Trap1a CRISPR/Cas9 KO Plasmid (m): sc-423500
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Trap1a 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 Trap1a 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 | |
Trap1a CRISPR/Cas9 KO Plasmid (m) | sc-423500 | 20 µg | $397.00 |
Overview
Trap1a encodes a mitochondrial HSP90 family chaperone that supports proteostasis by stabilizing and folding client proteins within the organelle. Trap1a influences mitochondrial respiration, reactive oxygen species homeostasis, and stress-adaptive signaling, integrating with pathways that regulate apoptosis and metabolic rewiring. By modulating oxidative phosphorylation efficiency and mitochondrial quality control, Trap1a contributes to cellular responses to hypoxia, nutrient limitation, and proteotoxic stress. Dysregulated TRAP1 activity has been linked to altered bioenergetics and stress tolerance observed across multiple disease-relevant contexts, including neurodegeneration and tumor-associated metabolic phenotypes, making it a useful target for mechanistic studies in mouse models.
Trap1a CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Trap1a gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Trap1a 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 Trap1a 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 Trap1a protein expression.
This CRISPR knockout system enables efficient generation of Trap1a-deficient cell models for investigation of Trap1a signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Trap1a exon(s) critical for Trap1a 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 Trap1a genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by Trap1a CRISPR/Cas9 KO Plasmid (m) and Trap1a CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Trap1a locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by Trap1a HDR Plasmid (m) and Trap1a HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Trap1a homology arms to support homology-directed repair at defined Trap1a 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.