEJ), leading to insertions or deletions that disrupt CEP55 function. By requiring dual sgRNA engagement at the target locus, the double nicking approach enhances editing specificity and provides a complementary CRISPR strategy for applications where additional control over targeting precision is desired.
To support efficient identification of edited cells, one plasmid encodes GFP for fluorescent visualization of transfected populations, while the companion plasmid carries a puromycin resistance gene for antibiotic selection. Together, these features support efficient enrichment of co-transfected populations and simplify the validation of CEP55-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.