SURF-1 CRISPR/Cas9 KO Plasmid (m): sc-423219
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SURF-1 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 SURF-1 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
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: SURF-1 Antibody (H-7): sc-365159
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SURF-1 CRISPR/Cas9 KO Plasmid (m) | sc-423219 | 20 µg | $397.00 |
Overview
Surf1 encodes SURF-1, a conserved inner mitochondrial membrane protein required for proper assembly of cytochrome c oxidase (complex IV) in the electron transport chain. By coordinating complex IV biogenesis, SURF-1 supports oxidative phosphorylation, mitochondrial membrane potential maintenance, and efficient cellular ATP production. Disruption of SURF1 function is linked to mitochondrial complex IV deficiency and Leigh syndrome–like neurodegenerative phenotypes, highlighting its importance for high-energy tissues. In mouse systems, Surf1 perturbation is widely used to interrogate mitochondrial proteostasis, respiratory chain remodeling, and stress-responsive signaling associated with impaired bioenergetics.
SURF-1 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Surf1 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Surf1 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 Surf1 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 SURF-1 protein expression.
This CRISPR knockout system enables efficient generation of Surf1-deficient cell models for investigation of SURF-1 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Surf1 exon(s) critical for SURF-1 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 Surf1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by SURF-1 CRISPR/Cas9 KO Plasmid (m) and SURF-1 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Surf1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by SURF-1 HDR Plasmid (m) and SURF-1 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Surf1 homology arms to support homology-directed repair at defined Surf1 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.