SURF-4 CRISPR/Cas9 KO Plasmid (m): sc-423221
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SURF-4 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-4 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 | |
SURF-4 CRISPR/Cas9 KO Plasmid (m) | sc-423221 | 20 µg | $397.00 |
Overview
Surf4 encodes SURF-4, an endoplasmic reticulum (ER) membrane cargo receptor that participates in selective export of secretory proteins from the ER to the Golgi via COPII-dependent trafficking. SURF-4 contributes to proteostasis by regulating ER retention versus forward transport, thereby influencing secretion efficiency and the cellular response to misfolded proteins. In mouse systems, Surf4 function intersects with pathways controlling lipid handling, extracellular protein abundance, and ER stress signaling, making it relevant to studies of metabolic regulation and secretory pathway homeostasis. Perturbation of SURF-4–mediated trafficking is used to model mechanisms linking secretion defects to cellular dysfunction and disease-associated phenotypes.
SURF-4 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Surf4 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Surf4 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 Surf4 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-4 protein expression.
This CRISPR knockout system enables efficient generation of Surf4-deficient cell models for investigation of SURF-4 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Surf4 exon(s) critical for SURF-4 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 Surf4 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by SURF-4 CRISPR/Cas9 KO Plasmid (m) and SURF-4 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Surf4 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by SURF-4 HDR Plasmid (m) and SURF-4 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Surf4 homology arms to support homology-directed repair at defined Surf4 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.