CTR9 CRISPR/Cas9 KO Plasmid (m): sc-423522
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CTR9 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 CTR9 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 | |
CTR9 CRISPR/Cas9 KO Plasmid (m) | sc-423522 | 20 µg | $397.00 |
Overview
Mouse Ctr9 encodes CTR9, a core subunit of the polymerase-associated factor 1 complex (PAF1C) that coordinates RNA polymerase II transcription elongation with chromatin regulation. CTR9 supports transcription-coupled histone modifications such as H3K4 and H3K36 methylation, influencing promoter-proximal pausing, mRNA processing, and maintenance of cell identity programs. Through these roles, CTR9 impacts pathways governing proliferation, differentiation, and genome stability, and altered PAF1C activity has been linked to dysregulated transcriptional networks relevant to cancer biology and developmental phenotypes. Ctr9 perturbation therefore provides a tractable entry point to study epigenetic control of gene expression and transcriptional homeostasis in mammalian cells.
CTR9 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Ctr9 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Ctr9 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 Ctr9 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 CTR9 protein expression.
This CRISPR knockout system enables efficient generation of Ctr9-deficient cell models for investigation of CTR9 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Ctr9 exon(s) critical for CTR9 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 Ctr9 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by CTR9 CRISPR/Cas9 KO Plasmid (m) and CTR9 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Ctr9 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by CTR9 HDR Plasmid (m) and CTR9 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Ctr9 homology arms to support homology-directed repair at defined Ctr9 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.