TRIP CRISPR/Cas9 KO Plasmid (m): sc-423499
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TRIP 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 TRIP 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 | |
TRIP CRISPR/Cas9 KO Plasmid (m) | sc-423499 | 20 µg | $397.00 |
Overview
Traip encodes TRIP, an E3 ubiquitin ligase that binds PCNA and functions in DNA replication–coupled genome maintenance. TRIP contributes to replication fork stability and coordinates ubiquitin-dependent responses to DNA damage, supporting resolution of replication stress and preservation of chromosome integrity. In mouse cells, TRAIP activity is linked to control of cell-cycle progression and mitotic fidelity through pathways that intersect with DNA repair and ubiquitin signaling. Perturbation of TRAIP-regulated processes is relevant to studies of genome instability phenotypes associated with developmental defects and cancer biology models.
TRIP CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Traip gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Traip 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 Traip 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 TRIP protein expression.
This CRISPR knockout system enables efficient generation of Traip-deficient cell models for investigation of TRIP signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Traip exon(s) critical for TRIP 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 Traip genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by TRIP CRISPR/Cas9 KO Plasmid (m) and TRIP CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Traip locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by TRIP HDR Plasmid (m) and TRIP HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Traip homology arms to support homology-directed repair at defined Traip 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.