TRIM10 CRISPR/Cas9 KO Plasmid (m): sc-422691
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TRIM10 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 TRIM10 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 | |
TRIM10 CRISPR/Cas9 KO Plasmid (m) | sc-422691 | 20 µg | $397.00 |
Overview
Mouse TRIM10 (Trim10) encodes a tripartite motif-containing E3 ubiquitin ligase implicated in ubiquitin-dependent control of protein stability and signaling complex turnover. TRIM family proteins commonly participate in regulation of innate immune signaling, stress responses, and cytoskeletal or differentiation-associated processes through modulation of ubiquitination and proteostasis. In hematopoietic contexts, TRIM proteins are frequently linked to lineage commitment and maturation programs, making Trim10 of interest for studying erythroid-associated regulatory networks and broader immune cell biology. Dysregulated ubiquitin pathway activity is a recurring feature of inflammatory and hematologic disease mechanisms, supporting the use of Trim10 perturbation to interrogate pathway dependencies in relevant mouse models.
TRIM10 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Trim10 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Trim10 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 Trim10 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 TRIM10 protein expression.
This CRISPR knockout system enables efficient generation of Trim10-deficient cell models for investigation of TRIM10 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Trim10 exon(s) critical for TRIM10 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 Trim10 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by TRIM10 CRISPR/Cas9 KO Plasmid (m) and TRIM10 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Trim10 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by TRIM10 HDR Plasmid (m) and TRIM10 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Trim10 homology arms to support homology-directed repair at defined Trim10 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.