CEP152 CRISPR/Cas9 KO Plasmid (m): sc-430248
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CEP152 CRISPR/Cas9 Knockout (KO) Plasmid (m) 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 CEP152 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
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CEP152 CRISPR/Cas9 KO Plasmid (m) | sc-430248 | 20 µg | $397.00 |
Overview
Cep152 encodes the centrosomal protein CEP152, a core scaffold required for centriole biogenesis and centrosome duplication in mouse cells. CEP152 cooperates with PLK4 and other centriole assembly factors to recruit and organize pericentriolar material, supporting microtubule nucleation and accurate bipolar spindle formation during mitosis. Disruption of CEP152 perturbs cell-cycle progression, triggers centrosome amplification or loss, and promotes genomic instability through defective spindle assembly and chromosome segregation. These processes connect CEP152 to pathways frequently interrogated in developmental biology, neurogenesis, and cancer-relevant mechanisms involving mitotic fidelity and DNA damage responses.
CEP152 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Cep152 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Cep152 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 Cep152 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 CEP152 protein expression.
This CRISPR knockout system enables efficient generation of Cep152-deficient cell models for investigation of CEP152 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Cep152 exon(s) critical for CEP152 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 Cep152 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by CEP152 CRISPR/Cas9 KO Plasmid (m) and CEP152 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Cep152 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by CEP152 HDR Plasmid (m) and CEP152 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Cep152 homology arms to support homology-directed repair at defined Cep152 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.