cyclin C CRISPR/Cas9 KO Plasmid (h): sc-402308
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- cyclin C 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 cyclin C 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 | |
cyclin C CRISPR/Cas9 KO Plasmid (h) | sc-402308 | 20 µg | $397.00 |
Overview
CCNC encodes cyclin C, a conserved cyclin that partners primarily with CDK8 and related kinases within the Mediator complex to modulate RNA polymerase II–dependent transcription. Through Mediator kinase signaling, cyclin C helps integrate cues from MAPK, Wnt/β-catenin, and other stress-responsive pathways to coordinate cell cycle control, differentiation programs, and adaptive transcriptional responses. Cyclin C has also been linked to mitochondrial dynamics and oxidative stress signaling, reflecting its role at the interface of nuclear transcription and cellular homeostasis. Dysregulation of CCNC-mediated transcriptional control has been associated with altered proliferation and gene expression programs observed across cancer and other disorders involving aberrant signaling and stress responses.
cyclin C CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the CCNC gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the CCNC 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 CCNC 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 cyclin C protein expression.
This CRISPR knockout system enables efficient generation of CCNC-deficient cell models for investigation of cyclin C signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting CCNC exon(s) critical for cyclin C 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 CCNC genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by cyclin C CRISPR/Cas9 KO Plasmid (h) and cyclin C CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the CCNC locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by cyclin C HDR Plasmid (h) and cyclin C HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by CCNC homology arms to support homology-directed repair at defined CCNC 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.