CPTI-M CRISPR/Cas9 KO Plasmid (m): sc-419787
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CPTI-M 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 CPTI-M 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 | |
CPTI-M CRISPR/Cas9 KO Plasmid (m) | sc-419787 | 20 µg | $397.00 |
Overview
Cpt1b encodes the muscle isoform of carnitine palmitoyltransferase 1 (CPTI-M), an outer mitochondrial membrane enzyme that controls long-chain fatty acid entry into mitochondria by generating acylcarnitines. As the rate-limiting step for mitochondrial β-oxidation, CPTI-M links lipid utilization to cellular energy homeostasis and interacts functionally with malonyl-CoA regulation, AMPK signaling, and broader PPAR-driven metabolic programs. In mouse tissues with high oxidative demand, Cpt1b activity shapes fuel selection, mitochondrial function, and lipid partitioning. Altered CPTI-M-dependent flux is frequently studied in the context of metabolic dysfunction, insulin sensitivity, and lipid-associated myopathies and cardiometabolic phenotypes.
CPTI-M CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Cpt1b gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Cpt1b 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 Cpt1b 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 CPTI-M protein expression.
This CRISPR knockout system enables efficient generation of Cpt1b-deficient cell models for investigation of CPTI-M signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Cpt1b exon(s) critical for CPTI-M 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 Cpt1b genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by CPTI-M CRISPR/Cas9 KO Plasmid (m) and CPTI-M CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Cpt1b locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by CPTI-M HDR Plasmid (m) and CPTI-M HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Cpt1b homology arms to support homology-directed repair at defined Cpt1b 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.