CTP CRISPR/Cas9 KO Plasmid (m): sc-419996
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CTP 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 CTP 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 | |
CTP CRISPR/Cas9 KO Plasmid (m) | sc-419996 | 20 µg | $397.00 |
Overview
Slc25a1 encodes the mitochondrial citrate transporter CTP, an inner membrane carrier that exports citrate/isocitrate to the cytosol in exchange for malate. This flux links the tricarboxylic acid cycle to cytosolic acetyl‑CoA production, supporting de novo lipogenesis, cholesterol biosynthesis, and acetylation-dependent regulation of gene expression, while also influencing redox balance through NADPH-generating pathways. By coordinating mitochondrial–cytosolic carbon transfer, CTP contributes to metabolic adaptation during proliferation and differentiation and can modulate inflammatory and stress-response programs. Dysregulated citrate transport has been associated with inborn errors of metabolism and broader metabolic phenotypes, making Slc25a1 a relevant target for studying mitochondrial metabolism and lipid homeostasis in mouse systems.
CTP CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Slc25a1 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Slc25a1 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 Slc25a1 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 CTP protein expression.
This CRISPR knockout system enables efficient generation of Slc25a1-deficient cell models for investigation of CTP signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Slc25a1 exon(s) critical for CTP 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 Slc25a1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by CTP CRISPR/Cas9 KO Plasmid (m) and CTP CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Slc25a1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by CTP HDR Plasmid (m) and CTP HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Slc25a1 homology arms to support homology-directed repair at defined Slc25a1 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.