SAMC CRISPR/Cas9 KO Plasmid (h): sc-414066
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SAMC CRISPR/Cas9 Knockout (KO) Plasmid (h) 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 SAMC 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 | |
SAMC CRISPR/Cas9 KO Plasmid (h) | sc-414066 | 20 µg | $397.00 |
Overview
Human SLC25A26 encodes SAMC (S-adenosylmethionine mitochondrial carrier), an inner mitochondrial membrane transporter that imports S-adenosylmethionine into the matrix to sustain mitochondrial methylation reactions. By supplying SAM for RNA, protein, and metabolite methyltransferases, SAMC supports mitochondrial gene expression, oxidative phosphorylation homeostasis, and redox-linked metabolic adaptation. Disruption of mitochondrial SAM transport perturbs one-carbon metabolism coordination between cytosol and mitochondria and can alter mtDNA/RNA processing and respiratory chain function. Variants affecting SLC25A26 activity have been associated with mitochondrial dysfunction phenotypes, making this gene relevant for mechanistic studies of mitochondrial disease biology and metabolic stress responses.
SAMC CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the SLC25A26 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the SLC25A26 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 SLC25A26 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 SAMC protein expression.
This CRISPR knockout system enables efficient generation of SLC25A26-deficient cell models for investigation of SAMC signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting SLC25A26 exon(s) critical for SAMC 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 SLC25A26 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by SAMC CRISPR/Cas9 KO Plasmid (h) and SAMC CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the SLC25A26 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by SAMC HDR Plasmid (h) and SAMC HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by SLC25A26 homology arms to support homology-directed repair at defined SLC25A26 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.