Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
CEP55 CRISPR/Cas9 KO Plasmid (h): sc-417522
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CEP55 CRISPR/Cas9 Knockout (KO) Plasmid (h) is a pool of plasmids, each encoding Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed for maximum knockout efficiency using sequences derived from the GeCKO v2 library
- gRNA sequences direct Cas9 to induce site-specific double-strand breaks (DSBs) in the CEP55 genomic locus, resulting in gene knockout through non-homologous end joining (NHEJ)
- The puromycin resistance and RFP genes are flanked by LoxP sites, enabling removal of selection markers via Cre recombinase (Cre Vector: sc-418923) after establishing stable knockout cell lines
- 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 CRISPR/Cas9 KO Plasmid (h) | sc-417522 | 20 µg | $397.00 |
Overview
CEP55 (centrosomal protein 55) is a cytokinesis regulator that localizes to centrosomes and the midbody, where it supports abscission by coordinating ESCRT machinery recruitment during late mitosis. Through interactions with midbody scaffolding proteins and membrane remodeling factors, CEP55 helps maintain faithful cell division, genome stability, and proper completion of the cell cycle. Dysregulated CEP55 expression has been linked to proliferative phenotypes and chromosomal instability observed across multiple cancer contexts, making it a useful node for studying mitotic control. CEP55 is also relevant to pathways governing centrosome dynamics, mitotic spindle organization, and checkpoint responses to cytokinetic failure.
CEP55 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the CEP55 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the CEP55 together with the Streptococcus pyogenes Cas9 nuclease. The plasmids also encode GFP, allowing fluorescent identification and enrichment of successfully transfected cells by fluorescence microscopy or flow cytometry.
The multi-guide design increases the likelihood of generating insertions or deletions (indels) that disrupt the CEP55 open reading frame following Cas9-mediated double-strand break formation. DNA breaks introduced by the CRISPR/Cas9 system are repaired through endogenous non-homologous end joining (NHEJ) pathways, frequently resulting in frameshift mutations that abolish CEP55 protein expression.
This CRISPR knockout system enables efficient generation of CEP55-deficient cell models for investigation of CEP55 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting CEP55 exon(s) critical for CEP55 function
- Co-expression of SpCas9 and sgRNA from a single plasmid for simplified delivery
- GFP reporter for identification of transfected cells
- Pool of plasmids targeting multiple CEP55 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by CEP55 CRISPR/Cas9 KO Plasmid (h) and CEP55 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the CEP55 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by CEP55 HDR Plasmid (h) and CEP55 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by CEP55 homology arms to support homology-directed repair at defined CEP55 target sites corresponding to the CRISPR/Cas9 KO designs. HDR donor availability may vary. See Related Products for availability.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.