TRIP12 CRISPR/Cas9 KO Plasmid (m): sc-420729
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TRIP12 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 TRIP12 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 | |
TRIP12 CRISPR/Cas9 KO Plasmid (m) | sc-420729 | 20 µg | $397.00 |
Overview
Trip12 encodes TRIP12, a HECT-type E3 ubiquitin ligase that catalyzes ubiquitin transfer to regulate protein turnover and signaling amplitude. In mouse cells, TRIP12 contributes to ubiquitin-dependent proteostasis and influences processes such as DNA damage responses, transcriptional regulation, and cell-cycle control by shaping the stability of key regulatory factors. As part of the ubiquitin–proteasome system, TRIP12-linked ubiquitination can affect stress adaptation and maintenance of genomic integrity. Altered ubiquitin ligase activity is frequently connected to dysregulated growth and neurodevelopmental phenotypes, making Trip12 a relevant target for mechanistic studies of cellular homeostasis and disease-associated pathways.
TRIP12 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Trip12 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Trip12 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 Trip12 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 TRIP12 protein expression.
This CRISPR knockout system enables efficient generation of Trip12-deficient cell models for investigation of TRIP12 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Trip12 exon(s) critical for TRIP12 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 Trip12 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by TRIP12 CRISPR/Cas9 KO Plasmid (m) and TRIP12 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Trip12 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by TRIP12 HDR Plasmid (m) and TRIP12 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Trip12 homology arms to support homology-directed repair at defined Trip12 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.